Researchers from Karolinska University have discovered a gene that reduces the severity of Covid infections by 20%. In theirpaper the scientists state that this explains why the disease’s symptoms are so variable, hitting some harder than others.
Why do some people fall severely ill from COVID-19 while others don’t? In addition to risk factors like age or obesity and plenty of other environmental factors, it also comes down to our varying genetic makeup. Therefore, researchers across the globe have begun the mammoth task of mapping the genes involved in making people more susceptible to catching SARS-CoV-2 (COVID-19) and developing a severe infection.
These large-scale efforts have thrown up more than a dozen genomic regions along the human chromosome containing large clusters of genes associated with severe COVID-19. However, the specific causal genes in these regions are yet to be identified, hampering our ability to understand COVID-19’s often selective pathology.
Now, scientists build on these findings to pinpoint a gene that confers protection from critical illness.
Neanderthal DNA protects against severe COVID-19
The previous studies from 2020 concentrated on the genetic data of people of European ancestry recorded by multi-disciplinary teams all over the world for the 1000 Genomes Project. This monumental collaboration uncovered a specific segment of DNA known as the OAS1/2/3 cluster, which lowers the risk of developing an acute COVID-19 infection by 20%. Inherited from Neanderthals in roughly half of all people outside of Africa, this segment is responsible for encoding genes in the immune system.
The genetic array came about as a result of the migration of an archaic human species out of the African continent about 70,000 years ago who mated and mingled DNA with Neanderthals reproduced in their offspring’s haplotypes, a set of inheritable DNA variations close together along a chromosome.
However, most human haplotypes outside Africa now include DNA from Neanderthals and Denisovans (an ancient human originating in Asia). Consequently, this ancient region of DNA is heaving with numerous genetic variants, making it challenging to distinguish the exact protective gene that could serve as a target for medical treatment against severe COVID-19 infection.
A possible solution is that people of African descent do not contain these archaic genes in their haplotypes, making them shorter and easier to decipher.
To test this theory, the researchers checked the 1000 Genomes project database for individuals carrying only parts of this DNA segment – focusing on individuals with African ancestry who lack heritage from the Neanderthals. Remarkably, the researchers found that individuals of predominantly African ancestry had the same protective gene cluster as those of European origin.
Genetic studies should be a multi-cultural affair
Once they established this, the researchers collated 2,787 COVID-19 cases with the genetic data of 130,997 individuals of African ancestry to reveal the gene variant rs10774671 G thought to convey protection against COVID-19 hospitalization. Their results correspond to a previous, more extensive study of individuals of European heritage, with analysis suggesting it is likely the only causal variant behind the protective effect.
Surprisingly, this previously ‘useless’ ancient variant was found to be widespread, present in one out of every three people of white European ancestry and eight out of ten individuals of African descent.
In evolutionary terms, the researchers write that the variant exists today in both these gene pools “as a result of their inheritance from the ancestral population common to both modern humans and Neanderthals.” Accordingly, their data adds more weight to the standard held theory that a common ancestor originated in Africa millions of years ago before sharing their DNA across the globe.
And while there’s much more to uncover regarding the newly discovered variant, the researchers can firmly suggest at this stage that the protective gene variant (rs10774671 G) works by determining the length of a protein encoded by the gene OAS1. As the longer version of the protein is more effective at breaking down the virus than the unaltered form, a life-threatening infection is less likely to occur.
Using genetic risk factors to design new COVID-19 drugs
Despite their promising results, the team cautions that the 1000 Genomes Project does not provide a complete picture of this genomic region for different ancestries. Nevertheless, it’s clear that the Neanderthal haplotype is virtually absent among individuals of primarily African ancestry, adding, “How important it is to include individuals of different ancestries” in large-scale genetic studies.
Senior researcher Brent Richards from McGill University says that it is in this way “we are beginning to understand the genetic risk factors in detail is key to developing new drugs against COVID-19.”
If these results are anything to go by, we could be on the cusp of novel treatments that can harness the immune system to fight this disease.
