I know — we’re all tired of the pandemic and we’re all hoping it’d be over by now. But unfortunately, the virus doesn’t really care about media fatigue or how tired we all are of this pandemic.
While substantial progress has been made on the vaccination front, new variants continue to emerge, and researchers warn that the pandemic is still not done yet. Now, a new Omicron variant (BA.2) is surging in several parts of the world, including the US, UK, and Hong Kong.
Researchers warned us from the beginning that until we reach herd immunity at a global level, new variants will continue to emerge and we’d still be stuck in a pandemic — and this is exactly what we’re seeing now. After the more contagious Delta variant came in and swooped over the Alpha and Beta variants, Omicron made it all look like a joke.
The contagiousness math adds up very quickly.
Alpha was 50% more contagious than the original Wuhan strain. Delta is 40-60% more contagious than Alpha. Omicron is 105% more contagious than Delta. Now, the BA.2 Omicron variant appears to be 30% more contagious than the original Omicron, and we’re seeing the number of cases spike accordingly.
The emergence of the new subvariant coincides with a wave of lifting restrictions. Countries (especially those with a relatively high level of vaccination) were quick to relax restrictions and ease the political, social, and economic pressure they were causing — but this has come at a cost.
In the UK, the BA.2 variant has become dominant, and while at some point it seemed that the Omicron wave would simply burn out in the country, we’re seeing a new surge in cases and hospitalizations are starting to follow.
What we know about BA.2 Omicron so far
While it clearly appears to be more transmissible (and will likely become dominant across the world), we still don’t know how severe this subvariant is. Lab experiments from Japan suggest that it may have Delta-like characteristics and may cause more severe illness.
“More importantly, the viral RNA load in the lung periphery and histopathological disorders of BA.2 were more severe than those of BA.1 and even B.1.1. Together with a higher effective reproduction number and pronounced immune resistance of BA.2, it is evident that the spread of BA.2 can be a serious issue for global health in the near future,” a study not yet peer-reviewed concludes.
However, a separate study from South Africa found that a similar proportion of individuals with BA.1 and BA.2 infections required hospitalization, and data from Denmark suggests similar hospitalization rates for BA.1 and BA.2.
As is always the case with new variants and subvariants, it’s hard to tell exactly how things stand in the beginning. It’s also curious that while it seems to be taking over in several parts of Asia and Europe, BA.2 transmission in the US seems relatively low.
Importantly, while Omicron BA.2 shows some ability to evade vaccine immunity, it seems that boosters still provide excellent immunity. Overall, BA.2 shows the already well-known Omicron ability to evade some of the protection offered by two shots — but three shots offer over 90% protection against hospitalization.
Long-term, it seems that booster-provided protection wanes in time, and the rate of booster shot delivery has also slowed down, presumably as people’s interest in the pandemic also wanes. But variants don’t care how much attention you’re paying.
Did we rip the bandaid too soon?
Another reason why BA.2 is spreading so quickly is that many countries have relaxed restrictions — or removed them altogether. Some researchers believe this was done too quickly.
In addition to extra transmissibility, the BA.2 subvariant also appears to be capable of escaping some of the treatments we have for COVID-19. While the original Omicron was capable of evading two of the four monoclonal antibody drugs used in infections in high-risk individuals, a study from New York University suggests that BA.2 can bypass a third drug, sotrovimab.
Researchers also caution that even mild cases can cause lasting brain damage (and potentially other problems as well). A study from Oxford found that the virus produces changes in the brain and may shrink grey matter.
Ultimately, the vast majority of people with booster shots should be able to evade the worst of the virus effects — but they can still be in for an unpleasant ride.
A growing body of evidence has implicated gut bacteria in regulating neurological processes such as neurodegeneration and cognition. Now, a study from Spanish researchers shows that viruses present in the gut microbiota can also improve mental functions in flies, mice, and humans.
They easily assimilate into their human hosts — 8% of our DNA consists of ancient viruses, with another 40% of our DNA containing genetic code thought to be viral in origin. As it stands, the gut virome (the combined genome of all viruses housed within the intestines) is a crucial but commonly overlooked component of the gut microbiome.
But we’re not entirely sure what it does.
This viral community is comprised chiefly of bacteriophages, viruses that infect bacteria and can transfer genetic code to their bacterial hosts. Remarkably, the integration of bacteriophages or phages into their hosts is so stable that over 80% of all bacterial genomes on earth now contain prophages, permanent phage DNA as part of their own — including the bacteria inside us humans. Now, researchers are inching closer to understanding the effects of this phenomenon.
Gut and brain
In their whitepaper published in the journal Cell Host and Microbe, a multi-institutional team of scientists describes the impact of phages on executive function, a set of cognitive processes and skills that help an individual plan, monitor, and successfully execute their goals. These fundamental skills include adaptable thinking, planning, self-monitoring, self-control, working memory, time management, and organization, the regulation of which is thought, in part, to be controlled by the gut microbiota.
The study focuses on the Caudovirales and Microviridae family of bacteriophages that dominate the human gut virome, containing over 2,800 species of phages between them.
“The complex bacteriophage communities represent one of the biggest gaps in our understanding of the human microbiome. In fact, most studies have focused on the dysbiotic process only in bacterial populations,” write the authors of the new study.
Specifically, the scientists showed that volunteers with increased Caudovirales levels in the gut microbiome performed better in executive processes and verbal memory. In comparison, the data showed that increased Microviridae levels impaired executive abilities. Simply put, there seems to be an association between this type of gut biome and higher cognitive functions.
These two prevalent bacteriophages run parallel to human host cognition, the researchers write, and they may do this by hijacking the bacterial host metabolism.
To reach this conclusion, the researchers first tested fecal samples from 114 volunteers and then validated the results in another 942 participants, measuring levels of both types of bacteriophage. They also gave each volunteer memory and cognitive tests to identify a possible correlation between the levels of each species present in the gut virome and skill levels.
The researchers then studied which foods may transport these two kinds of phage into the human gut -results indicated that the most common route appeared to be through dairy products.
They then transplanted fecal samples from the human volunteers into the guts of fruit flies and mice – after which they compared the animal’s executive function with control groups. As with the human participants, animals transplanted with high levels of Caudovirales tended to do better on the tests – leading to increased scores in object recognition in mice and up-regulated memory-promoting genes in the prefrontal cortex. Improved memory scores and upregulation of memory-involved genes were also observed in fruit flies harboring higher levels of these phages.
Conversely, higher Microviridae levels (correlated with increased fat levels in humans) downregulated these memory-promoting genes in all animals, stunting their performance in the cognition tests. Therefore, the group surmised that bacteriophages warrant consideration as a novel dietary intervention in the microbiome-brain axis.
Regarding this intervention, Arthur C. Ouwehand, Technical Fellow, Health and Nutrition Sciences, DuPont, who was not involved in the study, told Metafact.io:
“Most dietary fibres are one way or another fermentable and provide an energy source for the intestinal microbiota.” Leading “to the formation of beneficial metabolites such as acetic, propionic and butyric acid.”
He goes on to add that “These so-called short-chain fatty acids may also lower the pH of the colonic content, which may contribute to an increased absorption of certain minerals such as calcium and magnesium from the colon. The fibre fermenting members of the colonic microbiota are in general considered beneficial while the protein fermenting members are considered potentially detrimental.”
It would certainly be interesting to identify which foods are acting on bacteriophages contained within our gut bacteria to influence cognition.
Despite this, the researchers acknowledge that their work does not conclusively prove that phages in the gut can impact cognition and explain that the test scores could have resulted from different bacteria levels in the stomach but suggest it does seem likely. They close by stating more work is required to prove the case.
Researchers at the University of Washington have developed a new COVID-19 test that has the speed of over-the-counter antigen tests and the accuracy of medical-grade PCR tests.
Dubbed the ‘Harmony’ test, this diagnostic tool looks for the genetic material of the SARS-CoV-2 virus in test samples. However, unlike PCR tests, which can take several hours to produce a result, the Harmony kit can provide a diagnosis in under 20 minutes with high accuracy.
The test was designed to be low-cost and straightforward to use, according to the authors, in a bid to help everyone, from doctors to the public, to better detect and track coronavirus infections.
“We designed the test to be low-cost and simple enough that it could be used anywhere,” said Barry Lutz, a UW associate professor of bioengineering, an investigator with the Brotman Baty Institute for Precision Medicine, and senior author of the paper. “We hope that the low cost will make high-performance testing more accessible locally and around the world.”
The Harmony test uses a “PCR-like” approach to detecting the virus — samples are obtained using a nasal swab and processed with ready-to-use reagents using a series of simple steps. The kit is meant to be used with a low-cost detector that can be operated using a smartphone, which provides the results. Each detector can handle up to four samples at a time.
The team explains that one of their main reasons for designing this test kit was the need for affordable and easy-to-use COVID-19 tests that provide reliable accuracy. Many at-home antigen kits available today test for pieces of the virus, not traces of its genetic material, and are only about 80-85% accurate and may be less accurate with the Omicron strain. PCR (polymerase chain reaction) tests are much better — providing around 95% accuracy — but are slow and cannot be carried out at home, as they require specialized devices and training to process. The Harmony kit is meant to combine the strengths of both of these types of tests.
Preliminary results show that Harmony is 97% accurate for nasal swabs. The test detects three different regions of the virus’ genome to help keep it effective against new strains: if a new variant of the virus develops many mutations in one region, the test can still detect the other two. The Harmony kit can detect the Omicron strain.
