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Scooped by
Juan Lama
June 24, 2025 10:48 AM
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RetroVirox has launched a Summer Promotion with a 30% discount for antiviral and neutralization services against 4 viruses, including influenza, dengue, human metapneumovirus (HMPV) and respiratory syncytial virus (RSV). Discount applies to services initiated between July 1 and August 31 2025
Contact us at info@retrovirox.com for inquiries and additional info
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Scooped by
Juan Lama
April 3, 12:31 PM
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AI predicted that a forgotten breast cancer drug could be repurposed to treat many respiratory and gastrointestinal viruses, and subsequent animal tests suggests it may be right. A single drug has been found to inhibit a range of common viruses in lab studies, including coronaviruses, respiratory syncytial virus (RSV), norovirus, and influenza and hepatitis viruses. It will be tested in a clinical trial next year, raising hopes that the pill could one day be taken at home to relieve unpleasant symptoms or even limit infections if there were another viral pandemic. “As far as we can tell, this is the first drug that’s ever demonstrated activity across all these viral families,” says Daniel Haders, co-founder of Model Medicines, the California-based company leading its development. If it is approved, Haders envisages it being a pill that people could take if, for example, they have a flu-like illness but don’t know if it is influenza, covid-19, RSV or something else...
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Scooped by
Juan Lama
March 26, 12:39 PM
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The process by which viruses cause disease, viral pathogenesis, is the result of both infection of cells and the host immune response. A less studied but equally important contributor to viral pathogenesis is viral dissemination, the capacity of a virus to move from the primary site of infection, traverse physiological barriers, and gain access to secondary sites of infection. This dictates viral tropism and pathogenesis, but the mechanisms governing barrier crossing are incompletely understood. While the presence of viral receptors on cells is a major determinant of viral tropism and a prerequisite for infection, it does not completely explain the capacity of viruses to enter a tissue. Our recent work has begun to characterize the contribution of soluble viral proteins, acting as “viral toxins,” to viral dissemination, tissue tropism, and overall pathogenesis within an infected host. In this review, we discuss the characteristics of these viral toxins, which are soluble or surface-exposed viral proteins that can interact with endothelial and/or epithelial barriers, as well as immune cells, to trigger signaling pathways, resulting in the transient breakdown of cellular structures maintaining barrier integrity. The disruption of these barriers induces vascular leak and facilitates virus dissemination, influencing viral tropism and pathogenesis. Importantly, blocking this process prevents leak, viral dissemination, and severe disease during infection, highlighting the value of therapeutic intervention against viral toxin activity. Here, we summarize our current understanding of recently discovered viral toxins from the Flaviviridae, Coronaviridae, Nairoviridae, and Filoviridae. Published March 13, 2026 in MBio:
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Juan Lama
March 14, 12:26 PM
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Evidence suggests reactivations of the varicella-zoster virus may accelerate aging and raise dementia risk. Now scientists want to know if vaccines and antivirals could help protect the brain. The lecturer—a 63-year-old viral immunologist whose identity has been kept anonymous—suffered alarming symptoms, including impaired memory, waning concentration, and difficulty reading. While giving lectures to students, he found he had difficulty focusing and was often unable to finish sentences without pausing. But medical tests, including a brain biopsy, failed to get to the source of the problem, and over the next four years, his symptoms continued to progress. His decline would have likely continued unabated had he not heard about a case of encephalitis—serious brain inflammation caused by a reactivation of the varicella-zoster virus, most commonly associated with childhood chickenpox and, later in life, shingles. Remembering that his own symptoms had been preceded by a brief case of shingles, subsequent tests confirmed the patient had indeed experienced a reactivation of varicella-zoster. And so he decided to treat the problem with a course of acyclovir, an antiviral drug commonly prescribed to shingles patients. To his colleagues’ amazement, the Colorado lecturer’s symptoms quickly faded away and his cognition returned to normal. This remarkable case study, published in 2016, has inspired neurovirologists to look deeper into the connection between shingles and brain aging. For decades, shingles has been predominantly associated with a form of nerve pain known as postherpetic neuralgia, which can be so