If one in 10 cold infections are from coronaviruses, then antibodies produced from these illnesses could surely give a bit more protection against COVID-19, right? A new study has just provided the answer to this question by showing that immunity induced by colds can indeed help fight off the far more dangerous novel coronavirus.
A study from Imperial College London that studied people exposed to SARS-CoV-2 or COVID-19 found that only half of the participants were infected, while the others tested negative. Before this, researchers took blood samples from all volunteers within days of exposure to determine the levels of an immune cell known as a T cell – cells programmed by previous infections to attack specific invaders.
Results show that participants who didn’t test positive had significantly higher levels of these cells; in other words, those who evaded infection had higher levels of T cells that attack the Covid virus internally to provide immunity — T cells that may have come from previous coronavirus infections (not SARS-CoV-2). These findings, published in the journal Nature Communications, may pave the way for a new type of vaccine to prevent infection from emerging variants, including Omicron.
Dr. Rhia Kundu, the first author of the paper from Imperial’s National Heart & Lung Institute, says: “Being exposed to the SARS-CoV-2 virus doesn’t always result in infection, and we’ve been keen to understand why. We found that high levels of pre-existing T cells, created by the body when infected with other human coronaviruses like the common cold, can protect against COVID-19 infection.” Despite this promising data, she warns: “While this is an important discovery, it is only one form of protection, and I would stress that no one should rely on this alone. Instead, the best way to protect yourself against COVID-19 is to be fully vaccinated, including getting your booster dose.”
The common cold’s role in protecting you against Covid
The study followed 52 unvaccinated people living with someone who had a laboratory-confirmed case of COVID-19. Participants were tested seven days after being exposed to see if they had caught the disease from their housemates and to analyze their levels of pre-existing T cells. Tests indicated that the 26 people who tested negative for COVID-19 had significantly higher common cold T cells levels than the remainder of the people who tested positive. Remarkably, these cells targeted internal proteins within the SARS-CoV-2 virus, rather than the spike protein on its surface, providing ‘cross-reactive’ immunity between a cold and COVID-19.
Professor Ajit Lalvani, senior author of the study and Director of the NIHR Respiratory Infections Health Protection Research Unit at Imperial, explained:
“Our study provides the clearest evidence to date that T cells induced by common cold coronaviruses play a protective role against SARS-CoV-2 infection. These T cells provide protection by attacking proteins within the virus, rather than the spike protein on its surface.”
However, experts not involved in the study caution against presuming anyone who has previously had a cold caused by a coronavirus will not catch the novel coronavirus. They add that although the study provides valuable data regarding how the immune system fights this virus, it’s unlikely this type of illness has never infected any of the 150,000 people who’ve died of SARS-CoV-2 in the UK to date.
Other studies uncovering a similar link have also warned cross-reactive protection gained from colds only lasts a short period.
The road to longer-lasting vaccines
Current SARS-CoV-2 vaccines work by recognizing the spike protein on the virus’s outer shell: this, in turn, causes an immune reaction that stops it from attaching to cells and infecting them. However, this response wanes over time as the virus continues to mutate. Luckily, the jabs also trigger T cell immunity which lasts much longer, preventing the infection from worsening or hospitalization and death. But this immunity is also based on blocking the spike protein – therefore, it would be advantageous to have a vaccine that could attack other parts of the COVID virus.
Professor Lalvani surmises, “The spike protein is under intense immune pressure from vaccine-induced antibodies which drives the evolution of vaccine escape mutants. In contrast, the internal proteins targeted by the protective T cells we identified mutate much less. Consequently, they are highly conserved between the SARS-CoV-2 variants, including Omicron.” He ends, “New vaccines that include these conserved, internal proteins would therefore induce broadly protective T cell responses that should protect against current and future SARS-CoV-2 variants.”
Scientists have identified a previously unknown mutant strain in a fully vaccinated person who tested positive after returning from a short three-day trip to Cameroon.
Academics based at the IHU Mediterranee Infection in Marseille, France, discovered the new variant on December 10. So far, the variant doesn’t appear to be spreading rapidly and the World Health Organization has not yet labeled it a variant of concern. Nevertheless, researchers are still describing and keeping an eye on it.