The step that makes PCR tests so time- and technology-intensive is a series of a few dozen heating and cooling cycles. Temperatures need to be very accurately controlled during these cycles to maintain the integrity of the sample. The Harmony test uses a similar method, known as RT-LAMP (reverse transcription loop-mediated isothermal amplification), with the key difference being that this doesn’t require the same temperature cycling.
“This test operates at a constant temperature, so it eliminates the time to heat and cool and gives results in about 30 minutes,” said Lutz.
Together with two of his colleagues, Lutz set up a new company for the UW — Anavasi Diagnostics — which will take the Harmony kit from an experimental device to a commercially-available product. The team believes that the kit will first be available for clinics and other medical institutions, then in settings where monitoring for infections is required, such as workplaces or schools. After these needs are met, they will adapt the test for home use.
“For a long time, the options have been either a PCR test that is expensive and typically takes a day or more to get a result, or a rapid antigen test that gives fast results and is low cost, but typically has lower accuracy than a lab PCR test,” said Lutz. “From the first day, we designed our test to be manufacturable at low cost and high volume, while delivering fast results with PCR-like performance.”
“We plan to make our test accessible and affordable throughout the world,” he adds.
The paper “Harmony COVID-19: A ready-to-use kit, low-cost detector, and smartphone app for point-of-care SARS-CoV-2 RNA detection” has been published in the journal Science Advances.
Drug-resistant bacteria are a very concerning, and growing, threat. Now researchers at the Erasmus Hospital, Belgium, are working to recruit viruses in our fight against them.
The researchers report successfully treating an adult woman, who was infected with drug-resistant bacteria, using a combination of antibiotics and bacteriophages (bacteria-killing viruses). Such experiments are the product of several decades’ worth of research into the use of bacteriophages in humans. The results are encouraging and could pave the way towards such viruses having a well-established role in the treatment of drug-resistant bacteria.
The patient had been severely injured by the detonation of a bomb during a terrorist attack. She suffered multiple injuries, including one to her leg, that damaged it down to the bone. After surgery to have some of the tissue removed, she developed a bacterial infection on the leg. The bacteria responsible was Klebsiella pneumoniae, which is known to be resistant to antibiotics. It also creates biofilms that physically insulate affected areas from antibiotics.
Doctors tried to clear the infections, with no success, for several years. Left with no other options to try, her medical team suggested bacteriophage therapy, which they performed with assistance from researchers at the Eliava Institute in Tbilisi.
Bacteriophage therapy is not in medical use today as there are still concerns around the safety of using such viruses to treat humans with already-weakened immune systems, and many unknowns regarding when and how to best employ them.
To employ a bacteriophage in this role, one must be found that attacks the exact strain of bacteria that causes the infection. The researchers carried out a thorough search and testing process, and eventually found a suitable virus in a sample of sewer water. This was then isolated and grown in the lab, mixed into a liquid solution, and applied directly to the site of the infection. At the same time, the patient was put on a heavy antibacterial regimen.
Although it took three years of treatment, the patient is now free of the infection and able to walk again.
The team notes that their results showcase that such approaches can be effective treatment options when other avenues fail. However, they also explain that a better way of finding suitable bacteriophages must be developed before these interventions become viable in a practical sense. It simply takes too much time and effort to perform this search the same way the team did here for hospitals to realistically do this for multiple patients. There are currently no guarantees that a suitable virus will be found even if such a search is performed, as well.
The paper “Combination of pre-adapted bacteriophage therapy and antibiotics for treatment of fracture-related infection due to pandrug-resistant Klebsiella pneumoniae,” has been published in the journal Nature Communications.
After going through the experience of the COVID-19 pandemic, everybody is keen on predicting and avoiding the next big viral threat. New research at the University of Glasgow in the UK is harnessing the power of AI towards that goal.
Machine learning, an approach to data analysis whose goal is to teach machines how to automate certain tasks, could help predict the next zoonosis — a virus that jumps from an animal species to humans. Such pathogens are the most significant drivers of epidemics and pandemics and have been so throughout human history. The coronavirus was, very likely, also a zoonosis, one which jumped to humans from bats.
Manually sifting through all known animal viruses in an attempt to predict zoonosis is a monumental task. We estimate that there are around 1.67 million animal viruses out there, and although just a few should be able to infect humans, the work volume required for this task makes it simply not feasible in practical terms; especially as such predictions require specialized skills and laboratories.
This is where, a new study hopes, machines will come to the rescue.
Let the computer crunch it
“Our findings show that the zoonotic potential of viruses can be inferred to a surprisingly large extent from their genome sequence,” the study reads. “By highlighting viruses with the greatest potential to become zoonotic, genome-based ranking allows further ecological and virological characterization to be targeted more effectively.”
Predicting that a virus is likely to become a threat is not the same thing as actually preventing it from doing so, but it does go a long, long way in helping us prepare. That preparation would, in turn, lead to many lives saved, and much suffering avoided. It would also allow us to better monitor the behavior of particular threats, and focus preventative efforts more effectively.
In order to develop this AI, the team used the genetic sequences — full genomes — of roughly 860 virus species belonging to 36 families. The algorithm was trained to look for patterns in these (human-infecting) viral genomes alongside species-level records of human infection rates. Based on these datasets, viruses were assigned a probability of being able to infect human hosts. Its estimations were then compared to our best models of predicting a virus’ zoonotic potential. The authors used this step to both validate the estimations as much as possible, and to analyze patterns in these estimations across viral families.
“Although our primary interest was in zoonotic transmission, we trained models to predict the ability to infect humans in general, reasoning that patterns found in viruses predominantly maintained by human-to-human transmission may contain genomic signals that also apply to zoonotic viruses.”
Overall, the team reports, there are genetic features that seem to predispose viruses to infecting humans. These are largely independent of their taxonomy (evolutionary relationships to other viral species). Based on the AI’s estimations, they then developed machine learning models tailored specifically to look for these features across known viral genomes. We would still have to test any viral strain flagged by such a system in the lab in order to confirm that it can infect human cells, the author explain, before major resources are devoted to researching them and how to best counter them
This being said, a virus’ ability to infect human cells, by itself, is only one factor of its overall zoonotic potential. How virulent/infectious it is in humans, how easily it transmits between different hosts, and other environmental factors (such as a period of economic downturn or starvation, for example) have a sizable part to play in the formation of pandemics.
“These findings add a crucial piece to the already surprising amount of information that we can extract from the genetic sequence of viruses using AI techniques,” says study co-author Simon Babayan, from the Institute of Biodiversity, Animal Health and Comparative Medicine at the University of Glasgow.
“A genomic sequence is typically the first, and often only, information we have on newly-discovered viruses, and the more information we can extract from it, the sooner we might identify the virus’ origins and the zoonotic risk it may pose. As more viruses are characterized, the more effective our machine learning models will become at identifying the rare viruses that ought to be closely monitored and prioritized for preemptive vaccine development.”
The paper “Identifying and prioritizing potential human-infecting viruses from their genome sequences” has been published in the journal PLOS Biology.
In the past several months, the CDC has touted 20 seconds as the standard for all hand-washing activities, bringing a number of rarely sung happy birthdays, fight songs, and other multiple-second ditties out of the closet as a counter for the time period.
However, studies were short on why exactly 20 is the magic number. Well, now there is one.
Harder, better, faster, washer
In a new report out of the American Institute of Physics published in Physics of Fluids, researchers have created a model which captures the key mechanics of hand-washing. Turns out faster hand movement is better.
By simulating the motion you make when cleaning your hands, researchers estimated the time scales on which particles like viruses and bacteria were removed from your hands. Their model acted in two dimensions, with a wavy surface moving past another with a thin film of liquid separating the two — it’s imperfect but still good enough to get an idea. These wavy surfaces represented hands in their model due to the surface harshness on small spatial scales.
Particles would be trapped on the rough surfaces in wells of the hands, like the bottom of a valley. Vigorous movement and high water pressure would bring the particles to the surface and out of their little valley homes and out of your skin. According to Paul Hammond, author of the report, it turns out that 20 seconds is what he came up with in his model as the time to dislodge these particles from your hands.
“Basically, the flow tells you about the forces on the particles. Then you can work out how the particles move and figure out if they get removed,” said Hammond, who likened the process to scrubbing a stain on a shirt where the faster the motion the more likely it is to remove it. “If you move your hands too gently, too slowly, relative to one another, the forces created by the flowing fluid are not big enough to overcome the force holding the particle down.”
Hammond states that the model does not take into account chemical or biological processes that occur when using soap, but it’s pretty well known across the board that soap only improves the probability that your hands will, in fact, become cleaner.
“These viruses have membranes that surround the genetic particles that are called lipid membranes because they have an oily, greasy structure,” Thomas Gilbert, an associate professor of chemistry and chemical biology at Northeastern University, told the BBC. “It’s this kind of structure than be neutralized by soap and water.”
He explained that the dissolving of the outer “envelope” breaks up virus cells, and the genetic material, which is the RNA that takes over human cells in order to make copies of the virus, is swept away and destroyed because of the chemical or biological agents.
Just knowing how the physics of handwashing works can give us some clues as to how we can create more effective and environmentally friendly soaps, the researcher concludes.
“Nowadays, we need to be a bit more thoughtful about what happens to the wash chemicals when they go down the plughole and enter the environment.”
In the end, there is much more that goes into the story of handwashing, but this study does explain some puzzles and lay the foundation for future research. Truth be told, we’ve learned in the pandemic that we could all use a bit of work on our handwashing.
