Tag Archives: infection

Researchers successfully use viruses to clear years-old, antibiotic-resistant infection

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.

Stylized bacteriophages. Image via Pixabay.

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.

Viral helpers

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.

New vaccine shows protection against aerosol tuberculosis infection in monkeys

The new tuberculosis vaccine MTBVAC takes a new step as a candidate for universal vaccination against tuberculosis and an alternative to the current Bacillus Calmette–Guérin (BCG) vaccine, according to the results of the research published in the journal NPJ-Vaccines which shows the protection results of the MTBVAC vaccine compared to the current BCG vaccine in a model of respiratory tuberculosis in rhesus macaques.

The currently used BCG vaccine, based on a live attenuated form of Mycobacterium bovis isolated from cows and which, this year 2021, will make a 100 years since its first use in humans as a tuberculosis vaccine, continues to be the only licensed vaccine against the disease. After decades of research in this field, MTBVAC is the first and only vaccine based on the human pathogen Mycobacterium tuberculosis that has entered human clinical evaluation, a historic milestone in human vaccinology.

MTBVAC has shown its safety in Phase 1 studies in adults in Switzerland and in Phase 1b in newborns in South Africa, where Phase 2 studies are currently being carried out in tuberculosis-infected and uninfected adults and in healthy newborns to select the dose and study its safety and immunogenicity in a larger number of participants in order to support advanced Phase 3 efficacy evaluation in the target age-groups.

MTBVAC is the first and only live attenuated vaccine based on a human isolate of Mycobacterium tuberculosis designed and constructed by the research groups of Carlos Martin of the University of Zaragoza and of Brigitte Gicquel of Institut Pasteur in Paris

In this recently published study led by Dr. Sally Sharpe from Public Health England, a single dose of the MTBVAC vaccine administered intradermally has been found to confer significantly better protection against aerosol exposure to M. tuberculosis in Rhesus macaques when compared to BCG by the same route and dose of administration. Vaccination with MTBVAC resulted in a significant reduction in disease pathology induced by M. tuberculosis infection as measured by medical scan imaging in vivo, macroscopic pathological lesions examination, and pathological anatomy study of the frequency and severity of pulmonary granulomas.

This study consolidates previous preclinical and clinical safety and immunogenicity studies and represents a strong proof of concept of the efficacy of MTBVAC in the macaque model, the most relevant model of efficacy against respiratory tuberculosis, supporting and urging the clinical development of studies to demonstrate the efficacy of MTBVAC as a prophylactic vaccine against respiratory tuberculosis in humans. This would make MTBVAC an essential tool in the fight against tuberculosis.

Despite WHO’s declaration of tuberculosis as “global health emergency” in 1993, today the disease continues to be one of the leading causes of mortality caused by infectious diseases worldwide. The WHO Global tuberculosis report 2020 estimates that 1.4 million people died of tuberculosis in 2019 and it is estimated that as a consequence of the COVID-19 pandemic deaths from tuberculosis could increase by up to twenty per cent (20 %) in the next five years.

What is cellulitis? The infection that causes just one foot to get red

Example of cellulitis in left foot. Credit: Wikimedia Commons.

Cellulitis is one of the most common bacterial skin infections, characterized by tenderness, swelling, and redness around affected sites. Unlike other skin infections, which can be more superficial, cellulitis involves the skin’s deeper layers and can become life-threatening if left untreated.

According to the American Academy of Dermatology, about 15 million Americans suffer from cellulitis every year.

Although they might sound similar, cellulitis shouldn’t be confused with cellulite, which is a totally harmless skin condition that causes lumpy, dimpled flesh on the thighs, buttocks, and abdomen. Cellulitis is also often confused with stasis dermatitis because it also causes the legs to get red, itchy, and swollen. The main difference is that stasis dermatitis is treated with compression to get the fluid out of the legs, whereas cellulitis requires antibiotics.

What causes cellulitis?

The vast majority of cellulitis cases are caused by Streptococcus and Staphylococcus bacteria, which can cause infections when they enter through a crack, break, or cut in the skin. Lately, researchers have drawn attention to an increasing number of more serious cellulitis caused by methicillin-resistant Staphylococcus aureus (MRSA).

Theoretically, cellulitis can appear anywhere on the body, though by far the most common site of infection is the lower leg. However, any area of the skin that has been disrupted can be at risk of developing cellulitis, such as where you’ve had surgery, cuts, puncture wounds, animal bites, an ulcer, or dermatitis.

Besides injuries, such as cuts, fractures, burns, or scrapes, other risk factors for cellulitis include:

  • a weakened immune system as a result of diabetes, leukemia, HIV/AIDS, or certain medications;
  • skin conditions such as eczema and athlete’s foot, which can break the skin and allow bacteria to creep through;
  • chronic swelling in the arms or legs, a condition that typically occurs post-surgery;
  • obesity;
  • history of cellulitis since having cellulitis before makes you prone to develop it again.

What are the symptoms of cellulitis?

Credit: Wikimedia Commons.

The following symptoms may be signs of cellulitis:

  • Red area of skin that tends to expand
  • Swelling
  • Tenderness
  • Pain
  • Warmth
  • Fever
  • Red spots
  • Blisters
  • Skin dimpling

Cellulitis isn’t contagious. Although the skin infection is common and usually not cause for great concern if left untreated, cellulitis can spread rapidly throughout the body, causing potentially fatal sepsis. So the earlier the infection is treated, the better. A doctor’s appointment is mandatory, preferably that day, if a patient has both a red, swollen, tender rash and a fever.