The discovery of the B.1.640.2 mutation, dubbed IHU, was announced in the preprint server medRxiv, in a paper still awaiting peer review. Results show that IHU’s spike protein, the part of the virus responsible for invading host cells, carries the E484K mutation, which increases vaccine resistance. The genomic sequencing also revealed the N501Y mutation — first seen in the Alpha variant — that experts believe can make COVID-19 more transmissible.
In the paper, the clinicians highlight that it’s important to keep our guard and expect more surprises from the virus: “These observations show once again the unpredictability of the emergence of new SARS-CoV-2 variants and their introduction from abroad,” they write. For comparison Omicron (B.1.1.529) carries around 50 mutations and appears to be better at infecting people who already have a level of immunity. Thankfully, a growing body of research proves it is also less likely to trigger severe symptoms.
Like many countries in Europe, France is experiencing a surge in the number of cases due to the Omicron variant.
Experts insist that IHU, which predates Omicron but has yet to cause widespread harm, should not cause concern – predicting that it may fade into the background. In an interview with the Daily Mail, Dr. Thomas Peacock, a virologist at Imperial College London, said the mutation had “a decent chance to cause trouble but never really materialized. So it is definitely not one worth worrying about too much at the moment.”
The strain was first uploaded to a variant tracking database on November 4, more than two weeks before Omicron was sequenced. For comparison, French authorities are now reporting over 300,000 new cases a day thought to be mostly Omicron, with data suggesting that the researchers have identified only 12 cases of IHU over the same period.
On the whole, France has good surveillance for COVID-19 variants, meaning health professionals quickly pinpoint any new mutant strains. In contrast to Britain, which only checks three in ten cases for variants. The paper’s authors state that the emergence of the new variant emphasizes the importance of regular “genomic surveillance” on a countrywide scale.
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.
If we want to be able to feed the world, we’d best pay closer attention to pests.
According to current estimates, the world population is 7.7 billion. It took over 200,000 years to reach the first billion, and only 200 more years to reach 7.7 billion. By 2100, even conservative estimates put the world population at 11 billion — all of which will have to be fed. Considering that today, over 800 million suffer from chronic undernourishment, feeding the population of tomorrow will be quite a challenge.
Our agricultural productivity has increased dramatically in the 20th century, in a period often called “the Green Revolution.” Norman Borlaug, the “father” of the Green Revolution and the most prominent scientist associated with the movement, is credited with personally saving over 1 billion lives through his work.
However, with no other such revolution in sight, we will need to optimize production and reduce losses as much as possible — and one of the most important problems to consider are pests.
Pests and pathogens are an integral part of agriculture. They’ve been around since mankind has been growing crops, coevolving with agricultural plants. However, that’s not to say that we can’t do anything to fight them. Different methods have been employed, with varying degrees of success. But before we can talk about large-scale campaigns against pests, we first need to understand the big picture.
This is exactly where the new study comes in. Serge Savary, a researcher working at the French National Centre for Scientific Research, and colleagues, took on the gargantuan task of measuring global crop losses caused by pests and pathogens. They focused on the five most popular crops: wheat, rice, maize, potato, and soybean. Together, these crops make up almost half of mankind’s calorie consumption.
They found that at a global level, pets destroy:
21.5% of wheat crops;
30% of rice crops;
22.5% of maize crops;
17.2% of potato crops; and
21.4% of soybean crops.
This type of data is extremely valuable, especially as standardized information is difficult to compile across different regions and crops — and there is little in the way of good news.
All in all, almost one-quarter of this food is completely lost — and to make matters even worse, the highest losses are associated with regions with fast-growing populations and which are already struggling with malnutrition. These are also areas frequently hit by emerging or re-emerging pests and diseases.
Researchers hope that their work will serve as a guideline for policymakers and farmers alike. At a global scale, if we want to be able to feed the world, we need quick and efficient interventions in these areas.
There’s also another problem, a common culprit: climate change. It’s clear that climate change will affect plant-pathogen interactions, but it’s much less clear in what way. While they did not study this directly, Savary and colleagues quote another study, which ultimately concludes that “climate change will bring, above all, surprises.” Quite likely, they won’t be pleasant surprises.