TPOXX’s effectiveness against smallpox was established by studies conducted in animals infected with viruses that are closely related to the virus that causes smallpox, and was based on measuring survival at the end of the studies. More animals treated with TPOXX lived compared to the animals treated with placebo. TPOXX was approved under the FDA’s Animal Rule, which allows efficacy findings from adequate and well-controlled animal studies to support an FDA approval when it is not feasible or ethical to conduct efficacy trials in humans.
Smallpox, an acute contagious disease caused by the variola virus, was one of the most devastating diseases known to humanity and caused millions of deaths before it was eradicated. It is believed to have existed for at least 3,000 years.
The smallpox vaccine, created by Edward Jenner in 1796, was the first successful vaccine to be developed. He observed that milkmaids who previously had caught cowpox did not catch smallpox and showed that a similar inoculation could be used to prevent smallpox in other people.
The World Health Organization (WHO) launched an intensified plan to eradicate smallpox in 1967. Widespread immunization and surveillance were conducted around the world for several years. The last known natural case was in Somalia in 1977. The WHO declared smallpox eradicated in 1980, but since then many nations have expressed concerns that the variola virus, which causes smallpox, could be used as a bioweapon.
Similar to TPOXX, the FDA also approved Tembexa under its Animal Rule. Human safety data on Tembexa was based on clinical trials involving primarily patients who were treated with the drug after they received hematopoietic stem cell transplants.
In the animal study for Tembexa (brincidofovir), the efficacy was defined by measuring the animals’ survival by the end of the studies. Results demonstrated that more animals with smallpox who were treated with brincidofovir survived compared with animals who were treated with the placebo.
Not to make anyone feel uneasy after this whole pandemic thing, but a new study says there’s another viral threat looming on the horizon.
An international team of researchers is drawing attention to the fact that the Middle East respiratory syndrome (MERS-CoV), could mutate to become a global problem quite easily. While MERS has caused issues in the past and was highly lethal, it didn’t seem to be able to jump from one human to another, which limited its impact.
However, such an ability could be only a few mutations away for the virus. One subfamily of the virus is already able to infect humans, but luckily, it is still isolated from the main group. However, if these two were to come into contact, MERS could start the next pandemic.
Just one unlucky break
Pandemics, or the plagues of yore, usually start from zoonoses. These aren’t noses that like zoos at all. Rather, they’re pathogens that specialize in infecting animals but evolved to also infect human beings, at one point or another. Historically speaking, livestock is the main source of zoonoses, and the reason plagues used to ravage medieval Europe, where people and animals used to live in tight proximity with poor hygiene. Another element that makes zoonoses so dangerous is that, being a ‘new’ pathogen to humans, virtually nobody has any natural defenses against them.
SARS-CoV-2 was also a zoonosis, most likely originating from bats. The speed and ferocity with which the virus spread across the world, and the devastating effects it had on patients, are tragic reminders of just how dangerous such pathogens can become. But it’s not the only virus out there, not by far. Its big break, so to speak, what set it apart from other animal-borne viruses, was that it evolved the ability to infect a human cell — probably by accident.
MERS-CoV, a virus first seen in 2012 in Saudi Arabia, also has the potential to follow in its footsteps, according to a new study. During its initial outbreak, MERS killed around 40% of the patients it infected. However, it’s unlucky break was that it couldn’t pass from one person to another. Analyses at the time showed that virtually all cases of infection originated from dromedaries (camels). These animals, in turn, likely got it from bats.
Despite its lethality, the MERS outbreak remained a footnote of history, as it remained quite small in scope. Testing since then also seems to indicate that the danger is passing, as around 80% of the dromedaries tested so far — 70% of which live in Africa — have antibodies against the virus in their blood.
But, in a bid to find out why this virus didn’t infect many more people — especially curious considering how many dromedaries there are around, and how often people in Africa and Saudi Arabia interact with them — an international team of researchers took samples of the virus from multiple sites across the Middle East and Africa. Their goal was to identify and isolate individual strains (‘variants’) of the virus.
Those from Africa and the Middle East were separated into different clades, and were then compared from a genetic standpoint, and under lab conditions, using cultures of human lung cells. To their surprise, they found that African clades wouldn’t readily infect human cells. Those in the Arabian clade, however, would.
It all comes down to differences in the amino acids each clade uses in a particular protein — the S, or ‘spike’ protein. The team showed that African clade variants engineered to have the same amino acids in this protein as the Arabian clade had a much easier time infecting human cells.
One possible explanation for the difference between these two clades is that dromedary trade is “virtually one-way”, from Africa to the Middle East. In essence, this means that changes in the Arabian clade can’t percolate back into the African one, even if African clades do come into contact with Arabian ones. If the trade was to be reversed, however, or if a carrier animal makes its way back to Africa, the local population of viruses could become highly infectious to humans, sparking a new and deadly pandemic.
The paper “Phenotypic and genetic characterization of MERS coronaviruses from Africa to understand their zoonotic potential” has been published in the journal Proceedings of the National Academy of Sciences.
New research at the University of Zurich (UZH) points the way towards a new type of anti-tumor treatment. This, they hope, will help protect patients from the side effects of cancer therapy.
Tumors are notoriously tricky to eliminate. The new approach, therefore, involves using our own bodies to produce therapeutic compounds at the tumor’s exact location. This should dramatically limit the negative side effects of traditional interventions because, unlike chemotherapy or radiotherapy, this approach does no harm to normal healthy cells. In fact, this approach could, potentially, also be used for targeted delivery of medicine against COVID-19 directly to the lungs.
It all revolves around a genetically-modified respiratory virus (an adenovirus, to be exact) which delivers genes encoding anti-cancer and signaling compounds directly into tumor cells. Here, they cause the cells to produce the very substances that destroy them, as well as chemical signals such as cytokines, which tells our immune system that the tumor is a target.
“We trick the tumor into eliminating itself through the production of anti-cancer agents by its own cells,” says postdoctoral fellow Sheena Smith, who led the development of the delivery approach.
“The therapeutic agents, such as therapeutic antibodies or signaling substances, mostly stay at the place in the body where they’re needed instead of spreading throughout the bloodstream where they can damage healthy organs and tissues” adds Andreas Plückthun, who led the research effort.
The team christened their new approach SHREAD: SHielded, REtargetted ADenovirus. It draws on the previous work of the same team, including ways to guide the virus to particular areas of the body, as well as methods to hide them from our immune system.
In order to test their approach, the authors used SHREAD to induce a breast tumor in the mammaries of a lab mouse to produce trastuzumab, a clinically approved breast cancer antibody. In a few days, levels of the antibody inside the tumor itself were higher than they could have been if they were injected directly. At the same time, they were significantly lower in the bloodstream and other tissues compared to what’s seen with direct injections — this helps reduce side effects.
The team used high-resolution 3D imaging methods and tissues rendered totally transparent to see how the antibody creates pores in blood vessels of the tumor and destroys tumor cells from the inside out.
One of the best parts of this approach is that it’s not limited only to cancer. The authors explained that by insulating healthy tissues from significant levels of an active substance, it also opens the door for other therapies. For example, it makes it possible to more easily use ‘biologics’, a family of protein-based drugs. If administered using a traditional injection, such biologics would be too toxic for use, they explain.
The team is currently working on applying SHREAD to anti-COVID-19 therapies.
“By delivering the SHREAD treatment to patients via an inhaled aerosol, our approach could allow targeted production of COVID antibody therapies in lung cells, where they are needed most,” Smith explains. “This would reduce costs, increase accessibility of COVID therapies and also improve vaccine delivery with the inhalation approach.”
The paper “The SHREAD gene therapy platform for paracrine delivery improves tumor localization and intratumoral effects of a clinical antibody” has been published in the journal PNAS.
The COVID-19 pandemic caught the world off guard, showing just how woefully unprepared we are against spillovers of zoonotic viruses. But that doesn’t mean we weren’t warned. There are over 500,000 animal viruses that have the potential to cross to humans, and for decades, scientists have been calling the alarm that human activity is increasing the risk of spillover.
“It is highly likely that future SARS or MERS-like coronavirus outbreaks will originate from bats, and there is an increased probability that this will occur in China.” Sounds familiar? That’s the conclusion of a study published in early 2019 that was eerily prescient, and it’s not even the only study to come with this type of warning.
The rest, as they say, is history. The evidence so far indicates that SARS-CoV-2 is a wildlife spillover, with the virus originating in bats in China. Bats go out foraging and have numerous encounters with other animals, such as pangolins, badgers, pigs, and many others. Ultimately, the virus crossed to humans.
One good thing about this pandemic is that there is now an enormous amount of public support for measures meant to contain and avoid new outbreaks — although there’s a good chance this will decline as the imminent threat subsides. With this in mind, researchers at the University of California, Davis, have released a new web app called SpillOver, which ranks hundreds of wildlife viruses by their spillover risk.
“Our tool aims to rank the risks of spillover from newly-discovered viruses. Sadly, the risk of new diseases and another epidemic and pandemic resulting from human behaviors at high-risk transmission interfaces are high if we don’t act now. The tool allows you to create a personalized watchlist for a specific country or type of virus, etc. so that we can be prepared for the next one and help to stop it before human casualties or at least control it at the source,” Jonna Mazet, Professor of Epidemiology and Disease Ecology at the UC Davis School of Veterinary Medicine, told ZME Science.
The ranking is based on data collected from a myriad of sources, including new viruses first detected by PREDICT, a USAID project launched in 2009 designed to assess emerging pandemic threats. Hundreds of scientists and public health experts have already contributed to the database. Crowdsourcing is still available as any scientist can add data to existing viruses or assess the risk of new viruses using the ‘Rank Your Virus’ application in the tool.