How is cellulitis treated?

As is the case for other bacterial infections, cellulitis treatment usually involves a prescription of oral antibiotics. Doctors often turn to penicillin, cephalosporin or erythromycin, according to the American Osteopathic College of Dermatology (AOCD). Usually, the course of antibiotics lasts five to 10 days, although some doctors prescribe a two-week prescription.

The red area on your foot or other body part affected by cellulitis should start to improve within three days of starting antibiotics. But It’s important that you take the medication as directed and finish the entire course of medication, even after you feel better.

While taking antibiotics, you can reduce the pain by placing a cool, damp cloth on the site of infection. Elevating the affected part of your body can also help manage the pain, as well as over-the-counter pain medication.

The best thing you can do is to take steps to prevent cellulitis altogether. It’s important to wash a wound daily with soap and water, as well as change bandages at least daily. Applying a protective cream or over-the-counter ointments, such as Vaseline or Polysporin, can further reduce the risk of infection. Those who have diabetes and poor blood circulation need to take extra steps to prevent skin injury.

Resistance is futile: what viruses are, and why we’ll never ‘beat’ them

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?

Image via Pixabay.

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.

These proteins form the distinctive corona-like (‘crown’) structure of the coronavirus. Image via Pixabay.

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.

Viral morphology

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.

Image credits ZMEScience.

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.

An example of an enveloped virus infecting a cell.

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.

A mutated coronavirus, better at infecting cells, is now “dominant” in the 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.

cryogenic electron microscope image of a SARS-CoV-2 spike protein.
Image credits Andrew Ward lab / 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.

Some patients spread COVID-19 even a week after the symptoms dissipate

A new research letter reports that some patients who were treated for mild COVID-19 cases and released still had the virus in their systems up to eight days after the symptoms disappeared.

The SARS-CoV-2 virus seen under the electron microscope.
Image credits NIAID / Flickr.

The document was published online in the American Thoracic Society’s American Journal of Respiratory and Critical Care Medicine (link at the bottom of this article) and describes how half of the patients treated and released by the authors still carried the virus after their symptoms subsided. The findings should be taken with a grain of salt as we’re talking about a research letter and a small sample size of 16 patients treated in the same area — the Treatment Center of PLA General Hospital in Beijing.

“The most significant finding from our study is that half of the patients kept shedding the virus even after resolution of their symptoms,” said co-lead author Dr. Sharma, instructor of medicine at the Section of Pulmonary, Critical Care & Sleep Medicine in the Department of Medicine at Yale School of Medicine.

“More severe infections may have even longer shedding times.”

All the patients were treated between January 28 and Feb. 9, 2020, and were 35.5 years old on average.

The researchers took throat swabs from all patients on alternate days and analyzed them for the virus. The patients were discharged after they received a negative result by at least two consecutive (polymerase chain reaction) tests to show that they recovered. Yet, at least half of them were still spreading the virus after this stage.

Their initial symptoms included fever, cough, pain in the pharynx, and difficult or labored breathing. Two patients had diabetes and one had tuberculosis, neither of which affected the timing of the course of COVID-19 infection. All but one of them had an incubation period — the time between infection and symptom onset — of five days. Symptoms lasted, on average, for eight days and patients remained contagious for one to eight days after the symptoms passed.

And here is the bad news for those of us who are bravely hanging on during our second or third week in quarantine:

“If you had mild respiratory symptoms from COVID-19 and were staying at home so as not to infect people, extend your quarantine for another two weeks after recovery to ensure that you don’t infect other people,” recommended corresponding author Dr. Lixin Xie, a professor in the College of Pulmonary and Critical Care Medicine at the Chinese PLA General Hospital in Beijing.

“COVID-19 patients can be infectious even after their symptomatic recovery, so treat the asymptomatic/recently recovered patients as carefully as symptomatic patients,” the team advises medical personel.

The authors emphasize that they looked at a small number of patients who all had mild cases of infection and then recovered, adding that it’s unclear whether other, more vulnerable groups would show the same evolution of the disease. Further research is needed to establish whether the virus can maintain transmission in later stages of the infection in other groups as well.

The letter “Time Kinetics of Viral Clearance and Resolution of Symptoms in Novel Coronavirus Infection” has been published in the American Journal of Respiratory and Critical Care Medicine.

Surprisingly few infants contracted the COVID-19 coronavirus

The coronavirus outbreak seems to be largely avoiding infants, according to a new study.

Image credits U.S. Army / Sgt. 1st Class Raymond Moore.

New research looking into the cases of infants admitted to Chinese hospitals with the coronavirus (COVID-19) reports that, between December 8 and February 6, only nine such cases were recorded. As of February 14th, over 63,000 cases of coronavirus infections were recorded in China, making the number of infant cases surprisingly small in comparison. As of last week, the virus tallied over 45,000 infections worldwide and led to the deaths of over 1,000 people.

Must be this old to ride

The infants in this study were 1 to 11 months old and were admitted to the hospital with fever, coughs, or other mild respiratory symptoms, the team explains. None of them suffered any subsequent complications from the virus. Given the disproportionately low number of infant infections recorded, the authors propose that they may be less susceptible to the virus or have a lower risk of being exposed. Alternatively, it could be the case that infants contract the virus just as easily as everyone else but only develop a mild case and don’t require medical supervision.