severe that it was once cited as the leading cause of pain-related suicide in the elderly. Now, research is starting to reveal the devastating impact that shingles can have on brain health. According to Andrew Bubak, assistant professor of neurology at the University of Colorado Anschutz, the true burden of varicella-zoster “is totally underestimated. But it’s a very treatable virus.” In recent years, increasing numbers of studies have shown that the shingles vaccine appears to be capable of protecting the aging body and brain, and dementia specialists are taking note. In April 2025, a major study by researchers at Stanford University suggested vaccination against shingles could prevent one in five new cases of dementia. More recent studies have also linked getting a shingles vaccine to slower biological aging across a variety of measures. One explanation given for the findings is that the vaccine might be stimulating the immune system in a broadly beneficial manner. While there is likely some truth in this, additional research increasingly points to the value of avoiding shingles (or reactivations of the varicella-zoster virus) in the first place, with two separate studies finding associations between shingles and self-reported cognitive decline and dementia. Neurovirologists believe this emerging data underlines the importance of avoiding infection, through the childhood chickenpox vaccination—given to children in the US since 1995 and introduced in the UK in January 2026—and through the adult shingles vaccine and booster jabs in later life. Before the US started routinely vaccinating against chickenpox, more than 90 percent of children acquired the varicella-zoster virus in childhood. Following the infection, the virus takes up position in the peripheral nervous system—the neurons linking the brain and spinal cord to the limbs and organs—where it stays dormant, sometimes for decades. Varicella-zoster can reactivate in the body following various triggers, which range from acute stress to concussion, co-infections with Covid-19, immunosuppressive medications, and the general aging of the immune system. In many cases, such reactivations may be completely symptomless, with some studies suggesting many of us could unknowingly experience repeated “subclinical” reactivations—the virus reawakening from its dormant state without inducing visible symptoms—in mid- to later life. “We rely on specialized immune cells to continuously patrol the nervous system and keep the dormant virus suppressed,” says Tian-Shin Yeh, associate professor of medicine at Taipei Medical University and attending physician at Shuang Ho Hospital in Taiwan. “As we get older, these cells can become less effective, or exhausted.” Once varicella-zoster reactivates, several things can take place. The virus is part of the herpes family, members of which are particularly adept at infiltrating the brain and central nervous system due to their ability to exploit its internal transport mechanisms for their own use. “Our nerve cells contain molecular motors that shuttle cargo along the nerve fibers,” says Yeh. “Herpes viruses can commandeer these transport systems to move from peripheral tissues deep into the nervous system.”....
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Scooped by
Juan Lama
February 23, 11:16 AM
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An innovative approach supercharges the innate immune system to provide a first line of defence against respiratory infections. Imagine if a nasal spray could make you immune not only to the viruses that cause COVID-19 and influenza, but to all respiratory diseases. In a paper1 published in Science today, researchers describe a vaccine that has done just that. When given to mice, the vaccine protected them for at least three months against multiple disease-causing viruses and bacteria — including the SARS-CoV-2 virus that causes COVID-19 — and even quelling responses to respiratory allergens. If the research translates to humans safely and effectively, such a ‘universal vaccine’ could be offered to everyone at the start of each winter — and perhaps provide a first line of defence against future pandemics. Bali Pulendran, an immunologist at Stanford University in Palo Alto, California, and his group previously studied the Bacillus Calmette–Guérin (BCG) vaccine2, which provides temporary protection against numerous diseases and works by activating the innate immune system and keeping it active. This evolutionarily ancient system has a much broader reactivity than does the adaptive immune system — which is the one conventional vaccines utilize by teaching antibody-making B cells and T cells to recognize proteins found on specific pathogens. Activating the innate immune system can also induce the intrinsic capacity of the respiratory system’s epithelial cells to resist infection. These cells are the target of many pathogens. Double bulwark In the latest study, Pulendran’s team developed a universal vaccine that targets the innate immune system, with three components. The first two are drugs that stimulate specific receptor proteins that can activate innate immune cells, such as macrophages that reside in the lungs. The third component stimulates a population of T