Each of the 887 animal viruses compiled in SpillOver, most of which were new to science at the time of inclusion, has a risk score. Those with the highest risk are known zoonotic viruses that have already spilled over from wildlife to humans. For instance, SARS CoV-2 that causes COVID-19 ranks second, between the Lassa and Ebola viruses.
Why would the COVID-causing virus rank lower than Lassa, a virus that causes hemorrhagic fever and kills only 5,000 people a year? That’s because key information about SARS-CoV-2 is still missing, such as the number and range of its host species, which might paint a more accurate picture of the spillover risk for this species of coronavirus.
“SARS-CoV-2 was not discovered until it made people sick. That is the problem that we are trying to solve. We have all of the technology and scientific information we need to safely identify viruses and their transmission risks before they spillover, the world just needs the political will to act,” Mazet said.
Close to the top of the list, there are also newly identified viruses that have yet to spill over, but which nevertheless have a higher risk of becoming zoonotic than some known viruses. Unsurprisingly, many of them are coronaviruses, including a novel coronavirus provisionally named PREDICT_CoV-35, which ranks in the top 20.
It is in identifying such new viruses that have yet to spill over from bats or other animals to humans but have the potential to do so that the tool shines. By highlighting the riskiest viruses, experts can then perform further investigations and local authorities that can enact urgent measures meant to contain any possible viral leak to humans. It’s not too different from risk assessments used by banks and insurance companies to make informed decisions. As the ongoing pandemic has tragically shown, keeping an eye on other viruses like it could mean the difference between a normal life and a new pandemic — maybe even worse than this one.
“The biggest moments were often the most tragic ones — helping countries respond to more than 50 outbreaks of mystery diseases and terrible ones, like Ebola. Of course, the COVID19 pandemic has been the most devastating, but also illustrates the need for information on viruses in advance of spilling over, which is exactly what this tool aims to help us do: be prepared for Disease X,” Mazet said.
Using the open-source tool, anyone can compare and contrast the viruses included in the list. You can also filter the viruses based on certain attributes, such as viruses species, host species, and country of the first detection. Hundreds of scientists have already contributed to SpillOver’s database, and many more are welcome to do so. The more accurate the risk estimates for each virus, the better we can then prioritize efforts meant to contain them.
“We designed the tool to create and evolve the watchlist of newly-detected viruses that have not yet been recognized to cause disease in people but have spillover potential, just as SARS-CoV-2 did before the pandemic began. Identifying the risks associated with new viral discoveries is critical to protect us in the future. So far, we can say that the most life-saving change will come if we alter our behavior near and with wildlife and limit impacts to wildlife habitat to most quickly reduce spillover transmission risk,” Mazet concluded.
Hope against HIV, the human immunodeficiency virus, is closer than any time before. A new vaccine against this virus has shown promise in Phase 1 trials, leading to the production of efficient antibodies in 97% of participants.
HIV and AIDS, the condition it causes, are undoubtedly some of the most terrifying medical diagnoses one can hear today. Not only the horrendous symptoms, but also the fact that they’re incurable, make them so. But perhaps not incurable for much longer, as new research shows a promising way forward against this deadly disease and the pathogen that causes it.
Immunity at last
“We and others postulated many years ago that in order to induce broadly neutralizing antibodies (bnAbs), you must start the process by triggering the right B cells – cells that have special properties giving them potential to develop into bnAb-secreting cells,” explained Dr William Schief, a professor and immunologist at Scripps Research and executive director of vaccine design at IAVI’s Neutralizing Antibody Center, where the vaccine was developed.
“In this trial, the targeted cells were only about one in a million of all naïve B cells. To get the right antibody response, we first need to prime the right B cells. The data from this trial affirms the ability of the vaccine immunogen to do this.”
This vaccine, the product of a collaboration between the Scripps Research institute and non-profit IAVI draws on a novel vaccination approach to help patients develop antibodies against HIV. This approach involves triggering “naive B cells” in our bodies to produce broadly neutralizing antibodies that, in turn, fight the pathogen. It is hoped that these ‘bnAbs’ can attach to proteins called spikes alongside the surface of the HIV virus. These spikes stay very similar in structure and function across different strains of the pathogen, meaning the vaccine could be broadly efficient against it.
This ability to function across strains is a major selling point of this vaccine. HIV affects over 38 million people worldwide but a cure has not yet been forthcoming because the virus has a very fast mutation rate, meaning it can adapt to our immune system and traditional treatment approaches.
The vaccine is meant to be the first in a multi-step vaccination program that aims to coax our bodies into producing a wide range of bnAbs’s, potentially helping against other viruses that have been eluding us so far, according to Europeanpharmaceuticalreview.
The Phase 1 trial included 48 healthy adults who received either a placebo or two doses of the vaccine compound along with an adjuvant developed by GlaxoSmithKline. By the end of the trial, 97% of the participants in experimental groups (i.e. that didn’t receive a placebo) had the desired type of antibody in their bloodstream.
This is the first time we’ve been successful in inducing secretion of broadly-neutralizing antibodies against HIV, the team explains, with lead investigator Dr. Julie McElrath, senior vice president and director of Fred Hutch’s Vaccine and Infectious Disease Division calling it “a landmark study in the HIV vaccine field”.
“This study demonstrates proof of principle for a new vaccine concept for HIV, a concept that could be applied to other pathogens as well,” says Dr Schief.
“With our many collaborators on the study team, we showed that vaccines can be designed to stimulate rare immune cells with specific properties and this targeted stimulation can be very efficient in humans. We believe this approach will be key to making an HIV vaccine and possibly important for making vaccines against other pathogens.”
Needless to say, since this was only a Phase 1 trial, we’re still a considerable way away from seeing this vaccine in a shot. However, the results do pave the way towards a Phase 2, and (hopefully) a Phase 3 for the drug. For the next step, the team is going to collaborate with biotechnology company Moderna to develop and test an mRNA-based vaccine for the same task as their current compound — if successful, this would considerably speed up the process.
Still, for now, the compound works as a proof of concept. It shows that our immune systems can be primed and prepared to face even terrifying pathogens. “This clinical trial has shown that we can drive immune responses in predictable ways to make new and better vaccines, and not just for HIV. We believe this type of vaccine engineering can be applied more broadly, bringing about a new day in vaccinology,” concludes said Dr. Dennis Burton, professor and chair of the Department of Immunology and Microbiology at Scripps Research, scientific director of the IAVI Neutralizing Antibody Center and director of the NIH Consortium for HIV/AIDS Vaccine Development.
The same approach can also be used to try and create new vaccines for other stubborn diseases like influenza, dengue, Zika, hepatitis C, and malaria, the team adds.
The higher COVID-19 infection rates seen in black American communities compared to the overall averages could come down, at least in part, to their daily commute, a new paper explains.
We all felt the pressure that the pandemic has placed on our lives, but some of us have been having a way harder time than others. Sure, nobody likes being stuck inside for days on end, but we have to admit that it’s a luxury, and a privilege, for that to be our main gripe in a global pandemic that killed many thousands.
Minorities and poorer communities have borne the brunt of the hardship. We don’t know for sure exactly why, but it’s not hard to intuit how a lack of resources, poor socio-economic prospects, and social marginalization play into this. A new study comes to flesh out our understanding of these mechanisms by uncovering the role daily commuting patterns play in spreading the coronavirus through black American communities.
“The study suggests that taking into account daily commuting patterns of a social or ethnic group can be enough to explain most of the differential incidence of COVID-19 in African American communities during the first epidemic wave last year,” says Aleix Bassolas, Postdoctoral Research Assistant at Queen Mary.
The team used US census data from over 130 metropolitan areas to put together two types of geographical network. The connections between bordering census areas, together with commuting graphs, were used to chart the flow of people coming to and from their jobs across the nation. Their results suggest that coming into contact with other ethnic groups at their workplace or during their commute can account for the documented “infection gap” in society.
The higher than average incidence of COVID-19 recorded in black communities can be explained through this mechanism, the team notes. Predominantly-black communities in the US are some of the nation’s poorest and thus hardest-hit by the pandemic. For many of their members, sitting it out in quarantine simply isn’t an option, and they have to take a job outside of the home to keep families fed and rent paid.
In some areas of the U.S., COVID-19 incidence among such communities can be up to 5 times higher than the overall societal average. Previous research has shown that socio-economic factors can explain part of this infection gap, but not all of it.
In their study, the authors considered the effect that residential segregation (that people tend to live in areas where their ethnicity is the majority) and other forms of segregation such as commuting have on spreading or containing the disease. This was mediated by the groups’ diffusion segregation, which estimates how likely any group is to come into contact with groups of other ethnicities. A weekly tally of known COVID-19 cases during the early days of the pandemic was used to test the findings.
Strangers on the train
Random routes were simulated over the commuting graphs the team put together, which aimed to determine how long it would take for a person from a census tract to encounter individuals from another ethnic group for the first time. This approach showed that black Americans were the most exposed to other ethnicities — in essence, they’re the group most likely to come into contact with any of the other groups.
Later on in the pandemic, as restrictions on movement began to be implemented on a larger scale, public transport usage started to correlate strongly with the infection gap observed in different US regions.
The team also notes that diffusion segregation alone could explain the observed infection gap relatively well, while factors such as life expectancy or access to healthcare services had more of an influence on the disproportionately high CODIV-19 death rates seen in black communities.