The study has been published in Nature. DOI: 10.1038/s41559-018-0793-y
Researchers analyzing Northern Ireland soil report finding a previously unknown strain of bacteria that is effective against four of the top six drug-resistant superbugs, including MRSA.
A landscape from Boho, County Fermanagh, Northern Ireland. Image credits: Youngbohemian / Wiki Commons.
Folk remedies are rarely as useful as they’re touted — but in some rare instances, they can be surprisingly effective. This turned out to be the case with the soil found in the area of Boho, County Fermanagh, close to the border between Ireland and Northern Ireland.
The area has been inhabited since at least 4,000 years ago, and most notably, it was also inhabited in medieval times. Around the year 500, it was also inhabited by Druids — high-ranking healers and administrative figures of Celtic populations. There are mentions of the Druids (and some subsequent populations) using local soils to treat many ailments including toothaches, throat and neck infections.
Geologically, the area is very diverse, with habitats ranging from limestone karst to acidic bogs. As a result, the soils also exhibit a rare variability with an interesting chemistry. In this new study, researchers focused especially on an area of alkaline grassland called the Boho Highlands, which was touted as having healing properties.
Dr. Gerry Quinn, member of the research team and a previous resident of Boho, was aware of the legends surrounding the soil, so together with colleagues from Wales, Brazil, Iraq and Northern Ireland, he set out to analyze it and see whether there is some truth to these stories.
Within the soil, they discovered a new species of bacteria, which they call Streptomyces sp. myrophorea, so named because it produces a distinctive fragrance similar to that of oil of wintergreen (myrrh). This bacterium inhibited the growth of four of the top six multi-resistant pathogens, which the World Health Organization has highlighted as being responsible for healthcare-associated infections:
and Carbenepenem-resistant Acinetobacter baumanii.
Zone of inhibition produced by Streptomyces sp myrophorea on a lawn of MRSA. The bacteria is the brown spot, and the lighter color around the spot shows that it is inhibiting the spread of the MRSA which is surrounding it. Credit: G Quinn, Swansea University.
In other words, the bacterium is effective against 4 of the 6 most dangerous drug-resistant pathogens. To make it even more appealing, it also seems to halt both gram positive and gram negative bacteria, which differ in the structure of their cell wall, suggesting it could be a part of robust, broad-spectrum treatments.
However, the effect of this bacteria on the human body is not fully known. It’s also not exactly clear how the bacterium is fighting these drug-resistant pathogens — both matters are currently being investigated by the team.
The genome of the bacterium has also been sequenced. As more and more pathogens are developing drug resistance, finding new antibiotics to deal with them is crucial. Quinn and colleagues suggest that there are chances key elements might lie in some folk remedies, a field called ethnopharmacology. This isn’t to say that we should all trust folk remedies at the expense of established medicine — this is saying that within some natural environments, there may be compounds which could be harvested and used to deal with severe infections or to prevent the spread of pathogens. Professor Paul Dyson of Swansea University Medical School comments:
“This new strain of bacteria is effective against 4 of the top 6 pathogens that are resistant to antibiotics, including MRSA. Our discovery is an important step forward in the fight against antibiotic resistance.”
“Our results show that folklore and traditional medicines are worth investigating in the search for new antibiotics. Scientists, historians and archaeologists can all have something to contribute to this task. It seems that part of the answer to this very modern problem might lie in the wisdom of the past.”
Gerry Quinn also adds:
“The discovery of antimicrobial substances from Streptomyces sp.myrophorea will help in our search for new drugs to treat multi-resistant bacteria, the cause of many dangerous and lethal infections.”
“We will now concentrate on the purification and identification of these antibiotics. We have also discovered additional antibacterial organisms from the same soil cure which may cover a broader spectrum of multi-resistant pathogens.”
Journal Reference: Luciana Terra et al. A Novel Alkaliphilic Streptomyces Inhibits ESKAPE Pathogens, Frontiers in Microbiology (2018). DOI: 10.3389/fmicb.2018.02458.