All of the infants identified had at least one infected family member and became sick after their relatives fell ill. However, another study showed that infected mothers do not pass the virus to their children before or during birth through cesarean section. Samples of amniotic fluid from these mothers, as well as throat swabs from the newborns, showed no sign of COVID-19. Umbilical cord blood and breast milk were also found to be free of the virus. However, the authors of the second study caution that all the participants were already in their third semester, so it remains possible that the virus can spread to a fetus in the earlier stages of the pregnancy. Similarly, they all gave birth by c-section, so it is unknown whether vaginal delivery also insulates the newborn from the virus.

SARS and MERS, two coronaviruses related to the current outbreak of COVID-19, also seemed to ‘avoid’ infants. They didn’t pass to the newborns during birth and few cases of infant infections were recorded in general.

The paper “Novel Coronavirus Infection in Hospitalized Infants Under 1 Year of Age in China” has been published in the journal JAMA.


New app can hear if your child has an infected ear

A new smartphone app can detect ear infections in young children.

App paper funnel.

Image credits Dennis Wise / University of Washington.

Ear infections can be pretty hard to spot with children, especially very young ones. It has vague symptoms, from tug of the ears to fever, or there could be no observable symptoms at all. However, it can be painful and make it hard for children to hear, potentially even posing long-term threats. A new app developed by researchers at the University of Washington (UW) can determine the likelihood of such an infection with an accuracy of 85%

“Designing an accurate screening tool on something as ubiquitous as a smartphone can be game changing for parents as well as health care providers in resource limited regions,” said co-author Shyam Gollakota, an associate professor in the UW’s Paul G. Allen School of Computer Science & Engineering.

“A key advantage of our technology is that it does not require any additional hardware other than a piece of paper and a software app running on the smartphone.”

According to the National Institute of Health, “three of every four children have at least one episode by their third birthday,” and “almost half of those who get them will have three or more ear infections during their first three years.” It’s also one of the most common reason why parents visit a pediatrician. Luckily, they’re pretty easy to treat with antibiotics once discovered. A doctor can monitor and drain an infection if needed, which will relieve pain or hearing loss.

The team wanted to give parents a quick and reliable way of screening for the condition at home, to help them decide whether or not to take their child to the doctor. Their app generates a series of soft, audible sounds that are focused into the ear — through a small paper funnel you’ll craft — making the eardrum vibrate. By analyzing the sounds beaming back from the eardrum, the app can determine the likelihood that there is fluid behind it. It’s kind of like  “tapping a wine glass,” the team explains.


Image credits: University of Washington. All you need is a piece of paper to cut and fold into a funnel. This funnel is rested on the outer ear, and will serve to focus the sound into the ear canal. Each sound is 150 milliseconds long, and sounds similarly to a bird chirping. The team tested their app on 53 children between the ages of 18 months and 17 years at Seattle Children’s Hospital. About half of the children were scheduled to undergo surgery for ear tube placement, a common surgery for patients with chronic or recurrent incidents of ear fluid. The other half were scheduled to undergo surgery unrelated to the ears. They tested each child with the app immediately before surgery, giving them the perfect opportunity to see the app’s accuracy.

“What is really unique about this study is that we used the gold standard for diagnosing ear infections,” said co-first author Dr. Sharat Raju, a surgical resident in otolaryngology-head and neck surgery at the UW School of Medicine.

“When we put in ear tubes, we make an incision into the eardrum and drain any fluid present. That’s the best way to tell if there is fluid behind the eardrum. So these surgeries created the ideal setting for this study.”

Authors note that many of the children responded to the chirps by smiling or laughing. The algorithm itself was correct in 85% of the patients, which the team says is comparable to current methods that specialized doctors use. On tests involving younger children (15 children between nine and 18 months of age) it correctly classified all five ears that were positive for fluid and nine out of the 10 ears that were not.

The paper “Detecting middle ear fluid using smartphones” has been published in the journal Science Translational Medicine.


Why you shouldn’t pop your pimples — Really, you shouldn’t

Credit: Pixabay.

Popping pimples can be very tempting, but this is considered a bad idea by most dermatologists. Picking at your blemishes can spread infection and ultimately worsen your acne. It can also permanently scar your face. If you do insist on getting rid of the pimples, there are more hygienic and safe methods you should use — never do it with your bare hands, that’s for sure.

How pimples form

It helps the discussion if we first learn what causes blemishes.  It all starts in the hair follicles which contain the oil-secreting sebaceous glands. These glands are found the most on the face and scalp compared to other parts of the body, and there’s no coincidence why these areas are the most prone to pimples.

The glands’ function is to secrete oil to lubricate the hair, but when hair or skin dies the pores the oil oozes through are blocked. This creates an excess of oil in the pores which are forced by physics to expand under the skin in the shape of a water balloon. By this time, the skin looks red, puffy and infected.

When you squeeze a pimple, there’s a high risk of forcing debris of bacteria and dead skin deeper straight to the follicle. The follicle wall might rupture then and spill infected material into the dermis, which is the innermost layer of the skin. Even if you pull out a lot of that nasty goo, chances are infected material tunneled the dermis from below because of the pressure you exerted.

