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Antibiotics can destroy many types of bacteria, but increasingly, bacterial pathogens are gaining resistance to many commonly used …

Antibiotics can destroy many types of bacteria, but increasingly, bacterial pathogens are gaining resistance to many commonly used types. As the threat of antibiotic resistance looms large, researchers have sought to find new antibiotics and other ways to destroy dangerous bacteria. But new antibiotics can be extremely difficult to identify and test. Bacteriophages, which are viruses that only infect bacterial cells, might offer an alternative. Bacteriophages (phages) were studied many years ago, before the development of antibiotic drugs, and they could help us once again.

Image credit: Pixabay

If we are going to use bacteriophages in the clinic to treat humans, we should understand how they work, and how bacteria can also become resistant to them. Microbes are in an arms race with each other, so while phages can infect bacteria, some bacterial cells have found ways to thwart the effects of those phages. New research reported in Nature Microbiology has shown that when certain bacteria carry a specific genetic mutation, phages don’t work against them anymore.

In this study, the researchers used a new technique so they could actually see a phage attacking bacteria. Mycobacteriophages infect Mycobacterial species, including the pathogens Mycobacterium tuberculosis and Mycobacterium abscessus, as well as the harmless Mycobacterium smegmatis, which was used in this research.

The scientists determined that Mycobacterial gene called lsr2 is essential for many mycobacteriophages to successfully infect Mycobacteria. Mycobacteria that carry a mutation that renders the Lsr2 protein non-functional are resistant to these phages.

Normally, Lsr2 aids in DNA replication in bacterial cells. Bacteriophages can harness this protein, however, and use it to reproduce the phage’s DNA. Thus, when Lsr2 stops working, the phage cannot replicate and it cannot manipulate bacterial cells.

In the video above, by first study author Charles Dulberger, a genetically engineered mutant phage infects Mycobacterium smegmatis. First, one phage particle (red dot at 0.42 seconds) binds to a bacterium. The phage DNA (green fluorescence) is injected into the bacterial cell (2-second mark). The bright green dots at the cells’ ends are not relevant. For a few seconds, the DNA forms a zone of phage replication, and fills the cell. Finally, the cell explodes at 6:25 seconds. (About three hours have been compressed to make this video.)

The approach used in this study can also be used to investigate other links between bacteriophages and the bacteria they infect.

“This paper focuses on just one bacterial protein,” noted co-corresponding study author Graham Hatfull, a Professor at the University of Pittsburgh. But there are many more opportunities to use this technique. “There are lots of different phages and lots of other proteins.”

Sources: University of Pittsburgh, Nature Microbiology

Carmen Leitch

Streptococcus pyogenes, which is often called group A Streptococcus, infects people around the world. While estimates vary, these …

Streptococcus pyogenes, which is often called group A Streptococcus, infects people around the world. While estimates vary, these infections could be responsible for the deaths of over half a million individuals every year. The pathogen can also cause an illness known as scarlet fever, which usually occurs in kids between the ages of 5 and 15. Scarlet fever was once a major health threat for children, and there were infection rates as high as 20 percent in the early 20th century. The disease became less of a public health concern until its recent reemergence in the UK, Hong Kong, and mainland China.

Colorized scanning electron micrograph of Group A Streptococcus (Streptococcus pyogenes) bacteria (blue) and a human neutrophil (purple). Credit: NIAID

Isolates taken from patients have shown that S. pyogenes can carry resistance genes that shield it from the effects of antibiotics including tetracycline, erythromycin and clindamycin. These bacteria can also generate powerful toxins, like molecules called SSA and SpeC, known as superantigens, and an enzyme called Spd1.

While S. pyogenes infections are still rare, they can kill as many as 20 percent of people who are infected.

In 2019, a variant isolated in the UK, the so-called M1UK strep A variant, was shown to produce five times more strep A toxins compared to previous strains. The SpeA superantigen generated by this variant can short-circuit host immunity and was once known as the scarlet fever toxin. The M1UK variant also carried a few genetic mutations compared to previous strains, and one of those mutations was located close to the toxin gene. The findings have been reported in Nature Communications.