Medical nanobots are one step closer, as researchers developed simple nanorobots that can be propelled through blood to clear out bacteria and toxins.
Image credits Mate Marschalko / Flickr.
A team of engineers from the University of California San Diego has developed a class of ultrasound-powered robots that can scrub blood clean of bacteria and the toxins they produce. While still simple, the proof-of-concept nanobots could pave the way towards safe and rapid methods of decontaminating biological fluids — even in the bodies of living patients.
The team builds their nanorobots out of gold nanowires coated with platelet and red blood cell membranes. This hybrid membrane is what gives the nanites the ability to clear out biological contaminants. The platelet membrane binds to pathogens such as the antibiotic-resistant strain of Staphylococcus aureus, MRSA, while the red blood cell membranes can absorb and neutralize toxins produced by bacteria.
The gold nanobody is what lets the researchers move the bots around. The metal responds to ultrasound, giving the team the means to power them through the bloodstream without the use of engines or fuel. The bots need to be mobile in order to more efficiently mix with a fluid sample, speeding up the process of detoxification.
The nanobots were created using processes pioneered by the teams of Joseph Wang and Liangfang Zhang, professors in the Department of NanoEngineering at the UC San Diego Jacobs School of Engineering. Wang’s team designed and built the nanobots and the means of ultrasound-powered propulsion, while Zhang’s team developed the process used to coat these in natural cell membranes.
“By integrating natural cell coatings onto synthetic nanomachines, we can impart new capabilities on tiny robots such as removal of pathogens and toxins from the body and from other matrices,” said Wang.
“This is a proof-of-concept platform for diverse therapeutic and biodetoxification applications.”
Furthermore, the natural membranes prevent the nanobots from being ‘biofouled’ — a process by which proteins cake onto the surface of a foreign body, which would prevent the nanobots from functioning. The hybrid membranes were created from natural membranes, separated in one piece from platelets and red blood cells. These were then blasted with high-frequency sound waves, causing them to fuse together.
The nanobot binding to and isolating a pathogen. Image credits Fernández de Ávila et al., 2018, Science Robotics.
The robots’ bodies were constructed by then applying these membranes to gold nanowires through chemical means.
The finished devices are roughly 25 times smaller than the width of a hair, the team writes. Ultrasound waves can propel them up to 35 micrometers per second in blood. They were successful in cleaning blood samples contaminated with MRSA and associated toxins — after 5 minutes of being injected, the levels of bacteria and toxins were three times lower in treated samples than untreated samples.
If you’re like me and dream all starry-eyed about the day we’ll treat ourselves with nanobots, this research might make you feel quite happy inside. However, this work is at a very early stage. It’s also focused on something different — the team notes that, while their current nanobots can be used to treat MRSA in blood samples, they aim to have a device that can detoxify all kinds of biological fluids.
We still have a ways to go until then. For the near future, the team hopes to test their devices in live animal models, and to devise a way of creating the robot bodies out of biodegradable materials instead of gold.
The paper “Hybrid biomembrane–functionalized nanorobots for concurrent removal of pathogenic bacteria and toxins” has been published in the journal Science Robotics.
A rapidly spreading and lethal species of fungus that has devastated amphibian populations around the globe likely originated in East Asia. The authors of the new study say that monitoring and regulating the transit of amphibians, particularly those involved in pet trade, is essential in order to secure amphibian populations from such a dangerous and rapidly expanding disease.
A captive Oriental fire-bellied toad (Bombina orientalis) imported into Europe from South Korea. Credit: Frank Pasmans.
The fungus in question is Batrachochytrium dendrobatidis (Bd), also known as chytrid fungus. When it infects a host, the fungus causes a disease called chytridiomycosis, which attacks the animal’s skin, affecting the ability to regulate water and electrolyte levels. Eventually, the animal dies of heart failure. Frogs, toads, newts, and other amphibians across several continents are affected by the disease.
Previous attempts to discover the origin of this very dangerous and fairly recent pathogen suggested the fungus first appeared in South Africa, where it infected African clawed frogs (Xenopus laevis). It wasn’t along until this hypothesis was challenging as other research groups found that Bd samples taken from African frogs had too little genetic diversity.