Popping pimples can lead to:

  • Scarring. This is quite rare and happens when you pick a pimple so deeply so that you would get a hole. It can still happen though when some people get carried overboard.
  • Scabs. A big white head pimple can ruin your morning, especially if a meeting is due but living with it may be better than the alternative: a nasty, crusty scab. This happens because the skin thickens or darkens to protect itself from injury. Unfortunately, brown spots or hyperpigmentation is harder to clear up than a pimple itself and can take months to get rid of.
  • Infection. In some cases, medical attention may be required.
  • Pain. Especially the big ones — those hurt like hell.
  • New pimples. The good from a squeezed pimple can block other pores and lead to the formation of new pimples.

A hands-off approach when it comes to your skin may be for the best, even though it might seem socially awkward not to.

How to pop a pimple the right way

Whiteheads will come away by themselves in about a week, which might seem like an eternity to a teenager. If you really insist, there are some safe methods you can use to get rid of some pimples.

Use two cotton swabs instead of your fingers, or better yet a sterilized needle. Wait for the pimple to come to a head, then squeeze with the cotton swabs. Stop squeezing when you see blood and then spot-treat the pimple by applying a tiny bit of hydrocortisone. Make sure you apply it only on the zit.

Before attempting anything, it’s important you thoroughly wash your hands and rub alcohol on your fingers to sterilize them. Always apply pressure gently so you don’t push debris down the follicle.

If you have a nuclear meltdown on your face, then you could visit a dermatologist. The doctor will use special tools like a cortisone shot or even lasers to extract your whiteheads and blackheads or drain a cyst.

If it’s a blind pimple — big red bumps under the skin– then there’s nothing you can do. Attempting to pop it will only make it worse as you can get the skin injured. Wait for it.


Most common type of childhood leukemia is partly due to lack of exposure to microbes during infancy

British researchers claim they’ve found the likely cause of the most common childhood leukemia. After compiling more than 30 years of research, the team found that acute lymphoblastic leukemia (ALL) is caused by a combination of genetic factors and a lack of exposure to infection during infancy. This means that the disease can be preventable if steps are taken to prime the immune system during the child’s first year of life.


Credit: Pixabay.

Childhood acute lymphoblastic leukemia (ALL) is a type of cancer in which the bone marrow makes too many immature lymphocytes (a type of white blood cell). There are two main types of lymphocytes, B cells and T cells, and in children with ALL, too many stem cells become lymphoblasts, B lymphocytes, or T lymphocytes. These cells do not work like normal lymphocytes and are not able to fight infection very well.

ALL is the most common type of childhood cancer. It most often occurs in children ages 3 to 5 and affects slightly more boys than girls. In the United States, around  3,000 people younger than age 20 are diagnosed with ALL each year. Luckily, research has gone a long way in the past couple of decades, to the point that around 90 percent of cases are cured. However, for more than 100 years scientists have been debating the possible causes for ALL, including ionizing radiation, electricity cables, electromagnetic waves and man-made chemicals. None of these hypotheses have withstood scientific scrutiny.

Now, Professor Mel Greaves and colleagues from The Institute of Cancer Research, London, claim they have finally found out what causes ALL and have evidence to support their claims. According to Greaves, ALL develops due to a two-step genetic mutation before birth in the fetus stage. This mutation predisposes the children to leukemia; however, only 1% of children born with the genetic change go on to develop ALL. The leukemia is triggered later, in childhood, by exposure to one or more infections, which most often happens to be a flu virus infection.  

“This body of research is a culmination of decades of work, and at last provides a credible explanation for how the major type of childhood leukaemia develops. The research strongly suggests that ALL has a clear biological cause, and is triggered by a variety of infections in predisposed children whose immune systems have not been properly primed. It also busts some persistent myths about the causes of leukaemia, such as the damaging but unsubstantiated claims that the disease is commonly caused by exposure to electro-magnetic waves or pollution,” Graves said in a statement.

Studies carried out previously by Greaves and other researchers showed that twins with ALL had to have two mutations in order to develop cancer. The first mutation arises in the womb, leading to the production of a population of pre-malignant cells that spread to the other twin through the shared blood supply. The second mutation occurs after birth and is not present in the other twin. Population studies in people and animal experiments suggest that the second genetic mutation can be triggered by an infection. For instance, mice that had been engineered to have a leukemia-initiating gene went on to develop ALL after they were moved from an ultra-clean, germ-free environment to one that had common microbes.

Studies have shown that microbe exposure early in infancy such as daycare attendance or breastfeeding can offer protection against ALL. Most probably, the exposure to microbes primes the immune system.

Acute lymphoblastic leukemia is particularly prevalent in affluent societies and is increasing in incidence at around 1% per year. The new findings explain why this may be happening: a lack of microbial exposure can lead to an immune system malfunction that can trigger ALL. So, the problem is that a lack of infection can lead to a far more threatening infection later in life.

Now, Greaves and colleagues are investigating whether earlier exposure to harmless bugs could prevent this cancer in mice. If this happens, then ALL prevention measures could be taken such as exposing children to common but benign microbes.

“I hope this research will have a real impact on the lives of children. The most important implication is that most cases of childhood leukemia are likely to be preventable. It might be done in the same way that is currently under consideration for autoimmune disease or allergies – perhaps with simple and safe interventions to expose infants to a variety of common and harmless ‘bugs’,” said Greaves.