More research will be needed to know whether this variant has gotten better at moving from one person to another to cause infection.

Strep A is very rare, and the study authors noted that people should not be concerned about this novel variant at this time. Basic hygiene practices, like hand washing, can still protect us from dangerous germs like S. pyogenes. Strep A infections are spread through close contact with infected people, who may be coughing and sneezing. Other symptoms include a rash and fever.

The study authors also noted that these findings have highlighted the importance of developing a vaccine for Strep A infections.

An unrelated study reported in mBio has also revealed a different mutation that occurs in a Strep A variant that increases the production of a toxin called streptolysin O (SLO). SLO can help Strep A survive in the host, evade host immunity, and is destructive to host tissues. Variants that did not express SLO were not as virulent, noted the study authors.

Right now, scientists are working on a Strep A vaccine, as described in the video above.

Sources: Nature Communications, Griffith University, mBio

Carmen Leitch

Infections with many different types of bacteria including Streptococcus pneumonia, Listeria monocytogens, and Neisseria mengitidis can cause bacterial …

Infections with many different types of bacteria including Streptococcus pneumonia, Listeria monocytogens, and Neisseria mengitidis can cause bacterial meningitis. It’s estimated that every year over 1.2 million cases of bacterial meningitis happen around the world, and without treatment, this deadly disease is fatal to seven of ten people who are sickened by it. Even with antibiotic treatments, three of ten patients die. Survivors are left with issues like chronic headaches, seizures, loss of vision or hearing, and other neurological consequences. New research reported in Nature has revealed how bacteria are able to penetrate the meninges that surround and protect the brain to cause bacterial meningitis. The findings have shown that bacteria use neurons to evade immunity and infect the brain, and the work may aid in the creation of new therapeutics.

A digitally-colorized SEM image depicts of Streptococcus pneumoniae bacteria (lavender), as they were being attacked by a white blood cell (pink).  / Credit: CDC/ Dr. Richard Facklam

Right now, antibiotics can help eliminate the bacterial pathogens that cause this illness. But steroids are also needed to control the dangerous inflammation that can occur along with the infection. However, reducing inflammation also weakens the immune response, making it harder to get rid of the infection.

In this research, the scientists used Streptococcus pneumoniae and Streptococcus agalactiae bacteria, which can both cause bacterial meningitis in humans. They determined that when these bacteria get to the meninges, they release a toxin, which activates neurons in the meninges that sense pain. This pain neuron activation could explain why bacterial meningitis patients get horrible headaches, noted the researchers.

The activated pain neurons then release a signaling molecule called CGRP, which binds to a receptor called RAMP1 on the surface of immune cells called macrophages. Once CGRP binds to RAMP1 on macrophages, the immune cells are basically disabled, and they stop responding to bacterial infections like they normally would.

The link between CGRP and RAMP1 on macrophages also stops them from signaling to other immune cells, which allows the bacterial infection to not only penetrate the meninges but to spread infection.

This work was confirmed with the use of a mouse model that lacked the pain neurons that are activated by bacteria. Compared to mice with those neurons, the engineered mice had less severe brain infections when they were exposed to bacteria that cause meningitis. There were also lower levels of CGRP in the engineered mice compared to normal mice. The normal mice, however, had higher levels of bacteria in the meninges.

Additional experiments also showed that when mice were treated with drugs that block RAMP1, the severity of the bacterial infection was reduced. Mice treated with RAMP1 blockers were able to clear their infections faster too.

It may be possible to help the immune system clear cases of bacterial meningitis with medications that block either CGRP or RAMP1, potentially in conjunction with antibiotics. There are already drugs that can do this, and they are generally used to treat migraine.