Now, an international collaboration spanning 38 institutions reported their findings after sequencing the genomes of 234 samples collected from all around the world. Researchers looked at the minute differences between the genomes, identifying four distinct lineages. Three of them are distributed globally but a fourth appears only in Korea, in some of the frogs that are native in the region.
On a closer look, the Korean lineage contains much more genetic diversity than any other lineage. What’s more, the Korean Bd showed no history of global outbreaks within their genomes, which can only mean that the Korean chytrid strains were native to the region, and most closely resemble the ancestor of all modern Bd.
The team led by Simon O’Hanlon from Imperial College London estimated that the killer strain of Bd diverged from its most common ancestor between 50 and 120 years ago. That’s around the time intercontinental trade started rapidly expanding.
“Biologists have known since the 1990s that Bd was behind the decline of many amphibian species, but until now we haven’t been able to identify exactly where it came from,” O’Hanlon said in a statement.
“In our paper, we solve this problem and show that the lineage which has caused such devastation can be traced back to East Asia.”
According to the researchers, it is the human movement of amphibians — particularly through the pet trade — that has contributed the most to the spread of the pathogen around the world. Sightings of Asian strains of Bd in pet Oriental fire-bellied toads add weights to this idea.
The research suggests that since East Asia is ground zero for the deadly fungal pathogen, then ongoing trade in infected animals should be halted at once otherwise we risk threatening the already fragile amphibian biodiversity.
The International Space Station is becoming more and more independent. Now, astronauts can carry out microbial DNA sampling, which opens up exciting avenues for practical research.
NASA astronaut Kate Rubins poses for a picture during the first sample initialization run of the Biomolecular Sequencer investigation. Credits: NASA.
The mere idea of identifying microbes in space, without sending a probe back to Earth, was only a dream a few years ago. Now, thanks to the Genes in Space-3 project, NASA astronauts and biochemists have the ability to not only identify and treat microbial ailments in outer space but also potentially identify life on other planets. This also means that they can carry out a number of practical experiments in outer space — which they’ve already started.
The identification process has two parts: first, astronauts gather the microbial samples and subject them to Polymerase Chain Reaction — a technique commonly used in modern molecular biology to amplify copies of DNA segments across several orders of magnitude, generating thousands to millions of copies of a particular DNA sequence — then, they sequence and identify the microbes.
The first batch they sampled turned out to be regular microbes, like the ones commonly found in houses or anywhere that humans live. We truly tend to contaminate everything, and outer space seems to be no exception. What was somewhat surprising though was the sheer number of microbes they found on the space station.
“We have had contamination in parts of the station where fungi was seen growing or biomaterial has been pulled out of a clogged waterline, but we have no idea what it is until the sample gets back down to the lab,” said Sarah Wallace, NASA microbiologist and the project’s principal investigator at the agency’s Johnson Space Center in Houston.
“On the ISS, we can regularly resupply disinfectants, but as we move beyond low-Earth orbit where the ability for resupply is less frequent, knowing what to disinfect or not becomes very important,” said Wallace.
The need for on-site germ sampling became even more evident after the Johnson Space Center was damaged by Hurricane Harvey. The ISS was unable to send samples back to Earth — including microbial samples. Furthermore, as future manned missions are expected to be longer and longer, monitoring microbial activity aboard a shuttle will be much more important.
However, that’s still far off. For now, the most exciting prospect is studying microbial behavior and distribution in microgravity. Previous research has shown that floating in microgravity can give some microbes an unexpected genetic boost. Basically, researchers have found an increase in expression of virulence factors in Salmonella Typhimurium and increased biofilm production in Staphylococcus aureus. However, it’s unclear if this stays true for other microbes, or if different species behave in different ways. Bacterial response to microgravity is an increasingly useful area of study, and it’s one which NASA is tackling head-on.
We all know that flies are nasty and annoying, but most people just brush them off. Well, we might want to be more careful with them, as a new study shows that the two most common fly species can harbor more than 600 different bacteria.
Has this guy landed on your food? If so, you might want to think twice before eating. it. Image credits: Jon Sullivan.