“It’s exciting to think that, in future, childhood leukemia could become a preventable disease as a result of this work. Preventing childhood leukemia would have a huge impact on the lives of children and their families in the UK and across the globe,” said Professor Paul Workman, Chief Executive of The Institute of Cancer Research, London.

Scientific reference: Mel Greaves, A causal mechanism for childhood acute lymphoblastic leukaemia, Nature Reviews Cancer (2018). DOI: 10.1038/s41568-018-0015-6.

Some people can really tell if you look sick, new study reports

How good are you at telling if someone’s sick? A new study finds that at least some people are quite good at identifying facial cues.

Composite, overlaid images of the 16 individuals, sick (left) and healthy (right). Image credits: Audrey Henderson/St Andrews University.

Detecting and avoiding sick people is a vital aspect of limiting exposure to diseases, and its likely that many of our ancestors lived and died by how well they could do it. Since the advent of modern medicine, however, that internal radar has somewhat lost in importance. Previous studies have shown that obvious symptoms of disease facilitate identification — but what of non-overt displays? Clinical neuroscientist John Axelsson wanted to see just how good people are at detecting such displays, and what cues they follow in the process.

“Almost no knowledge exists on whether humans can detect sick individuals, and if so by what cues”, he writes in the study. “Here, we demonstrate that untrained people can identify sick individuals above chance level by looking at facial photos taken 2 h after injection with a bacterial stimulus inducing an immune response.”

Axelsson and his team, which included neuroscientists and psychologists from Germany and Sweden, injected eight men and eight women with a molecule found in bacterial membranes. The idea was to generate a bodily response to the pathogens in the subjects without actually making them sick. It was still a bit unpleasant, but the subjects did receive $430 for their troubles.

The team then photographed each subject 130 minutes after they received the injection (when they said they felt most unwell). Some days later, they also gave participants a placebo (saline) injection and photographed them. They then had 60 students from universities in Stockholm identify the sick photos. The students had a significantly better guess rate than random: 62%, compared to 50%, which would have been completely random. Out of 2,945 ratings for the 32 different facial photos, 1,215 were sick people. Volunteers got it right 775 times and wrong 440 times. This is pretty impressive, but it’s still only semi-accurate, seeming to suggest that we only superficially look at cues. Still, results might significantly improve in real life scenarios.

Researchers theorize that we are much better at identifying people we’re familiar with because we’re much more in tune with their facial features and day to day behavior. Also, sick people often act differently, which could also be an important tell. For instance, they tend to be less talkative and tired even before other symptoms kick in. By the time obvious cues like sneezing or coughing emerge, it may already be too late to avoid contagion. Odors might also be a significant cue — previous studies have already shown that when we’re sick, our body odor tends to change. So while the face is the main thing we look at, it doesn’t really paint the whole picture.

Next, scientists analyzed what cues people were using to identify the disease. They found that we focus on the skin and the eyes, as well as the overall appearance of tiredness.

“Acutely sick people were rated by naive observers as having paler lips and skin, a more swollen face, droopier corners of the mouth, more hanging eyelids, redder eyes, and less glossy and patchy skin, as well as appearing more tired. Our findings suggest that facial cues associated with the skin, mouth and eyes can aid in the detection of acutely sick and potentially contagious people,” the study concludes.

Looking at how we identify other sick people isn’t only a scientific curiosity. Researchers say it could have significant benefits for public health. Helping people improve their disease-identifying skills could help them avoid contagion, even if they don’t realize it. The next step, researchers say, is to figure out to what extent this is a learned behavior. They want to see if doctors and trained professionals are better than average people at detecting disease symptoms.

Journal Reference: John Axelsson et al. Identification of acutely sick people and facial cues of sickness. DOI: 10.1098/rspb.2017.2430


Drug-resistant candida outbreaks in the UK despite hospital efforts to control it

Over 200 UK patients in more than 55 hospitals have been infected or colonized by a highly drug resistant strain of fungus, Candida auris.


Image via Pixabay.

Three of these hospitals have seen large outbreaks of C. aureus, all of which were since officially declared over by health authorities. Luckily, nobody lost their lives. In fact, no deaths have been attributed to the fungus since it was first found in the UK back in 2013. However, during these latest outbreaks, some 50 patients developed clinical infections and 27 developed blood infections, which can be life-threatening. Most of the UK cases had been detected by screening, rather than investigations for patients with symptoms.

The scary thing about the C. aureus is how fast it’s emerging, and the sheer anti-fungal resistance this thing seems to possess. It was first identified in Japan in 2009 and has spread to more than a dozen countries since. The CDC lists around 100 known instances of the fungus in nine US states so far, and a further 100 where it didn’t cause an infection.

Most people who contract the fungus don’t develop an infection or only develop a mild one. Which is very bad news for those patients because if you do, things take a sharp turn south. The fungus can be deadly if contracted by patients with weakened or compromised immune systems, but the real risk is developing an invasive infection. Over a third of those who develop an invasive infection with C. auris die, though there were no reported deaths in the UK outbreak.

Such an infection can become almost impossible to beat back with drugs because C. auris is highly resistant to a broad spectrum of anti-fungal compounds. Every case in the UK so far has shown reduced responsiveness to fluconazole, the bread-and-butter of antifungal defense. Most of them were resistant to multiple other drugs, and some are resistant to all three main classes of antifungal drugs used to treat Candida and other fungal infections.