Sources: Harvard Medical School, Nature

Carmen Leitch

In recent years, we have learned a lot about the crucial role gut microbes play in our health …

In recent years, we have learned a lot about the crucial role gut microbes play in our health and well being. The extent of their influence can be surprising at times. Research has shown that gut microbes can impact the repair of tissue damage by fueling the production of a type of immune cell called Tregs, or regulatory T cells. These cells reside in various tissues and help regulate inflammation and immunity in different organs. But new work has shown that Tregs can also move around the body and respond when they are called to help fix injuries and tissue damage, such as in the muscles and liver. The findings, which used a mouse model and still have to be confirmed in humans, have been reported in the journal Immunity.

Image credit: Pixabay

There are Tregs that reside in the colon, and these cells are known to play an important role in the maintenance of gut health. The immune system in the gut has to protect us from infection while also ignoring the harmless or beneficial microbes in the gut microbiome. Gut microbes have also been known to affect Treg production. But colonic Tregs were thought to stay in the gut. In this study, the investigators found colonic Tregs among muscle cells.

First study author Bola Hanna, a research fellow in immunology at Harvard Medical School (HMS) noticed cells that looked like gut-derived Tregs among muscle tissue. The researchers wanted to known more about these mysterious cells. First, they confirmed the identity of the Tregs by analyzing gene expression and molecular characteristics. This indicated that these cells were just like colonic Tregs. Next, the investigators tagged those cells and watched as they moved around the bodies of a mouse model. The researchers assessed the antigens on these cells as well, confirming that they were equivalent to Tregs from the gut.

When a mouse model was created to lack these Tregs, and was then subjected to muscle injury, the mice had high levels of inflammation and difficulty healing. When healing did happen, it was accompanied by scarring.

In another experiment, mice were given antibiotics to reduce the levels of gut microbes. Once again, when muscle injury occurred, it took longer to heal. But if the gut microbiome was restored, normal healing commenced.

The colonic Tregs are promoting healing in muscles by reducing the levels of an inflammatory molecule called IL-17.

The investigators also found evidence of gut Tregs in different organs including the kidneys, liver, and spleen. In a mouse model of fatty liver disease, there were unusually high levels of colonic Tregs compared to healthy mice, suggesting that Tregs are influencing inflammation in a variety of tissues.

In the mouse model of fatty liver disease, symptoms got worse when the mice lacked Tregs, which also seems to confirm that colonic Tregs are playing an important role in countering the effects of inflammation due to fatty liver disease.

“Our observations indicate that gut microbes drive the production of a class of regulatory T cells that are constantly exiting the gut and act as sentries that sense damage at distant sites in the body and then act as emissaries to repair that damage,” explained senior study author Diane Mathis, a professor of immunology in the Blavatnik Institute at HMS. This work may also help scientists create therapies for fatty liver disease.

Sources: Harvard Medical School, Immunity

Carmen Leitch

The SARS-CoV-2 virus and the illness it causes, COVID-19, have made an indelible mark on our lives. It …

The SARS-CoV-2 virus and the illness it causes, COVID-19, have made an indelible mark on our lives. It seems that is also true in more ways than one; new research has shown that when the virus infects cells, portions of the viral genome integrate into the genome of host cells in a phenomenon known as reverse transcription. While this is a relatively rare even for SARS-CoV-2, so many people have been infected with the virus that integration has probably happened many times. Scientists have now used several techniques to show that SARS-CoV-2 can integrate into a host cell genome, and the findings have been reported in the journal Viruses. This study is confirmation of previous work reported in the Proceedings of the National Academy of Sciences in 2021.

Colorized scanning electron micrograph of a cell (red) infected with the Omicron strain of SARS-CoV-2 virus particles (blue), isolated from a patient sample. Image captured at the NIAID Integrated Research Facility (IRF) in Fort Detrick, Maryland. Credit: NIAID

This research may help explain why some people continue to test positive for the virus long after their infection has subsided and they have recovered. In reverse transcription, RNA molecules, in this case from SARS-CoV-2, are transcribed into cDNA, a flip of the typical process in which active genes are transcribed into RNA molecules. Those reverse-transcribed cDNA molecules are then stitched into the host cell genome. If some of those cells are captured during a COVID-19 test, PCR would recognize and amplify the viral DNA in the host cell, causing a positive test result.