cells, which are part of the adaptive immune system. Their task is to keep sending signals to the innate immune system to maintain its active state. The vaccine contains an immunogenic protein from chicken eggs, and in experiments in which it was omitted, immunity quickly waned. Mice that were given four doses of the nasally delivered vaccine developed immunity to SARS-CoV-2 and other coronaviruses, plus to bacteria that cause certain respiratory infections. Another novel benefit was that the activated pathways also suppressed the mechanisms that mediate hypersensitivity to house dust mites, thereby preventing allergic asthma. Analyses of how the protection works revealed what Pulendran calls a two-bulwark system, in which an initial mucosal barrier limits pathogen entry into the lungs. “Then,” he says, “this mucosal vaccination has set up the lung immune system, so that it is extraordinarily rapid in eliciting the virus-specific immune response to send off those few viruses that slip through the initial bulwark.” Bridge vaccine “It’s really a fantastic paper, and it’s exciting. The data look very clear to me,” says Akiko Iwasaki, an immunobiologist at Yale University in New Haven, Connecticut. “If it works in humans, that would be really quite remarkable.” Zhou Xing, an immunologist at McMaster University in Hamilton, Canada, says that people who are familiar with the advances in mucosal vaccines over the last decade will not be surprised by the findings. “We call it a ‘bridge vaccine’,” he says — the idea of leveraging the innate immune system to generate non-selective pathogen protection. Both Xing and Iwasaki warn that translating the effectiveness seen in mice into clinical therapies for people isn’t straightforward. Xing fears that without advanced aerosol delivery methods, a nasally delivered vaccine in humans won’t reach the lungs to activate the immune pathways described here. (The small size of mice means that both nasal sprays and pathogens can easily access their lungs.) Xing also says that roll out of the vaccine on a large scale could prove impractical if people need four doses. Because this approach puts the immune system in a state of constant hypervigilance, it could also come with potential side effects. “The cost–benefit ratio is something that one has to assess very, very cautiously in humans,” Pulendran says. If no problems are encountered in an initial, dose-escalation safety trial, a second trial would then use controlled infections, he predicts. That is, sometime after vaccination, healthy volunteers would be deliberately exposed to the influenza virus, for example, to see if they are protected.If they are, a new form of preventive medicine might be in the offing. “Mice provide you with the conceptual framework and evidence of how it could work,” Pulendran says. “But really, the proof of the pudding is: does it really work in humans?” Study published in Science (feb. 19, 2026): https://www.science.org/doi/10.1126/science.aea1260
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Scooped by
Juan Lama
February 18, 2:40 PM
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The US Food and Drug Administration has reversed course and will review a new mRNA flu vaccine from Moderna, the pharmaceutical company said Wednesday. About two weeks ago, the FDA sent Moderna a letter in which it refused to accept the application to review its first mRNA seasonal flu vaccine — a rare move by the federal agency that raised concern about another setback for the technology that’s been a target of some Trump administration health officials. The FDA told Moderna that its application didn’t contain an “adequate and well-controlled” trial because the control arm didn’t reflect the “best-available standard of care in the United States at the time of the study,” according to the letter, that Moderna posted online. It didn’t identify any safety or efficacy concerns, the company said. But Moderna has since met with the FDA and “proposed a revised regulatory approach” with different pathways by age, according to a news release from the company. Moderna is now “seeking full approval for adults 50 to 64 years of age and accelerated approval for adults 65 and older, along with a post-marketing requirement to conduct an additional study in older adults,” the news release said. “Discussions with the company led to a revised regulatory approach and an amended application, which FDA accepted,” Andrew Nixon, a spokesperson for the US Department of Health and Human Services, said in a statement. “FDA will maintain its high standards during review and potential licensure stages as it does with all products.” If the FDA approves the vaccine, it could be available for people ages 50 and older for the upcoming 2026-2027 flu season. Last week, Moderna said that the initial refusal from the FDA was inconsistent with previous feedback from the agency. “We appreciate the FDA’s engagement in a constructive Type A meeting and its agreement to advance our application for review,” Moderna CEO Stéphane Bancel said in a statement. “Pending FDA approval, we look forward to making our flu vaccine available later this year so that America’s seniors have access to a new option to protect themselves against flu.”