This resistance also allows C. auris to spread through the environment and between patients with surprising ease. One in three of the UK hospitals hit by the recent outbreak reported difficulty in eliminating the fungus from their premises for more than a year. The fungus was found on “the floor around bed sites, trollies, radiators, windowsills, equipment monitors and key pads, and also one air sample.” In light of these findings, healthcare officials have implemented new protocols, such as having healthcare workers wear better protective equipment and isolating all patients colonized or infected by the fungus.

Despite the risk, officials want to assure the UK public that their hospitals are safe.

“Our enhanced surveillance shows a low risk to patients in healthcare settings. Most cases detected have not shown symptoms or developed an infection as a result of the fungus,” Dr Colin Brown of Public Health England’s national infection service told the BBC.

But the rapid emergence of the fungus, combined with its high drug resistance, has public health officials worried. A CDC report this July highlighted the yeast as a “serious global health threat.”

Oral sex might be helping the spread of unstoppable bacteria

Who thought oral sex might be bad for the planet? According to the World Health Organization (WHO), drug-resistant gonorrhea is spreading at an alarming pace, and oral sex is helping fuel it.

Gonorrhea affects about 0.8% of women and 0.6% of men, with an estimated 33 to 106 million new cases each year (out of the almost 500 million cases of sexually transmitted infections). In recent years, some instances of the bacteria have become drug-resistant and almost impossible to treat, prompting the WHO to list it as one of the world’s biggest health threats. There are reasonable concerns that it might simply become incurable.

Speaking to the BBC, Prof Richard Stabler, from the London School of Hygiene & Tropical Medicine, expressed the gravity of the situation:

“Ever since the introduction of penicillin, hailed as a reliable and quick cure, gonorrhoea has developed resistance to all therapeutic antibiotics. In the past 15 years therapy has had to change three times following increasing rates of resistance worldwide. We are now at a point where we are using the drugs of last resort, but there are worrying signs as treatment failure due to resistant strains has been documented.”

There are three main ways to tackle this issue: developing new antibiotics, preventing its spread, and vaccines. The first one is not looking so good. Dr. Manica Balasegaram, from the Global Antibiotic Research and Development Partnership, said:

“The situation is fairly grim. There are only three drug candidates in the entire drug [development] pipeline and no guarantee any will make it out.”

The second part is all about limiting its spread. There’s no realistic way we can stop all infected people from having unsafe sex, especially since gonorrhea is often without any visible symptoms. This is where oral sex is stepping into the scene.

It’s hard to say if people are doing more of it nowadays because data on it is so scarce. In fact, oral sex fits an interesting position in our society: most people do it, but we never talk about it. A 2001 survey in the UK found that 77.9% of men and 76.8% of women have given and/or received oral sex in the past year. Rates are similar in Europe and the US. It’s important to realize that oral sex also passes on a lot of infections — just like regular sex does. Gonorrhea, genital herpes, and syphilis are easily passed this way, whereas, chlamydia, HIV,  hepatitis A, hepatitis B, and hepatitis C, genital warts, and pubic lice are passed less frequently. So if you’re having safe sex but unprotected oral sex, you’re still at some risk.

Of course, doctors acknowledge that this will change few people’s minds, but at least it’s important to acknowledge it.

The last, and probably decisive, course of action will be vaccines. Current control measures are inadequate and seriously threatened by the rapid emergence of antibiotic resistance, a 2014 study reports, highlighting the need for a gonorrhea vaccine. Such a vaccine has been demonstrated on mice populations, but human trials have yet to be carried out.

wound licking

Is licking your wounds actually a good thing?

wound licking

Credit: Flickr

When faced with a minor cut or bruise, most people will instinctively lick the site of injury. It’s almost second nature as if it’s inscribed in our DNA. Everybody does it — humans, dogs, virtually anyone with a tongue and saliva. There’s even a widely used idiom, ‘lick your wounds’, which means to spend time getting back your strength or happiness after a defeat or bad experience.

You’ve likely done it countless times so far and you’re still alive. So, without even doing proper science we at least know that licking a wound isn’t fundamentally bad. But does it accelerate healing in any way or does it just act like a comforting placebo?

Wound licking: good or bad?

A 2008 study published by Dutch researchers suggests putting saliva in contact with an open wound comes with many benefits. It seems a certain compound of saliva called histatin not only kills bacteria, preventing infections, but also accelerates healing.

The researchers first collected epithelial cells from the inner cheek then cultured them in multiple petri dishes until the surface was completely covered in cells. An incision was then made in the cell layer by scratching away a small area of the cells.

One dish was bathed in isotonic fluid containing the same number of dissolved particles as blood. But other dishes were bathed in glorious human saliva. Sixteen hours later, the scientists reported the saliva-treated artificial wound was almost completely closed while untreated dishes had a substantial part of the ‘wound’ still open. Then, it was only a matter of singling each saliva component to find out which one was responsible for the accelerated healing property.

“This study not only answers the biological question of why animals lick their wounds,” said Gerald Weissmann, MD, Editor-in-Chief of The FASEB Journal, “it also explains why wounds in the mouth, like those of a tooth extraction, heal much faster than comparable wounds of the skin and bone. It also directs us to begin looking at saliva as a source for new drugs.