This study has also shown that simply inserting viral RNA into cells is not enough to cause genomic integration, so it seems unlikely based on the evidence we have now that mRNA from the COVID-19 vaccines would cause integration into cells’ DNA.

“This paper puts our data on a very firm footing. Hopefully, it will clarify some of the issues raised in the discussion that followed the first paper, and provide some reassurance to people who were worried about the implications for the vaccine,” said corresponding study author Rudolf Jaenisch, a founding member of the Whitehead Institute.

Since the integration of the SARS-CoV-2 genome into cells’ DNA is unusual, the researchers had to use a very sensitive method called digital PCR, which detects very specific genetic sequences, to identify instances in which viral RNA had been integrated into the genome of a cell.

The digital PCR results found viral RNA that had been reverse-transcribed to cDNA in about 4 to 20 of every 1,000 cells, but this includes all molecules of the sort, whether they ended up being integrated into a genome or not. Thus, the researchers suggested that viral integration is even more rare than that.

Whole genome sequencing can be used to show when that integration also occurred, because those events are typically accompanied by a reverse transcription complex called LINE1. The LINE1 sequences act as an indicator of integration. However, WGS is usually only used on a handful of cells, so when other investigators looked for those sequences, they could not usually be found.

“Because the human cell genome coverage by whole genome sequencing is very limited, you would need to run the sequencing experiment many times in order to have a good chance of detecting one viral genome copy,” explained postdoctoral researcher and first study author Liguo Zhang.

In this study, the researchers created cells that would overexpress LINE1, and make viral integration more common artificially. This time, the digital PCR showed that viral cDNA appeared in fourteen to twenty of every 1,000 cells, and WGS identified instances of integration along with LINE1. Further work with a tool called TagMap confirmed viral integration without overexpressing LINE1.

“This is unambiguous proof of viral genomic integration,” Zhang said. When this approach was repeated with cells that were treated with SARS-CoV-2 vaccine, there was no evidence of integration.

“We need to do further testing, but our results are consistent with vaccine RNA not integrating,” Jaenisch said.

Sources: Whitehead Institute for Biomedical Research, Viruses

Carmen Leitch

Adult T-cell leukemia/lymphoma (ATLL) is a rare type of cancer that impacts T cells, a crucial immune cell …

Adult T-cell leukemia/lymphoma (ATLL) is a rare type of cancer that impacts T cells, a crucial immune cell that plays an important role in fighting infection. ATLL tends to be aggressive, and can manifest in the blood as leukemia, in the lymph nodes as lymphoma, or other tissues like the skin. ATLL has been associated with human T-cell lymphotropic virus type 1 (HTLV-1) infections, although fewer than five percent of people with this virus end up developing ATLL. Right now, clinicians cannot predict which people with HTLV-1 infections will get ATLL. While some types of ATLL tumors can be surgically removed, survival prospects for these patients is not good.

Image credit: Pixabay

A recent article published in Genes & Cancer noted that even though a monoclonal antibody that can treat ATLL called mogamulizumab has recently been approved, the survival rate is still poor.

Viruses are known to change gene expression in host cells, and HTLV-1 is no different. Previous work reported in PLOS Pathogens showed that when HTLV-1 infects cells, it causes a huge number of genetic and epigenetic changes with viral proteins it generates called Tax and HBZ. These many genetic changes could be interfering with chemotherapeutics and may render them less effective, suggested researcher Tatsuro Jo of the Nagasaki Genbaku Hospital.