“Our results confirm that knowing where people have to commute to, rather than where they live, is potentially much more important to curb the spread of a non-airborne disease,” says Dr. Vincenzo Nicosia, Lecturer in Networks and Data Analysis, at Queen Mary and corresponding author of the paper.
“Policymakers need to take into account specific mobility patterns and needs, as well as differences in the mobility and commuting habits of different ethnic and social groups when deciding on the most effective non-pharmaceutical countermeasures against COVID-19 and similar non-airborne diseases.”
The approach used here can easily be applied to other countries such as the UK, but it’s dependent on them having quality, detailed records of commuting data. Not every government has access to those, they explain.
The paper “Diffusion segregation and the disproportionate incidence of COVID-19 in African American communities” has been published in the Journal of the Royal Society Interface.
Most bats do not have rabies. According to the US Centers for Disease Control and Prevention (CDC), even among bats submitted for rabies testing, only about 6% had rabies. Rabies can only be confirmed in a laboratory but any bat that is active by day or is found in a place where bats are not usually seen like in your home or on your lawn or attic could be rabid. A bat that is weak and unable to fly could potentially be sick.
A man died of rabies in Limoges, in southwest central France, most probably after being bitten or scratched by a bat, as reported recently by the Institut Pasteur. This is a first in mainland France. The sixty-year-old succumbed to encephalitis, an inflammation of the brain of unexplained origin, in August 2019. A partnership established between the Necker hospital and the Pasteur Institute, aimed at identifying the causes of undocumented encephalitis, led to the genetic analysis of post-mortem samples. These analyzes at Necker Hospital in Paris showed that he had contracted a lyssavirus, European Bat LyssaVirus type 1 (EBLV-1), sheltered by bats.
“This shows that there are cases of rabies that we can miss”
“It is thanks to this retrospective diagnosis that this case was brought to light. This shows that there are cases of rabies that can be missed, ” explained Laurent Dacheux, deputy head of the national reference center for rabies at the Institut Pasteur.
“The trace of this virus was identified at that time, in November 2020. In the midst of the coronavirus , and this discovery went unnoticed”, continues Laurent Dacheux. This exceptional case was finally mentioned in a popular science article on the Mesvaccins.net site and highlighted by the regional daily Le Populaire du Center .
In contact with bats
“It has been thirty-five years since a death of this type has occurred in the world. And in mainland France, this is indeed a first,” assures Laurent Dacheux.
In 2019, a 21-year-old man died of rabies after coming into contact with a bat on Vancouver Island in the Canadian province of British Columbia. Health official Bonnie Henry confirmed that the man came into contact with a rabid bat in mid-May, began showing symptoms six weeks later, and died in July 2019.
Why don’t people get the rabies vaccine?
Rabies is a fatal disease. Each year, tens of thousands of people are successfully protected from developing rabies through vaccination after being bitten by an animal like a bat that may have rabies.
In some cases, people who died of rabies knew they were bitten by a bat. They did not go to a doctor to seek medical help because they were not aware that bats can have rabies and transmit it through a bite. In other cases, it is also possible that young children may not fully awaken due to the presence of a bat (or bite) or may not report a bite to their parents. Most bats have small teeth which may leave marks that can disappear quickly.
Which animals can be infected with rabies?
Any mammal can contract rabies. Rabies is most often reported in mammals that tend to come in contact with humans or live near human settlements, including bats, raccoons, skunks, and foxes. Cases of rabies have also been reported in deers, woodchucks, mongoose, opossums, coyotes, wolves, and monkeys. Pets and domesticated animals that are mammals can easily get the disease if bitten by another animal that is already infected. Cases in pets and other domesticated animals have been reported in dogs, cats, cows, horses, and rabbits.
If you are bitten by an animal – or if infectious material (such as saliva) from an animal gets into your eyes, nose, mouth, or a wound – it is important to wash the affected area thoroughly with soap and water and get medical advice immediately. Whenever possible, the animal should be captured and sent to a laboratory for rabies testing.
No other year in living memory has been as heavily influenced by a virus as 2020. But what exactly are viruses, what makes them tick, what about them made us all put our lives on hold?
The short of it is that viruses are biological machines, supremely well-adapted to a single survival strategy. And this strategy is quite simple — viruses find living cells, infect them, and hijack their biochemical machinery to reproduce. They’ve done away with (or perhaps never developed in the first place ) anything that doesn’t directly help them perform that task, all the way down to the most fundamental traits of living organisms: viruses aren’t really alive, but they’re not not-alive either.
Their simplicity works to make viruses easy to ‘build’ (so they’re plentiful) and hard to detect and destroy. In fact, we still have very few reliable medicines against viruses (they’re known as ‘antiviral’ compounds), and they often only work on particular kinds or lineages of viruses. We’ve managed to put a man on the moon and put stars inside a bomb, but for all our achievements, humanity’s best defense against these pathogens is still our own bodies and immune systems. This becomes a bit scary when you consider that viruses very definitely outnumber any and all living things on the planet.
But I’m getting ahead of myself. Let’s start from the beginning:
General viral structure
Viruses are acellular. This means they are not made from cells nor do they have a cellular structure. This also means that all those fancy components you may or may not have learned about in cellular bio 101 — organelles, plasma membranes, ribosomes, etc — have nothing to do with a virus. They’re also exceedingly tiny, typically around 20–300 nanometers in diameter, though a few are larger. To put things into perspective, if a bacterium was the size of a soccer field, a virus would be around the size of three soccer balls put side-by-side. An animal cell would be the town around it.
One such pathogen (an individual, fully-assembled virus is referred to as a ‘virion’) is about as simple a biological machine as you can make and still have it work. They include a core that houses their nucleic acid (genetic material), an outer coat of proteins or ‘capsid’, and that’s pretty much it. That’s all you need to make a working virion. However, some fancier models can have additional features, such as an outer membrane shamelessly stolen off a host cell, different proteins (or glycoproteins) that can help them infect targets, or other structural elements. Capsids are constructed from proteins known as capsomeres. Them, alongside any membrane viruses have, typically tend to be peppered with glycoproteins that serve as binding or access keys into certain cells.
By and large, viruses are classified into one of four groups based on their structure: filamentous, isometric (or icosahedral), enveloped, and head and tail. We’ll be getting to them in a second. One interesting characteristic of viruses is that across all strains, their complexity seems to be in no way related to the complexity of their hosts. The most complex and intricate structures we’ve seen in viruses belong to bacteriophages, pathogens that infect bacteria (which are the simplest living organisms).
What shape a virion takes, as well as the presence or absence of an envelope, has little bearing on what species it can infect and what the symptoms would be, but they’re still very useful classification criteria because they’re relatively easy to check.
The shape and size of viruses tends to be consistent among different lineages, and quite distinctive for each.
Filamentous viruses have long, cylindrical bodies; plant viruses often employ this shape, including the TMV (tobacco mosaic virus). Icosahedral or isometric viruses look pretty much like spheres, or spheres with flattened faces. They get their name from the icosahedron, a polygon with 20 faces (like the dice you use in Dungeons and Dragons), although they don’t necessarily have to have that exact shape. One icosahedral virus you may know personally is the rhinovirus (which causes the common cold). Enveloped viruses have a membrane that surrounds their capsid, which is produced from bits of a cell’s membrane modified with viral proteins. The HIV virus is an enveloped virus, as most animal viruses tend to be. Finally we have head and tail viruses, which have a ‘head’ similar to icosahedral viruses and a ‘tail’ that resembles filamentous ones — they often infect bacteria.
Filamentous viruses are also known as ‘helical’, as their capsomers are arranged around a coil of genetic material, forming a helix. Them, alongside icosahedral viruses are sometimes called ‘simple’ viruses, while head and tail ones (or other shapes) are known as ‘complex’ viruses.
The presence of a membrane can help facilitate infection and provide protection against the host’s immune system (as it’s made from pilfered parts of cells). Enveloped viruses tend to rely completely on their membrane for infection. Its glycoproteins exploit cells’ natural pathways through the membrane to allow infections. They act as ‘keys’ to the protein ‘locks’ that are typically employed to allow nutrients or other elements through the lipid layers of the membrane. But through this, they become vulnerable to inactivation by compounds that interact with fats, such as soap. This is the case for the coronavirus, for example, which is why handwashing is so effective against it.
All of this is very swell, to be sure, but why are viruses so interested in getting inside cells? So glad you asked — here’s why:
The viral life cycle
The central idea to keep in mind here is that viruses aren’t technically alive. They have some of the trappings of living things — genetic material, they’re made of organic matter — but they also lack most essential elements of life, most notably the ability to reproduce by themselves. But that’s all fine and dandy, as far as viruses are concerned, because everyone else can do it for them.
Think of viruses as weaponized USB sticks. For the most part, they’re inert. Viruses have no metabolism, they don’t expend energy, they don’t move on purpose and they don’t chase their prey. They just float around, and every infection begins with a random encounter between a virus and a host. Once they make contact with an appropriate cell, a six-step process unfolds: attachment, penetration, uncoating, replication, assembly, and release.
Attachment and penetration are pretty self-explanatory. They involve the virion coming into contact with and attaching to the host cell, and the subsequent penetration through its membrane. Attachment is governed by the type of binding proteins on the capsid and the transfer proteins on the cell wall — if they’re compatible, the process can unfold. Penetration involves the transfer of viral genetic material through the membrane, which leaves the capsid outside the cell; in this step, the virion basically injects its genetic data into the host cell. Note that some enveloped viruses use other tricks to get inside the cell, most notably by fusing their membranes with that of the cell or tricking it into eating the virus. Once inside, the capsid degrades and the genetic material is released, representing the Uncoating phase.