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Scooped by
Juan Lama
February 17, 11:53 AM
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In Massachusetts, Moderna is pulling back on vaccine studies. In Texas, a small company canceled plans to build a factory that would have created new jobs manufacturing a technology used in vaccines. In San Diego, another manufacturing company laid off workers. When Robert F. Kennedy Jr. was picked in November 2024 to become the next health secretary, public health experts worried that the longtime vaccine skeptic would wreak havoc on the fragile business of vaccine development. Those fears are beginning to come true, according to executives and investors involved with companies that develop and sell vaccines and the technology that is best known for the Covid vaccines. At conferences and in interviews, they described the emerging consequences of the Trump administration’s dismantling of the longstanding federal support for vaccines. “There will be less invention, investment and innovation in vaccines generally, across all the companies,” Dr. Stephen Hoge, the president of Moderna, said in an interview. The Trump administration said it was not discouraging innovation. But investors have grown hesitant to bet on a field that has fallen out of favor in Washington. Major manufacturers are reporting declining sales of their shots. Smaller companies are taking the brunt of the impact, with some stocks whipsawing in response to the changes...
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Scooped by
Juan Lama
February 12, 11:55 AM
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Researchers at the Helmholtz Institute for One Health (HIOH), a site of the Helmholtz Centre for Infection Research (HZI), together with an interdisciplinary team of partners, have identified the fire-footed rope squirrel (Funisciurus pyrropus) as a likely natural reservoir of the monkeypox virus (MPXV). Their study was published today in the renowned scientific journal Nature. The discovery was based on the detailed investigation of an mpox outbreak among wild sooty mangabeys (Cercocebus atys) in Taï National Park, Côte d’Ivoire. Scientists combined ecological, behavioral and molecular evidence to document, for the first time, the interspecies transmission of MPXV in the wild, from fire-footed rope squirrels to sooty mangabeys. A deadly outbreak among mangabeys For decades, the researchers now at HIOH have worked closely with the Taï Chimpanzee Project to monitor the health of wild chimpanzees, sooty mangabeys and other wildlife in Taï National Park, Côte d'Ivoire — a long-term commitment that proved essential to detecting this transmission event. In early 2023, the team identified an outbreak of mpox in a well-studied group of sooty mangabeys: About one third of the group showed clinical signs of disease, and four infants died. Viral genome sequencing revealed that the virus detected in the infected monkeys was nearly identical to an MPXV strain identified in a fire-footed rope squirrel found dead 12 weeks earlier nearby. In an attempt to link both observations, the team analyzed fecal samples from the mangabeys, seeking evidence of pre-outbreak MPXV circulation and contact between the host species. One sample collected eight weeks before the outbreak onset contained DNA from both the virus and the rope squirrel, providing strong evidence of interspecies transmission at this moment. Behavioral data supported these findings. Sooty mangabeys from this group have already been observed catching and eating fire-footed rope squirrels, which provides a direct route for the transmission of viruses. Squirrels under suspicion: now confirmed Squirrels have long been suspected as potential reservoirs for MPXV. The first isolation of the virus from a wild animal was from a rope squirrel (Funisciurus anaerythrus) captured in the Democratic Republic of the Congo in 1985. In 2003, imported squirrels infected with MPXV were also among the rodents suspected to have been the source of an mpox outbreak in pet prairie dog owners in the US. Yet, these animals had never been shown to be directly responsible for an outbreak in another species in nature. The new study is a breakthrough that starts unveiling how the pathogen circulates in the wild. What this means for human health As hunting pressure has reduced populations of larger game species, rodents such as squirrels are increasingly hunted and consumed by humans, which likely heightens the risk of human exposure and zoonotic transmission of MPXV. Therefore, confirming the direct involvement of fire-footed rope squirrels in interspecies transmission carries important public health implications. “Identifying the animal sources of the virus and the exposure routes that lead to inter-species transmission are key steps towards understanding spillover mechanisms and developing effective prevention measures to mitigate the risk of transmission to humans,” says Livia V. Patrono, one of the senior authors at HIOH. The