Most people are aware that flies can carry dangerous pathogens, but few people are aware of the extent of that danger. To shed some light on said pathogens, researchers used DNA sequencing techniques to study the collection of microbes found in and on the bodies of the house fly (Musca domestica) and the blowfly (Chrysomya megacephala). In total, they analyzed DNA found on 116 flies from three different continents. They found that the house fly, which is virtually ubiquitously in the world, can carry up to 351 types of bacteria, while the blowfly, limited to the warmer parts of the world, carried 316. All analyzed individuals carried a large number of pathogens.
“We believe that this may show a mechanism for pathogen transmission that has been overlooked by public health officials, and flies may contribute to the rapid transmission of pathogens in outbreak situations,” said Donald Bryant, Ernest C. Pollard Professor of Biotechnology and professor of biochemistry and molecular biology, Penn State.
Stephan Schuster, former professor of biochemistry and molecular biology, Penn State, and now research director at Nanyang Technological University, Singapore says that the flies’ legs especially can carry bacteria from one surface to another.
“The legs and wings show the highest microbial diversity in the fly body, suggesting that bacteria use the flies as airborne shuttles,” said Schuster. “It may be that bacteria survive their journey, growing and spreading on a new surface. In fact, the study shows that each step of hundreds that a fly has taken leaves behind a microbial colony track, if the new surface supports bacterial growth.”
Researchers used a scan electron microscope to find where bacterial cells and particles attach to the fly body. The electron microscope captures an up-close look at the head of a blowfly in this picture. Image credits: Ana Junqueira and Stephan Schuster.
Since both flies are carrion species, they’re quite likely to pick up a swarm of bacteria and then pass them on to us. They also use feces or decaying, rotting corpses to nurture their young, which not only makes them pretty disgusting but also dirty and dangerous. Feces and decaying organic matter are a haven for flies, but they’re also a haven for bacteria (including nasty ones).
However, researchers say that there is some good news to come from their research. They believe that flies could be used as “drones” to research how pathogen-prone an environment is. Basically, they say we could release clean flies into an area, they would naturally pick up the bacteria from said area, and scientists could recapture and analyze them, thus learning what pathogens hide there.
The study also revealed that the two fly species share over 50 percent of their microbiome and that flies from urban areas tended to carry more bacteria than their rural counterpart. The potential, then, for flies to carry diseases may increase when more people are present. But most importantly, researchers want the general population to pay more attention to flies and their interaction with our food.
“It will really make you think twice about eating that potato salad that’s been sitting out at your next picnic,” Bryant said. “It might be better to have that picnic in the woods, far away from urban environments, not a central park.”
It’s a bird! No, it’s a plane! No, it’s… microbes ?! High up in the atmosphere, 10.000 meters above ground, researchers have found over 100 species of bacteria doing just fine in stormy clouds.
The eye of Hurricane Earl in the Atlantic Ocean, seen from a NASA research aircraft on Aug. 30, 2010. This flight through the eyewall caught Earl just as it was intensifying from a Category 2 to a Category 4 hurricane.
Each year, hundreds of millions of tons of dust, water and man-maned pollutans make their way into the atmosphere, often traveling between distant locations or even between continents on jet streams. Of course, along with these massive quantities, some microbes get sucked up too – but even though bacteria have been known to survive in the most extreme environments, researchers weren’t expecting them to do so good high up in the air. It’s suspected that some of them are able to feed up there, creating a thriving ecosystem 10 km above our heads.
The discovery came up rather accidentally; a team of scientists based at the Georgia Institute of Technology in Atlanta hitched a ride on nine NASA airplane flights aimed at studying hurricanes. Previous studies had identified some microorganisms in those environments, but no attempt had been made to catalog and understand them – especially while driving your plane through a raging hurricane.
But despite extremely dangerous conditions and several other practical issues, scientists are a sturdy bunch; they managed to collect thousands upon thousands of airborne microorganisms floating in the troposphere about 10 kilometers over the Caribbean, as well as the continental United States and the coast of California; no difference was found between microbes above air or land.