In regards to this genetic data, first know that it can be either DNA or RNA (some virions that carry RNA are known as ‘retroviruses’). Viruses can carry single or double strands of DNA (‘ssDNA’ or ‘dsDNA’ viruses respectively) or RNA (‘ssRNA’ or ‘dsRNA’). Single strands can be either sense or antisense. Sense strands are those used actively as instructions to create proteins (messenger RNA, or ‘mRNA’), while antisense RNA are their mirror complementaries and serve as a template to create strands of mRNA.
Now, the moment we’ve all been waiting for: what does this genetic material encode? Well, the complete information on how to build the virus, naturally! Once the viral material enters the cell, it will hijack its ‘code’ to make it produce more viral genetic material, capsid elements, and anything else that is needed to Replicate the original virus. DNA viruses typically use a cell’s biochemical machinery to create more DNA (for the new viruses) that is then transcribed into mRNA, and this mRNA is used to start protein synthesis. RNA viruses use their genetic code as a direct template for more RNA (for the new viruses) and mRNA that is consumed in protein synthesis. Retroviruses such as HIV contain RNA that must first be copy-pasted into the host’s DNA — but they also have the right protein, ‘reverse transcriptase’, for the job.
If a cell lacks the know-how required to build these various elements, the viral genome instructs it on what needs to be done. This is best exemplified by retroviruses. Reverse transcription or retrotranscription involves turning a strand of RNA into a double-strand of DNA which is then inserted into the host genome; in very broad lines, it’s reverse-engineering, like creating a full blueprint on how to build a car by just looking at the car. Very nifty. Bacteria and cells do use reverse transcription, but typically for what could be considered data maintenance work. It’s unclear whether this is a natural ability of all cells or if it was inherited from ancient viruses that grafted the needed genes into their hosts (which goes to show that viruses can be a driver of evolution).
The bits and pieces that the cell creates will spontaneously self-Assemble into new virions inside the cytoplasm. Finally, they Release (or ‘egress’) out of the cell. Exactly how this takes place varies from strain to strain. Some viruses (especially enveloped ones, including HIV) gradually exit the cell through budding — a process through which they also gain their membrane covering — which keeps the host cell alive. Most commonly, however, virions are released when the cell is so full of viruses that it bursts open (and dies in the process).
Lytic vs Lysogenic
Now, viruses may seem evil, but they’re not out to kill you. In fact, they will occasionally put in the effort to not hurt their host, especially during times when prey cells are rare and harder to find.
The process of a cell ripping apart, the breaking down of its membrane, is known as ‘lysis’. Under normal circumstances, virions follow the lytic cycle, which is the one described above that ends in the death of the cell. Such an event sees several hundred virions released from the dying cell, around 100 to 200 individual particles, as a rule of thumb.
The lysogenic cycle is a bit more covert — it produces something known as a ‘temperate’ or ‘non-virulent’ infection. Through the lysogenic cycle, a virion lies dormant and hidden inside the host cell genome, waiting for the right time to strike. During this time, it uses inhibitor genes so that the host cell doesn’t read the viral information, leaving it free to hang around unimpeded. The cell also profits by gaining immunity from reinfection with the same virus.
But when the cell experiences some kind of stressor (such as exposure to UV light or chemical agents) that weaken these inhibitors, its automatic DNA-repair systems detect the intruder, activate, and cut it out of the genome. After this point, the viral genetic material activates and the steps of replication, assembly, and release resumes as per normal conditions, and the infection spreads.
Why are viruses a thing?
We don’t really know. They’re too simple for us to reliably extract information on their evolutionary history from them. They’re not exactly alive, but they can and do evolve and mutate when reproducing in cells. They also have an annoying habit of copy-pasting genes from and onto their hosts, which further muddies the waters.
What we do know is that they are the single most successful group on the planet. A paper published in the journal Nature in 2011 puts their immense scale into perspective. Although it cautions that these estimates are “mostly based on ‘back of the envelope’ calculations and should therefore be viewed as they were intended: ballpark figures aiming to inspire”, they’re still no less impressive.
“If all the 1 × 1031 viruses on earth were laid end to end, they would stretch for 100 million light years. Furthermore, there are 100 million times as many bacteria in the oceans (13 × 1028) as there are stars in the known universe. The rate of viral infection in the oceans stands at 1 × 1023 infections per second, and these infections remove 20–40% of all bacterial cells each day.”
“There are about 200 megatonnes of carbon in viruses in the ocean, which is equal to about 75 million blue whales,” explains Curtis Suttle, a Distinguished University Scholar and Professor at the University of British Columbia in another paper. “In fact, in a litre of coastal seawater there are more viruses than there are people on the planet.”
“If aliens randomly sampled Earth they would see a planet dominated by microbial life, most of which would be viruses,” Suttle adds. “On average, there are about 10 million viruses and a million bacteria per litre of seawater or freshwater. If we compare the number of viruses in the oceans to the number of stars in the universe, there are about 1023 stars in the universe [and] about 10 million-fold more viruses in the ocean.”
These numbers showcase why humanity can never truly hope to ‘defeat’ viruses — it hasn’t ever been an option. But one of the best, and perhaps most chilling ways to illustrate this is the legacy viruses have left in us.
Viruses have, to the fullest extent of the word, become a part of us. It’s estimated that around 8% of the genome of modern humans is viral, meaning it has been passed from a virus into a cell, down through the generations, and we still carry that around. By contrast, only between 1% and 2% of our genome was inherited from the Neanderthals.
We are more ‘virus’ than we are our closest relatives.
“What we learn from our study is that, in general, viruses have major roles in driving evolution,” one researcher explained. “In the long-term, viruses have positive impacts to our genome and shape evolution.”
While the general principles of evolution are fairly straightforward, the details behind the process is immensely complex. What if someone told you, for instance, that viruses help fine-tune evolution; that these dreaded organisms that aren’t really organisms can help push the survival of a species? As weird as it sounds, that’s one takeaway from the two studies published by the Cincinnati Children’s Perinatal Institute and at Azabu University in Japan.
The scientists looked at lab mice and human sex cells, or to be more precise, at the germline cells — the cells that form the egg, sperm, and the fertilized egg that pass on their genetic material to the progeny (offspring).
Specifically, they looked at the set of all RNA of these sex cells, something called transcriptomes.
These transcriptomes contained either the male or the female half of chromosomes passed on as genetic materials when species mate. In other words, they define the unique character of sperm and egg as they pass on genetic information to the next generations.
The two published papers look at some of the processes behind these transcriptomes. Satoshi Namekawa, principal investigator on both papers, combined biological testing of mouse models and human germline cells with computational biology to see how genes are produced and reorganized following sexual reproduction. He found that a key element in this process is something called super-enhancers.
“One paper, Maezawa and Sakashita et al., explores super-enhancers, which are robust and evolutionally conserved gene regulatory elements in the genome. They fuel a tightly regulated burst of essential germline genes as sperm start to form,” Namekawa said.
Super-enhancers are regulated by two molecules that act as gene control switches. This is where the second study comes in, Namekawa explains.
“The second study, Sakashita et al., involves endogenous retroviruses that act as another type of enhancer – gene regulatory elements in the genome – to drive expression of newly evolved genes. This helps fine tune species-specific transcriptomes in mammals like humans, mice, and so on.
Endogenous retroviruses are normal components of the human genome and account for around 8% of our DNA — in fact, they account for over 5% of many mammals’ DNA. Also referred to as “jumping genes”, these retroviruses have traditionally been considered threats because they can disrupt some genes. However, over the past few decades, researchers have found that these viruses can actually act as regulatory elements for our genome.
This is exactly what Namekawa and colleagues have found. Endogenous retroviruses can help fine-tune transcriptomes, essentially helping a species’ evolution and diversity.
Super-enhancer switching drives a burst in gene expression at the mitosis-to-meiosis transition, Nature Structural & Molecular Biology, DOI: 10.1038/s41594-020-0488-3
Several months ago, an interesting correlation emerged: countries that had a mandatory BCG vaccine for tuberculosis seemed to have lower mortality rates from the coronavirus.
Some researchers interpreted this as a potential protective effect offered by the vaccine, while others only saw it only as a “shred of evidence.” Now, a peer-reviewed study adds more evidence to the idea that the tuberculosis vaccine could help protect against COVID-19.
It’s already been over half a year since mankind started battling the dreaded novel coronavirus — and the fight is far from over. But, as time passes, we are at least learning more and more about the virus and how we can become more resistant against it.
We’re dealing with a very unusual pathogen and in many ways, it’s not behaving as we anticipated. For instance, it’s puzzling why some developing countries seem to have lower mortality rates than some developed countries, which presumably have better health systems.
There are several differences that could help explain that discrepancy (such as lower average age or simply that developing countries are doing a poorer job at data gathering), but one theory suggests something else might also be at play: the BCG vaccine, used against tuberculosis.
The BCG vaccine was first introduced in 1921, and it is now on the World Health Organization’s List of Essential Medicines, a list of the ‘safest and most effective medicines’ needed in a society. The BCG vaccine is no longer prevalent in the developed world, however, because tuberculosis itself is not that prevalent in the developed world. That may play a role in the COVID-19 pandemic, a group of researchers says.
“In our initial research, we found that countries with high rates of BCG vaccinations had lower rates of mortality,” explained Escobar, an affiliate of the Global Change Center housed in the Fralin Life Sciences Institute. “But all countries are different: Guatemala has a younger population than, say, Italy, so we had to make adjustments to the data to accommodate those differences.”