In the HTLV-1 genome, there is an opportunity, however. Its genome is completely different from the human genome, so the viral proteins generated during HTLV-1 infection are excellent therapeutic targets. ATLL survivors have been found to carry cytotoxic T lymphocytes that work against the HTLV-1 Tax protein. People who survive ATLL over the long term may have been able to activate strong antitumor mechanisms.

Jo added that some people who have lived for a long time after an ATLL diagnosis, and prior to the approval of mogamulizumab, had also developed herpesvirus infections. It’s been suggested that herpes infections can trigger powerful cellular immunity mechanisms.

“Although contracting herpes simplex or herpes zoster is unpleasant, the mechanism by which these herpesvirus infections can produce a therapeutic effect on refractory ATLL via the activation of the host’s cellular immunity is extremely interesting and worth further study,” said Jo.

Sources: Impact Journals LLC, Genes & Cancer

Carmen Leitch

Though the COVID-19 pandemic has waned, SARS-CoV-2 is still with us, and we still need diagnostic tests. Scientists …

Though the COVID-19 pandemic has waned, SARS-CoV-2 is still with us, and we still need diagnostic tests. Scientists have been improving those tests in several ways. Researchers are developing a test that can rapidly diagnose new COVID-19 infections within hours of exposure. A combination flu and COVID-19 test has recently been approved by the US Food and Drug Administration (FDA) and is now available to consumers for use at home. A COVID-19 home test with greater sensitivity has also been created and will hopefully reach the market soon.

Image credit: Pixabay

Typical COVID-19 tests identify viral particles in swabs of the nostrils, throat, and/or cheeks. But those tests are best used during certain windows, and they can miss active infections when there isn’t much viral material available because a person is asymptomatic, or the infection has not yet set in and begun to replicate robustly. A totally new type of test uses a different approach, and aims to detect the immune response to the virus. The work has been published in Cell Reports Methods.

A viral infection activates the expression of a variety of immune genes, which are transcribed into mRNA molecules. The test detects certain levels of those mRNA molecules. The researchers used blood samples collected during the COVID-19 pandemic to validate their results; the test detected COVID-19 infections, even in asymptomatic people, with 98.4 percent accuracy.

More work is still needed to improve the test. For example, it uses blood samples and not nasal swabs. The scientists also need to verify that it can distinguish between different types of viral infections, like COVID-19 and the flu. But the researchers are hopeful that the diagnostic test will be available in the near future.

A combination flu and COVID-19 test is already on the market. The FDA recommends the test for anyone with symptoms of a respiratory tract infection symptoms. It’s called the Lucira COVID-19 & Flu Home test. It does not require a prescription, requires nasal swabs that can be collected by the user at home, and results are available in about 30 minutes.

While samples have to be collected by an adult, the test can be used on anyone older than 2. There is a small risk of false negatives, noted the FDA, so if respiratory infection symptoms exist and the test is negative, people may still want to follow up with their healthcare provider.

Scientists have also developed a much more sensitive test for COVID-19 that can be used at home. The work was reported in ACS Infectious Diseases.

At-home tests change color when an antibody-linked reporter molecule latches onto viral particles in a sample. But that color change is very faint when few viral particles are present. PCR-based tests are good for disease detection because only very small amounts of viral material have to be present; they are then amplified by PCR. But special equipment is needed for PCR.

This new, sensitive test has added an amplification step to a test that can be used at home. A hybridization chain reaction (HCR) boosts the signal of reporter molecules instead. The viral protein gets tagged with a DNA molecule, which can act as a scaffold that more reporter molecules can bind to. Thus, every viral particle triggers the emission of a much stronger signal.

When the sensitive test was compared to tests that are on the market, it was 2.5 times more sensitive than the best, and 100 times more sensitive than the worst. The researchers are now working to get the new test to the market.