Another added benefit of wound-licking is that small wounds and injuries can be cleansed of debris like dust, infected tissue, and other contaminants.

There are some risks, though

Though there are proteins and enzymes in saliva that promote wound healing, it’s worth remembering that our mouths are also host to scores of bacteria. It’s estimated that there are over 100 million microbes composing more than 600 different species in each milliliter of saliva. These bacteria are completely harmless as long as they stay in the mouth and there are no open wounds inside it. In fact, mouth bacteria are responsible for some of the most common diseases in humans, particularly gum disease and tooth decay (cavities).

As such, in some cases, licking your wounds may be a bad idea, especially if you have a history of decreased immunity. For instance, there’s one odd case reported in a 2002 paper published in the New England Journal of Medicine. The paper describes how German doctors were forced to amputate the thumb of a diabetic man who licked a small wound inflicted from falling off his bike. The diabetic patient had fallen victim to necrotizing fasciitis, which can destroy tissue in as little as 12-24 hours and absent urgent medical care can be fatal. Subsequent examination revealed two types of bacteria: Eikenella corrodens, commonly found inside the mouth, and Streptococcus anginosus, often found on the skin and in the throat, were responsible for the infection. It should be noted that this sort of infection is rare and only occurs if the victim is vulnerable somehow; in this case suffering from diabetes.

And don’t let pets lick your wounds, seriously

There are as many bacteria in our bodies as are human cells. This flora, as scientists call it, includes skin bacteria, mouth bacteria or gut bacteria, as well as yeast and other eukaryotes. Our immune system has adapted to this flora and learned to live in harmony with it. Each person’s flora is unique and absent many types of bacteria, we wouldn’t be able to survive. However, getting exposed to foreign bacteria can be very dangerous.

Your dog will have its own colonized set of bacteria and yeast flora. If you raised the dog since he was a pup, then it’s likely his flora has come in contact with yours so you’ve become immune. That being said, don’t trust someone else’s dog to lick your cut finger or bruise. You shouldn’t let your own dog do it, for that matter.


Animals lick their wounds because they have no other recourse. We humans, however, are blessed with knowing how to use soap and water, as well as disinfectants and, if required, antibiotics. Licking your own wound or letting your pet do it for you shouldn’t cause disease, but it does come with risks. In most cases, the safest thing to do with your mouth is to ask for help. Otherwise, just use a band-aid.


New infections cause dormant viruses to reactivate

Herpes viruses are almost impossible to eliminate from your body. While other viruses succumb when they are defeated by the immune system, the herpes virus remains in the body forever, lying in wait, sometimes reactivating years later. A new study has found that new infections may weaken the body just enough to favor the reawakening of herpes.

Herpes virus

Artistic representation of the herpes virus. Via Gofolic.

For quite a while, scientists have been trying to figure out exactly why the virus sometimes reactivates, even after lying dormant for decades. Herpes, which has been associated to cancer, could be combated with more efficiency if researchers understand the underlying mechanisms of the pathogen. Now, a team has found that interactions with other infections later in life are the catalysts for the awakening.

“Probably 95 percent of us have been infected with at least one herpes virus, but many people never have a problem with it,” said study co-author Rolf Renne, a professor of molecular genetics and microbiology in the UF College of Medicine and a member of the UF Genetics Institute and the UF Health Cancer Center. There are eight herpes viruses that infect humans, causing diseases that range from cold sores and chickenpox to mononucleosis and cancer. “The question has been: What happens to reactivate these viruses to cause disease?”

To me, this information was quite shocking. The fact that Renne, one of the leading voices in the field believes that almost all of us have been infected is quite worrying – especially when in the vast majority of the cases the virus is never truly eliminated from the body.

What they found in this research is that a protein called interferon gamma keeps herpes in check, which explains why the virus typically remains dormant in the body. But when the immune system is challenged, especially when fighting an infection,  another protein called interleukin 4 was released, which not only blocked interferon gamma from doing its job but also directly activated virus replication. Again, the big problem here is not the herpes virus in itself – but rather that when the virus reactivates, it infects new cells, and significantly increases the chances of a cancerous tumor developing.

“The fact that the virus can ‘sense’ the immune reaction to a worm and respond by reactivating is a remarkable example of co-evolution,” said senior author Dr. Herbert W. Virgin IV, of Washington University in St. Louis. “We think other interactions between multiple infectious agents and the immune system will be discovered over time that we will view as similarly sophisticated or maybe even devious. Understanding these interactions will help us survive in a complex microbial world.”

Their findings are quite intuitive – it seems rather safe to assume that the weakening of the body favors the reemergence of dormant virus, but intuitive is not science.

Source: University of Florida

Adelie penguins going about their way. Photo :Peter & J. Clement/

New bird flu infects Antarctic penguins

Adelie penguins going about their way. Photo :Peter & J. Clement/

Adelie penguins going about their way. Photo :Peter & J. Clement/

It’s so cold even penguins get the flu in the Antarctic. Seriously, researchers report in a paper published in the journal mBio how they identified a new strain of influenza that infects Adelie penguins which breed in huge colonies on the rocky Antarctic Peninsula. The virus itself seems to be dormant as the penguins don’t exhibit any visible flu symptoms, yet the findings do raise important questions like how influenza spreads over the world in extremely isolated regions such as the Antarctic.