authors recommend increasing awareness among people who come into contact with squirrels and other wildlife, such as children. In addition, they call for a deeper understanding of MPXV ecology in reservoir species – especially squirrels – as well as in intermediate hosts, particularly non-human primates, in MPXV-endemic regions, to strengthen evidence-based prevention strategies. One Health approach more relevant than ever The findings underscore the importance of a One Health approach that recognizes the links between human, animal, and environmental health. “This discovery was only possible thanks to long-term ecological research, continuous health monitoring and systematic sample collection in the Taï National Park,” says Fabian Leendertz, senior author, director of HIOH and co-director of the Taï Chimpanzee Project. “We need to maintain and expand this kind of effort to better understand and hopefully reduce the risks posed by emerging infectious diseases, including mpox – we need to strengthen prevention.” Josef Penninger, Scientific Director of the Helmholtz Centre for Infection Research, adds: “This study also highlights the value of close cooperation with our African partners. Only through strong, trust-based collaborations with local authorities and research institutions can we effectively tackle zoonotic diseases and make an impact, not just regionally, but globally.” Study published in Nature (feb. 11, 2026): https://www.nature.com/articles/s41586-025-10086-y
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Scooped by
Juan Lama
February 6, 11:55 AM
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The establishment of human intestinal enteroids (HIEs) as a model for human norovirus (HuNoV) replication has been transformative for studying this leading cause of gastroenteritis. However, indefinite passaging of HuNoVs in HIEs remained a challenge, necessitating the use of patient stool samples as viral inocula. Using RNA-seq, we identified CXCL10, CXCL11, and CCL5 as up-regulated chemokines, suggesting their potential as host restriction factors. TAK-779, a CXCR3/CCR5/CCR2 antagonist, enhanced GII.3 HuNoV replication and viral spread in a dose- and time-dependent manner, enabling successful passaging of GII.3 HuNoV in two different HIE lines and generation of viral stocks. Sequencing passaged virus revealed one consensus change in the major capsid protein and several dynamic adaptations, suggesting emergence of variants. TAK-779 also enhanced replication of GI.1 and GII.17 strains, but not GII.4, suggesting strain-specific host interactions. This breakthrough in passaging provides insight into HuNoV-host interactions, establishes a scalable in vitro system for virus propagation, and opens avenues for structural, biochemical, and therapeutic studies. Published in Science Advances (Feb. 4, 2026): https://www.science.org/doi/10.1126/sciadv.aeb0455
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Scooped by
Juan Lama
February 2, 11:41 AM
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Key to the success of influenza A virus as a pathogen are its numerous tactics of immune evasion. To suppress anti-viral cellular and organismal responses, influenza A virus encodes several immunomodulatory proteins, including the endoribonuclease PA-X. PA-X decreases inflammation and immune responses in in vivo infections by limiting host gene expression. PA-X is conserved in 99% of all influenza A viral strains, pointing to its importance as a crucial immunomodulator. However, it is not yet known how PA-X activity alters the antiviral response in the human airway or how it benefits the virus. To define how influenza A virus uses this protein to evade immune responses, we characterized the impacts of PA-X on the host response to infection in the infected and bystander cells of the airway epithelium using a 3D ex vivo model. We discovered that PA-X exerts a dual action on immune responses, dampening aspects of both the innate and adaptive immune systems. Consistent with reports in model organisms, PA-X significantly decreases secretion of multiple cytokines from airway epithelium, including IFN-λ, which likely plays a role in its ability to reduce inflammation and lung damage. In addition, we revealed that PA-X decreases and delays MHC I antigen presentation from infected cells. This reduction likely aids influenza A virus in hiding from antigen-specific T cells and allows the virus to successfully replicate prior to immune detection. This new function for PA-X highlights how influenza A virus employs active mechanisms to block immune detection, in addition to tolerating high levels of antigen mutations to escape it. Moreover, as evasion of recognition by the adaptive immune system is particularly important during infections of animals and humans with pre-existing immunity, this immunomodulatory activity may be key to the longevity of influenza A viruses and their continued circulation. Preprint in bioRxiv (Jan. 31, 2026): https://doi.org/10.64898/2026.01.30.702929