Working with NIH researchers, Escobar collected coronavirus mortality data from around the world. The team then adjusted that data for relevant variables such as population density, age, income, and access to health services. Even after they controlled for all these variables, the correlation still stands: countries with higher rates of BCG vaccinations have lower peak mortality rates from COVID-19.
Strikingly, Germany seems to offer good support for this theory, a separate study finds. Prior to the country’s unification in 1990, West Germany and East Germany had different BCG vaccinations. West Germany provided BCG vaccines from 1961 to 1998, while East Germany started earlier, but stopped in 1975. This implies that older Germans in former East Germany would have more protection than their western peers — and this is exactly what recent data has shown: western German states have mortality rates that are 2.9 times higher than those in eastern Germany.
It’s also not entirely surprising that the BCG vaccine would offer such protection. There is systematic review evidence showing that BCG vaccination prevents respiratory infections (pneumonia and influenza) in children and the elderly. BCG has also been shown to provide broad cross-protection from a number of viral respiratory illnesses in addition to tuberculosis, so it’s reasonable that it could do the same for COVID-19.
“The purpose of using the BCG vaccine to protect from severe COVID-19 would be to stimulate a broad, innate, rapid-response immunity,” said Escobar.
However, Escobar stresses that this is still preliminary research, and more work is still needed to validate the results. If confirmed, it would also be necessary to assess just how strong this protective effect is, and how this could (perhaps) be used to our advantage.
“We’re not looking to advise policy with this paper,” Escobar said. “This is, instead, a call for more research. We need to see if we can replicate this in experiments and, potentially, in clinical trials. We also need to come back to the data as we get more information, so we can reevaluate our understanding of the coronavirus pandemic.”
For now, this remains a noteworthy idea that warrants further investigation. There are already clinical trials underway to assess if and how BCG vaccination in adults can also confer protection from severe COVID-19.
A virus is essentially a tiny piece of genetic material, either made of RNA or DNA. The entire viral particle, known as a virion, consists of this genetic material and an outer shell of protein that encases it called a capsid. Some viruses have a second protective layer known as the envelope.
Viruses are what you’d call obligate parasites, meaning they have to invade foreign cells in order to hijack their biological machinery and replicate. Viruses cannot replicate on their own and without a host, they’re doomed for extinction.
Because they can’t self-replicate like other living cells (among other things), most biologists believe viruses cannot be classed as life forms. Their classification as living beings can get complicated because, at the same time, viruses are subjected to evolutionary pressure just like any living creature.
For instance, viruses can mutate at insanely fast rates, allowing different strains to emerge that are better adapted to infecting hosts, thus begetting more replication.
The smallest of all microbes, viruses are notorious for their contagious behavior. People have generally learned to be afraid of viruses due to their potential to cause illness, from the benign common cold to the frightening Ebola and HIV, or, most recently, the novel coronavirus that has triggered an unprecedented pandemic.
Over thousands of years, viruses have been responsible for killing countless people. The 1918 Spanish flu pandemic killed 50 to 100 million, while 200 million were killed by smallpox during the 20th century alone.
However, not all viruses are necessarily bad. Some have proven instrumental as research tools and as vital components in vaccines and other modern therapies.
How do viruses spread?
The existence of a virus is intertwined with that of its host, but how does it spread?
Depending on the virus, they can infect virtually all types of cells, be they plant, bacterial, or animal cells.
In order to do so, the virus first needs to gain access. The largest organ in the human body, our skin, is a fantastic insulator, protecting our cells and tissues from foreign pathogens. However, it is not foolproof — respiratory passages, such as the mouth and nose, as well as the eyes, allow external particles to enter the body. Open wounds can also act as gateways for viruses, bacteria, and other pathogens.
Once inside the body, the virus cannot reach its infectious potential if it’s not capable of attaching itself to host cell surfaces. To do so, viruses have to be able to recognize and bind to certain receptors on the surface of the cells, like a lock and key. This is why viruses can infect only certain species of hosts and only certain cells within that host.
If the virion can bind to the receptor, it can then immediately inject its genome through the membrane of the cell. Once inside, it instructs the host cell to produce viral proteins through transcription and translation, while halting the synthesis of RNA and proteins that the cell would have used to function properly.
The last stage of viral replication is the release of the new virions produced in the host organism. This usually happens when a cell is exhausted and dies, bursting to release millions of virions that are capable of infecting adjacent cells and repeating the replication cycle.
How viruses cause sickness (and use it to their advantage)
Although cells can get damaged and die due to the viral replication cycle, a person will fall ill and exhibit symptoms of disease mainly as a result of the immune response to the virus. In its attempt to control and purge the virus from the body, the immune system will also attack healthy cells. Sometimes, this can get out of control, resulting in a so-called “cytokine storm”, which in some COVID-19 patients can trigger wide scale damage to virtually all major internal organs.
The shrewd virus will use the host’s sickness to its advantage. For instance, a person that has symptoms of the common cold will have a runny nose and cough, and the respiratory fluids that they expel contain copious amounts of rhinovirus. Most of these viruses expelled through sneezing or coughing will not find a host and die. But eventually, some will meet new hosts, and restart their cycle of viral replication — one host at a time.
Contact between viruses and susceptible hosts can occur through various means.
A virus can stay suspended in the air attached to aerosols, which a person can inhale, thus gaining access to the body. Alternatively, a person might touch a contaminated surface or shake hands with an infected person, only to later touch their mouth, nose, or eyes. Some viruses replicate inside intermediate hosts, such as insects, using them as vectors of transmission. The Zika virus, for instance, is spread by mosquitoes when they bite humans.
The novel coronavirus that caused the COVID-19 pandemic is believed to originate in bats, which can harbor thousands of different viruses without getting sick themselves. Scientists believe that the virus then jumped to other animals, such as the pangolin, which were consumed in wet markets in Wuhan by local people. For this reason, many wildlife organizations are fighting to ban wet markets and the trade of wildlife in order to stave off future pandemics.
How large is a virus?
Viruses are the smallest microorganisms out there, although their size can vary rather wildly. The Porcine Circovius that infects pigs is only 17 nanometers wide, while the hefty Tupanvirus measures 2.3 micrometers, making it almost 1,000 times larger. If these figures don’t make much sense, imagine that the poliovirus, which is 30 nanometers across, is around 10,000 times smaller than a grain of salt.
At this scale, it’s impossible to observe viruses even with modern optical microscopes. It’s no wonder that it took scientists a lot time to confirm their existence.
Towards the end of the 19th century, scientists were well aware that microorganisms could cause disease. However, they mostly knew about bacteria, while the notion of viruses still escaped them.
Science’s incursion into the world of viruses first began when researchers were investigating the tobacco mosaic disease, for which the responsible pathogen couldn’t be identified.
In 1886, German chemist Adolf Mayer crushed diseased tobacco leaves and poured the resulting juice into the veins of healthy tobacco leaves. Sure enough, the leaves later developed the yellowish speckling characteristic of the disease. But despite his best efforts, Mayer couldn’t find the bacteria which he was certain was responsible for the disease.
Six years later, in 1892, Dmitri Ivanovksy, at the time a student in Russia, replicated Mayer’s experiment. However, he introduced an additional step: before injecting the juice into healthy tobacco leaves, Ivanovsky passed the juice through a Chamberland filter. This filter is fine enough to capture bacteria and other known organisms, but even after the sieving, the liquid concoction still caused disease when it encountered tobacco leaves.
Researchers still had no clue what was causing tobacco mosaic disease, but at least now they knew that whatever microorganism was responsible for the disease was smaller than anything they knew.
Dutch scientist Martinus Beijerinck also replicated the experiment, coming to the same results as the German and Russian researchers. However, he had some important insights to share. Beijerinck believed that the cause of tobacco disease wasn’t bacterial in origin, but rather by a “filterable virus”. The word ‘virus’ actually describes ‘poisonous liquids’ in Latin.
It wasn’t until much later, in 1939, that scientists confirmed the existence of the tobacco mosaic virus using an electron microscope — the only scientific instrument capable of imaging objects of such small scale.
Nature needs viruses
There may be at least one million different types of viruses circulating in the world, 320,000 of which might be capable of infecting mammals, a 2013 study found.
That sounds frightening. It means everywhere you look there are thousands of different viruses, some capable of infecting human cells.
However, viruses aren’t inherently bad. Like all things in nature, they exist for a reason. Most viruses cannot infect humans and play important roles in ecosystems, maintaining a balance between various stakeholders, from plants and insects to humans.
If there were no viruses, life as we know it may even collapse.
“If all viruses suddenly disappeared, the world would be a wonderful place for about a day and a half, and then we’d all die – that’s the bottom line,” Tony Goldberg, an epidemiologist at the University of Wisconsin-Madison, told BBC Future. “All the essential things they do in the world far outweigh the bad things.”
This is all very counter-intuitive: viruses sustain life, rather than destroy it.
One way they keep ecosystems in check is by infecting bacteria. Viruses that infect bacteria are called ‘phages’ (from Greek phagein, meaning “to devour”), and we’d all be in deep trouble without them.
Phages are the main regulators of bacterial populations, especially in the ocean. If all viruses somehow magically disappeared overnight, we’d all be overrun by bacteria in a matter of weeks or perhaps even days. Not just humans, but all life on Earth would probably find itself out-competed by bacteria.
And although this isn’t fully understood yet, scientists think that some viruses can give organisms an advantage. For instance, viruses seem to play a role in the process that turns cellulose from grass into milk in cows.