Bird flu strikes penguins

Researchers at a World Health Organization flu lab in Australia, led by Aeron Hurt, trekked down to the Antarctic Peninsula a year ago and collected oral samples from two distinct colonies. Using a laboratory technique called real-time reverse transcription-PCR, the researchers found avian influenza virus (AIV) genetic material in 3 percent of the samples.

[NOW READ] Climate change causes penguin colonies to decline by a third

The researchers managed to culture four viruses, demonstrating that live infectious virus was present. All of these were H11N2 influenza viruses that were highly similar to each other, yet when their genomes were compared with those from a database spanning all known animal and human influenzas there was nothing quite alike on the planet. Apparently, this penguin influenza is unique.

This suggests that it has been isolated for many decades — presumably hiding out in the penguins’ digestive and respiratory tracts, or possibly frozen in Antarctic ice. So where did they come from and in Antarctica of all places?

[ALSO READ] Dutch researchers create super-influenza, with the capacity to kill billions

Four of the gene segments were most closely related to North American avian lineage viruses from the 1960s to 1980s. Two genes showed a distant relationship to a large number of South American AIVs from Chile, Argentina and Brazil. Using a molecular clock to incorporate the evolutionary rate of each AIV gene segment, the researchers estimated that the virus has been evolving for the past 49 to 80 years without anyone knowing about it.

Concerning this South American connection, it may be possible that long distance migratory birds are the root of the virus’ spreading. The yellow-billed pintail duck, for instance, is known to stray from South America and end up on the Antarctic Peninsula. This coupled with penguins’ utter contempt for hygiene, despite their tuxedo, fancy-like appearance, may have helped spread the virus.

“The large amount of penguin feces in colonies during summer, which in some cases is so significant it can be observed on satellite images, presumably facilitates (viral) transmission by the fecal-oral route,” the scientists note.

While the penguin influenza hasn’t caused any illness yet, it’s still interesting to follow. Scientists might gather from this how often, for instance, infectious viruses can reach isolated communities and far away places like Antarctica and what animals are most vulnerable.

New Treatment for Gonorrhea Acts like a Vaccine, Preventing Reinfection

A first step has been taken towards an effective treatment for Gonorrhea – with drug resistant strains on the rise, this moment comes just at the right time, merely days after the U.S. Centers for Disease Control (CDC) placed the STD on a list of “urgent threats” in the fight against drug-resistant bacteria.


Gonorrhea (colloquially known as the clap) is a common sexually transmitted infection which affects more than 700,000 people in the United States each year. It’s a serious disease, but nothing really dramatic – or at least that’s how the situation was up until a few years; in the past decade,has progressively developed resistance to the antibiotic drugs prescribed to treat it. According to the CDC the bacteria which causes the disease in humans initially leads to painful inflammation and discharge, but if not treated properly, can cause infertility and can even be fatal. Researchers from the University at Buffalo, think that the answer doesn’t lie in more powerful drugs, but in making the body react better to the threat.

They showed that the disease could be cured by introducing into the genital tract a cytokine, or immunoregulatory protein, known as interleukin-12 (IL-12), which is also currently investigated as an anti-cancer agent. Michael Russell, a microbiologist and immunologist at S.U.N.Y. Buffalo has been working on the STD for some 20 years, and he his studies seem to indicate that it directly affects immune systems.

He tested his method on mice and…

“And it worked,” he says, “very nicely.”

Not only did mice treated with IL-12 respond more quickly to antibiotics, they were also significantly less likely to contact the same strain a month later – which is a constant problem with gonorrhea. Of course, the drug has the potential to do wonders against the disease, but Russell wants to push things even further – transform the infection into a “living vaccine”:

“Since the second world war,” Russell says, “we’ve been treating infections by throwing antibiotics at them. Now that bacteria are emerging with antibiotic resistance, we have nothing else in the pipeline to deal with gonorrhea.” But the IL-12 treatment, he says, can turn the infection into a “live vaccine,” allowing the body to develop immunity.

However, even with the massive amount of pressure caused by the imminent antibiotic-resistant germ crisis, the method is miles away for being suitable for humans. But eventually he hopes to see this novel approach to the treatment of gonorrhea and other infectious diseases.


Dogs can be trained to detect extremely dangerous superbug

Researchers had already known that dogs can sniff out hospital superbug Clostridium defficile from stool samples of patients, but now, a really cute beagle has been trained to sniff out the bacteria from the air in the hospital.

Cliff – the beagle

C. difficile infection generally occurs in patients who have been recently admitted in hospitals and were previously on antibiotics. In this research, scientists from Netherlands have trained a dog which can detect the distinct smell in the bacteria’s stool.

They chose a two-year old beagle, called Cliff, for this study; beagles are known not only for their absolute cuteness, but also for their sharp sense of smell – for which they are commonly employed as detection dogs.

Cliff’s detection abilities were tested, as he was asked to sniff 50 stool samples from the people who had the infection and 50 stool samples that were from healthy people; his results were remarkable, being able to identify all 50 positive samples and 47 out of the 50 negative samples. What’s even better was not only that he was super effective at sniffing out the bug, but he was also very quick. It took him less than 10 minutes per case – the official test takes several days and is quite costly.

“This could have great potential for C. difficile infection screening in healthcare facilities and thus contribute to C. difficile infection outbreak control and prevention,” researchers conclude.