The first surprise was to see that over 60% of the samples they collected were still alive; they cataloged a total of 314 different families of bacteria in their samples, but it’s not yet clear if any of them are pathogens. This research seems to back up the idea that storms act as “elevators” for microbes, plucking them off Earth’s surface and carrying them high into the sky, says Dale Griffin, an environmental and public health microbiologist with the U.S. Geological Survey in St. Petersburg, Florida, who was not involved in the study.
What’s interesting is that 2 of the 17 most common families of bacteria in the upper troposphere feed on oxalic acid – one of the most common chemical compounds in the sky, raising a pertinent question: is the high atmosphere actually an ecosystem?
“That’s a big question in the field right now,” Griffin says. “Can you view [the atmosphere] as an ecosystem?”
We shouldn’t jump to conclusions too soon though warns David Smith, a microbiologist at NASA’s Kennedy Space Center in Florida. He has studied bacteria in the air above Oregon’s Mount Bachelor in a separate study, and found that they hibernate during their long, aerial trip.
“While it’s really exciting to think about microorganisms in the atmosphere that are potentially making a living, there’s no evidence of that so far.”
Even if they spend their atmospheric trip in dormancy, they could still play a key role in climate. How so? Well, most microbial cells are the perfect size and texture to cause water vapor to condense or even form ice around them, which means they could actually “seed” clouds, having a substantial effect on weather and climate.
In what can only be described as a milestone in biological and genetic engineering, scientists at Stanford University have, for the first time ever, simulated a complete bacterium. With the organism completely in virtual form, the scientists can perform any kind of modification on its genome and observe extremely quickly what kind of changes would occur in the organism. This means that in the future, current lab research that takes extremely long to perform or is hazardous in nature (dealing with lethal strains of viruses for instance), could be moved almost exclusively to a computer.
The researchers chose a pathogen called Mycoplasma genitaliumas their target for modeling, out of practical reasons. For one, the bacterium is implicated in a number of urethral and vaginal infections, like its name might imply as well, however this is of little importance. The bacterium distinguishes itself by having the smallest genome of any free-living organism, with just 525 genes. In comparison, the ever popular lab pathogen, E. coli has 4288 genes.
Don’t be fooled, however. Even though this bacterium has the smallest amount of genetic data that we know of, it still required a tremendous amount of research work from behalf of the team. For one, data from more than 900 scientific papers and 1,900 experiments concerning the pathogen’s behavior, genetics, molecular interactions and so on, were incorporated in the software simulation. Then, the 525 genes were described by 28 algorithms, each governing the behaviour of a software module modelling a different biological process.
“These modules then communicated with each other after every time step, making for a unified whole that closely matched M. genitalium‘s real-world behaviour,” claims the Stanford team in a statement.
Thus, even for an organism of its size, it takes that much information to account for every interaction it will undergo in its lifespan. The simulation work was made using a 128-node computing cluster, and, even so, a single cell division takes about 10 hours to simulate, and generates half a gigabyte of data. By adding more computing power, the computing process can be shortened, however its pretty clear that for more complex organisms, much more resources might be required.
“You don’t really understand how something works until you can reproduce it yourself,” says graduate student and team member Jayodita Sanghvi.
Big leap forward for genetic engineering and CAD
Emulating for the first time a living organisms is fantastic by itself, and is sure to set the ground for the development of Bio-CAD (computer-aided-design). CAD is primarily used in engineering, be it aeronautic, civil, mechanical, electrical and so on, and along the years has become indispensable, not only in the design process, but more importantly in the innovation process. For instance, by replacing the insulating material for a boiler in CAD, the software will imediately tell the engineer how this will affect its performance, all without having to actually build and test it. Similarly, scientists hope to achieve a similar amount of control from bio-CAD as well. The problem is that biological organisms need to be fully described into the software for bio-CAD to become lucrative and accurate.
“If you use a model to guide your experiments, you’re going to discover things faster. We’ve shown that time and time again,” said team leader and Stanford professor Markus Covert.
We’d love to see this research expanded forward, which most likely will happen, but we’re still a long way from modeling a human – about 20,000 genes short.