Sources: California Institute of Technology, ACS Infectious Diseases, The Associated Press, Simons Foundation, Cell Reports Methods

Carmen Leitch

The Centers for Disease Control and Prevention (CDC) has issued an alert about a rise in extensively drug-resistant …

The Centers for Disease Control and Prevention (CDC) has issued an alert about a rise in extensively drug-resistant (XDR) Shigella infections (shigellosis). There has been a concerning increase in drug resistance among Shigella infections in the United States; they rose from zero in 2015 to 5 percent in 2022. There are few treatment options for these infections, the bacteria are easy to transmit from one person to another, and few microbes need to be transmitted for illness to occur. The microbes generally spread through the fecal-oral route, which means contaminated food and water can also cause the illness. The bacteria are also transmitted during sexual contact. The XDR strains of Shigella can also share those resistance genes with other bacteria. Therefore, the CDC is especially concerned about these infections, and is calling on health professionals to watch for cases of XDR shigellosis.

A medical illustration of drug-resistant, Shigella sp. bacteria / Credit: CDC/ Antibiotic Resistance Coordination and Strategy Unit / Medical Illustrator: Stephanie Rossow

Shigella causes abdominal cramping and diarrhea that can be bloody; it may also cause fever or tenesmus, a feeling of flu bowels. Usually, these infections resolve on their own after a few days, and only supportive care, such as hydrating fluids, are needed. Antibiotics can shorten the duration of the illness, reduce the likelihood of transmission to others, and can also prevent complications.

Strains of XDR Shigella are resistant to many popular antibiotics that are usually used to treat shigellosis, including azithromycin, ciprofloxacin, ceftriaxone, trimethoprim-sulfamethoxazole (TMP-SMX), and ampicillin. Right now, there is no consensus on the best way to eliminate XDR Shigella. Strains of resistant Shigella include Shigella sonnei and Shigella flexneri.

Shigella infections tend to impact certain populations, including children between the ages of 1 and 4. International travelers, and men who have sex with men are other groups who tend to have higher than usual rates of shigellosis.

There have been 232 confirmed cases that have occured in recent years that the CDC has information about, and of those cases, 82 percent were men, 13 percent were women and 5 percent were children. While only 41 of these individuals answered questions about sexual activity, 88 percent of them reported male-to-male sexual contact.

The CDC has noted that clinicians should consider shigellosis when patients, particularly young children, international travelers, or men who have sex with men present with acute diarrhea.

A diagnosis is usually confirmed with a stool sample, particularly for patients who will receive antibiotics. Tests can also be performed to determined whether Shigella strains are susceptible to antibiotics.

Source: CDC

Carmen Leitch

Rheumatoid arthritis (RA)  is a complex, chronic inflammatory disease that is thought to affect about one percent of …

Rheumatoid arthritis (RA)  is a complex, chronic inflammatory disease that is thought to affect about one percent of the world’s population. RA happens when a person’s own antibodies attack joint tissue, causing painful swelling, stiffness, and redness. Some research has suggested that there is a link between RA and gum disease.

Image credit: Pixabay

Gum disease is estimated to affect up to 47 percent of adults, and in the disorder, oral microbes can move to the blood after the gums start to bleed. An increase in disease activity has been observed in RA patients who also have gum disease. Gum disease has been shown to be more common in RA patients who carry a certain type of antibodies, called anti-citrullinated protein antibodies (ACPAs), though ACPAs are often found in the blood of individuals with RA. The presence of ACPAs can often predate the diagnosis of RA by a few years.

A new study investigated the connections between these observations. In this work, the researchers collected blood samples from a small group of ten people with RA, five with and five without gum disease. These samples were collected every week for one year, and the investigators assessed the expression of both human and bacterial genes in those samples.

Certain types of inflammatory immune cells carried gene expression signatures that were associated with the autoimmune flares of arthritis patients who also had periodontal disease, as well as the presence of certain oral bacteria in the blood.

Many of these oral bacteria were chemically altered by deimination; they were citrullinated. Citrullination can change the structure and function of proteins. Although citrullination can be a part of the normal function of tissues, high levels of citrullination have been linked to inflammation.