Viruses are truly frightening when they break out on a global scale, unleashing pandemics. From Europe’s Black Death during the Middle Ages to the Spanish flu around the time of the First World War, pandemics have been known to change the course of society. The current COVID-19 is no exception, likely unleashing a new world order.
Pandemics like COVID-19 can shock the economy and medical systems to the point that they can collapse. This is why it’s important we don’t have too many pandemics in the future — and the best way to avoid such scenarios is to protect the natural world.
A strain of the coronavirus seen in Europe and the United States is significantly more infectious than the initial virus, according to findings from Scripps Research.
The strain is characterized by a mutation that dramatically increases the number of spike proteins on the virus’ surface, explains senior author Hyeryun Choe, a virologist at Scripps. These spikes represent the biochemical mechanism via which the virus gains entry into human cells.
More of a bad thing
“The number—or density—of functional spikes on the virus is 4 or 5 times greater due to this mutation,” says Hyeryun Choe, PhD.
“Viruses with this mutation were much more infectious than those without the mutation in the cell culture system we used.”
The coronavirus gets its name from these spikes, which resemble a crown. Apart from their aesthetics, these spikes enable the virus to access our cells using the ACE2 receptors on their membrane.
The mutation identified by this study, called D614G, doesn’t directly influence the number of spikes. What it does do, however, is to cause a different amino acid to be used in these spikes — glycine instead of aspartic acid — which makes their structures more flexible. Due to this, more spikes can survive from the moment the virus is produced to when it infects a host as they’re less likely to break off.
So although the mutation acts on the flexibility of these spikes, the net result is a virus that’s much more stable over time and retains a greater ability to infect cells.
No such link has yet been confirmed or infirmed, but the team says that such mutations could help explain why outbreaks in Italy or New York were rampant and quickly overwhelmed the medical resources available, while other areas fared much better, at least initially.
Still, to the best of our knowledge today, the SARS-CoV-2 variant that spread in the earliest outbreaks lacked the D614G mutation, but it is now dominating in much of the world, the team explains. In February, no sequences deposited to the GenBank database showed the D614G mutation. By March, it appeared in 1 out of 4 samples. and in 70% of samples by May, the team reports. ICU data from New York and elsewhere reports a preponderance of the new D614G variant as well, they add.
Mutation is a natural part of biology and that all viruses acquire tiny genetic changes as they reproduce. Most don’t have any bearing on the virus’ ability to infect our cells.
The team further notes that the findings are based in lab experiments with harmless viruses engineered to produce key coronavirus proteins. Further research would be needed to determine whether this mutation also impacts the transmissibility of the virus in real-world situations. For now, however, serum isolated from infected people worked just as well against engineered viruses with and without the D614G mutation, suggesting that potential vaccines should protect against both strains.
It is still unknown whether this small mutation affects the severity of symptoms of infected people, or increases mortality, the scientists say.
The paper “The D614G mutation in the SARS-CoV-2 spike protein reduces S1 shedding and increases infectivity” has been published in the pre-print site bioRxiv and is undergoing peer-review.
Containing the coronavirus crisis without proper intel is like shooting in the dark. Until we can find a vaccine or cure, we need to know everything there is to know about the virus’ behavior in order to properly manage resources and manpower. Otherwise, we risk living the rest of the year (and perhaps following ones) going from lockdown to lockdown.
Some important characteristics that should be precisely known include the mortality rate, the virus attack rate, the average viral load and the minimum infectious dose, the basic reproductive number (which tells you how many people a single individual can infect, or how contagious the virus is), as well as how long an infected person remains contagious.
This last bit is the subject of a new study by researchers at Singapore’s National Centre for Infectious Diseases and the Academy of Medicine, who tested 73 COVID-19 patients. Their analysis revealed that, on average, the virus could not be isolated or cultured after 11 days after the onset of illness — this was true despite viral RNA being detected with PCR tests.
Much confusion around positive tests and infectious cases
In other words, a person might still test positive despite signs of obvious recovery. However, just because there is still viral material in a person’s respiratory fluid doesn’t mean they’re infectious.
This explains a lot of very weird things we’ve seen in relation to this virus, such as people testing positive for weeks on end. Because of such cases, many have been worried that people can get sick with COVID-19 many times after recovery or that the human body cannot produce sufficient antibodies to become immune to the coronavirus.
Instead, this study suggests that people really do build immunity — it’s just that our PCR tests are so sensitive that they can pick up even tiny traces of the virus. What’s more, these viruses may not be able to replicate in other hosts 11 days after the onset of symptoms.
The implications are huge. This means that many protocols currently in place for managing COVID-19 patients need to be rethought or entirely discarded. For instance, in many countries, COVID-19 patients are not allowed to be discharged from the hospital until they have two consecutive negative tests.
In light of these findings, hospitals could discharge a patient after symptoms have disappeared and/or at least 14 days have passed from the onset of illness. This way, many valuable hospital beds can be cleared for new patients.
The findings are in line with other previous studies that investigated how long the individuals remain infectious. One study on COVID-19 patients from Hong Kong concluded that an infected person can pass the virus on to other people a few days before the onset of symptoms, with infectiousness peaking right when the symptoms appear, then declining over the next 7 days. These findings are supported by another study on Chinese patients which concluded that significant viral shedding likely begins two to three days before symptoms first appear and that the number of whole viruses that are expelled declines after people begin feeling sick.
Another study on Taiwanese COVID-19 patients offers hints about the infectiousness of the virus from another angle. The authors of the study tested people who were in close contact with the COVID-19 patients, finding that secondary cases arose within 5 days of the initial host’s onset of symptoms. Contacts made after this period did not result in new cases.
Finally, a study from Germany that cultured the virus from throat and lung samples found that the virus could replicate and infect other cells in the first week of symptoms, but none after day 8 — that’s in spite of the samples showing high viral loads in PCR tests.
A positive test doesn’t mean the patient is still sick or contagious
These studies all seem to suggest that viral replication quickly drops one week after symptom debut and that patients stop spreading viable viruses after the second week of illness.
They also speak volumes about the faultiness of RNA detection by PCR testing, which so many hospitals and countries see as a gold standard of COVID-19 outcome success. Instead, patients could be discharged based on other criteria as well, like the time elapsed since the onset of illness. This would help free up resources for new patients.
And, perhaps most reassuringly, the findings suggest that SARS-CoV-2 isn’t really some superbug. People who’ve tested positive again and again after weeks of illness probably aren’t getting reinfected after recovery. Instead, it’s just a matter of tests picking up residual viral material.
Hopefully, similar studies will soon answer how contagious asymptomatic cases are as well, as this is another important missing piece of the puzzle.
For now, this much seems very likely with regard to the behavior of the coronavirus: people can pass it on as early as a few days before symptoms appear, but no later than 14 days after the onset of symptoms, regardless of positive PCR tests.
Coronavirus carriers can infect their environment with the pathogen even before showing symptoms, according to a new study from the Cleveland Clinic.
The findings are based on an analysis of several surfaces in the hotel rooms of two presymptomatic Chinese students who were quarantined before being diagnosed with the disease. This study highlights the role and importance of quarantine in preventing the spread of COVID-19, and why it’s essential that we stick to isolation measures even if we’re ‘feeling fine’.
Hiding in plain sight
“The detection of SARS-CoV-2 RNA in the surface samples of the sheet, duvet cover, and pillow cover highlights the importance of proper handling procedures when changing or laundering used linens of SARS-CoV-2 patients,” the authors explain.
“In summary, our study demonstrates that presymptomatic patients have high viral load shedding and can easily contaminate environments.”
The study looked at the hotel rooms of two students who returned to China from studying abroad on March 19 and March 20. They did not show any symptoms of viral infection initially, but were moved to the hotel for quarantine as a precautionary measure.
On the second day in quarantine, they both tested positive for COVID-19 — they were still asymptomatic at this time — and were hospitalized for monitoring and treatment.
Their rooms were closed off after they tested positive, and various surfaces throughout were sampled about three hours after the tests. The team took swabs from door handles, light switches, faucet handles, thermometers, television remotes, pillow covers, duvet covers, sheets, towels, bathroom door handles, toilet seats, and toilet flushing buttons, among other frequently-touched areas.
A total of 22 samples were collected from the two rooms. Eight of them tested positive for COVID-19. Six were from the same patient, identified as Patient A, and were harvested from the light switch, bathroom door handle, sheet, duvet cover, pillow cover, and towel. In Patient B’s room, positive samples were detected on a faucet and pillowcase.
The team notes that they saw larger viral loads after prolonged contact with sheets and pillow covers, suggesting that the pathogens found this environment particularly cozy. However, overall, the main take-away from this study is how carriers, even presymptomatic ones, can cause “extensive environmental contamination of SARS-CoV-2 RNA in a relatively short time.”
Such findings come to fill in the puzzle of how the coronavirus behaves in the environment. Previous studies have recorded its ability to survive on various surfaces, which varied between three hours and seven days, depending on the material. The present study comes to show how it can get there in the first place, and at which parts of its life cycle.
All in all, the coronavirus seems to easily spread to our environments, even before we know we have it. It’s also content to survive there for quite a long time, too, ready to hitch a ride on our hands towards our face. These two factors contribute to making it such a contagious virus, and they’re why the 14-day quarantine measures were instituted in the first place.
It’s also why such measures are still one of our most effective ways in curbing its spread.
The paper “Detection of Severe Acute Respiratory Syndrome Coronavirus 2 RNA on Surfaces in Quarantine Rooms” has been published in the journal Emerging Infectious Diseases.