Citrullination can also create targets for ACPAs; when the normal, unconverted forms of the oral bacteria were incubated with ACPAs, the antibodies did not react, but when the citrullinated oral bacteria were exposed to ACPAs, there was a reaction. ACPAs appear to be bound to oral microbes in RA patients.

The findings have been reported in Science Translational Medicine.

The study noted that the immune response to oral microbes could be influencing RA flares, that oral microbes can trigger a specific antibody reaction in patients with both RA and gum disease, and that RA flares cause varying immune signatures, which could reflect different flare triggers.

It could be that gum disease repeatedly causes the immune system to respond, and as the immune system keeps reacting and repeatedly increasing inflammation, RA may eventually begin to emerge. More work will be needed, however, to fully understand whether gum disease is playing a causative role in the development of RA.

Source: Science Translational Medicine

Carmen Leitch

A variety of studies have shown that when the air is drier, viral particles can linger there longer. …

A variety of studies have shown that when the air is drier, viral particles can linger there longer. These findings have now been confirmed in an analysis of particles of a virus that is very similar to the one that causes COVID-19, SARS-CoV-2. Although previous work has shown that relative humidity levels affect the length of time of a virus stays infectious in the air, this is the first to factor in the effect of saliva, which helps shield viral particles. The data can help explain why people tend to get more sick during winter, when humidity levels drop significantly indoors. It also stresses the importance of good ventilation systems and other mitigation efforts for preventing the spread of illness. The work has been reported in PNAS Nexus.

Dr. Mark Hernandez, S. J. Archuleta Professor of Civil and Environmental Engineering, and CU PhD graduate Marina Nieto-Caballero, now a postdoctoral researcher at Colorado State University, standing inside a bioaerosol chamber in the Environmental Engineering disinfection laboratory at the Sustainability, Energy and Environment Complex (SEEC). Credit  Patrick Campbell/University of Colorado

This study used a mammalian coronavirus that is very similar to SARS-CoV-2. Particles containing this virus remained infectious for twice as long when air was drier. These particles are normally expelled with saliva, which acts like a protective shield, particularly when humidity is low.

Although civil engineers typically design and maintain buildings so their indoor relative humidity will stay between 40 and 60 percent, the reality is a bit different, and varies widely depending on the climate of the region. The researchers suspected that these humidity levels were influencing the spread of SARS-CoV-2.

To test that theory, the investigators engineered airborne particles containing virus, with and without saliva. These were then released into large, sealed chambers with relative humidity levels of 25, 40, and 60 percent.

The saliva protected the virus at every humidity level, and at 40 and 60 percent relative humidity, half of the airborne viral particles were still infectious one hour after release. Half of the airborne particles were still infectious two hours after release at 25 percent humidity; as the relative humidity dropped, the virus was still pathogenic for much longer.

“It shows this virus can hang around for quite a while, hours even. It’s longer than a class, longer than the time you’re in a restaurant, longer than the time you take to hang out in the cafe. An occupant may come in, spread coronavirus in the air, and leave. Depending on architectural factors, then someone else could walk into that space with potent doses still hanging around,” said senior study author Mark Hernandez, a Professor of Civil and Environmental Engineering at the University of Colorado at Boulder.

The virus is probably also contaminating air for longer than it takes typical ventilation systems to eliminate it. Thus, additional mitigation strategies like filtration could reduce transmission, suggested the study authors.

“I hope this paper has an engineering impact in our buildings, for example, in schools and hospitals, so that we can minimize the infectivity of these viruses in the air,” said lead study author Marina Nieto-Caballero, PhD.

Increasing indoor humidity levels could help reduce risk for people who live in naturally arid environments, but that can be inefficient and expensive, said Hernandez. We can use strategies that we already know about instead, like opening windows, using inexpensive air filters, and increasing ventilation rates to introduce more fresh air, Hernandez added.

Sources: University of Colorado at Boulder, PNAS Nexus

Carmen Leitch