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Scooped by
Juan Lama
January 25, 12:11 PM
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A dairy cow in the Netherlands appears to have been infected with H5N1, the first report of this deadly avian influenza virus having spread to cattle outside of the United States. According to a detailed letter the Dutch agriculture minister sent to the country’s parliament today, a cat on a dairy farm in the province of Friesland died from H5N1 last month, which led veterinary authorities to sample blood and milk from cattle at the farm. One cow had antibodies to the virus in its milk, but no samples tested positive for the virus itself. “There are also no signs of avian influenza spreading to other dairy farms,” the minister wrote. The cow had mastitis and respiratory problems last month, the minister noted, and its milk was not processed. Also, milk from the farm is pasteurized, which inactivates the virus. “This means that there is very little chance that virus from the infected cow has ended up in the milk for human consumption,” the minister stressed. It’s unclear how the virus arrived at the farm or how the cat and cow became infected. Epidemiologist Marion Koopmans of Erasmus Medical Center praised the Dutch government’s surveillance network. “Kudos to our animal health authorities for their alertness,” Koopmans said. She notes that the country performed a large-scale screening for the virus in dairy cattle in 2024 in response to the unprecedented outbreak of H5N1 in U.S. dairy cows—which spread rapidly across many states—but did not find it. Cows infected with H5N1 typically have fever and produce less milk, which also becomes discolored. Most recover. None of the people living or working at the Dutch farm have had any flulike illnesses recently. H5N1 on dairy farms in the U.S. has infected some humans, mainly causing pink eye. Flu researchers worry the spread of the bird virus in cattle herds will give it more opportunity to adapt to mammals and better transmit between them, potentially posing a serious threat to human health. The Netherlands, Europe’s largest exporter of eggs, is going through the most severe outbreak of H5N1 avian influenza in years. Since October 2025, more than three dozen farms have had outbreaks and more than 1.5 million chickens, turkeys, and ducks have been culled to stop the virus’ spread, according to government data. Many wild birds have died as well. More samples from the dairy farm are being tested this weekend.
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Scooped by
Juan Lama
January 22, 11:37 AM
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Vaccines may do far more than prevent infections. The way that some inoculations train your immune system could also reduce the risk of cancer, stroke, or heart attacks, and possibly guard against dementia. New evidence shows that the shingles vaccine is linked to slower aging, with benefits that can last for several years after vaccination. The researchers found that among more than 3,800 participants in the US aged 70 or older, those who received the shingles vaccine after age 60 scored better on composite measures of biological aging than those who were unvaccinated. Vaccinated participants also showed biological markers tied to lower inflammation and slower "molecular and overall biological aging," the researchers report. The associations remained even after accounting for demographic and health differences between the two groups. While the study does not provide conclusive proof that the shingles vaccine leads to healthier aging outcomes, the findings add to several other observational studies linking the vaccine to widespread health benefits in later life, especially for the heart and brain. "By helping to reduce this background inflammation – possibly by preventing reactivation of the virus that causes shingles – the vaccine may play a role in supporting healthier aging," explains Kim. "While the exact biological mechanisms remain to be understood, the potential for vaccination to reduce inflammation makes it a promising addition to broader strategies aimed at promoting resilience and slowing age-related decline." Shingles, also known as herpes zoster, is triggered by a reactivation of the varicella zoster virus that causes chickenpox. Most people are infected in childhood, after which time the virus lies dormant in their nervous systems. For the average, healthy person, shingles doesn't pose a threat until later in life, which is why the two-dose vaccine is generally recommended for those over 60. About 30 percent of unvaccinated people will develop shingles in their lifetime. The first version of the shingles vaccine was only licensed for use in the US in 2006, and now we have a newer version, which may have even better results for a person's ongoing health. Only future, long-term studies can say for sure. The power of the shingles vaccine is yet to be determined, but the possibilities are profound. Study published (Jan. 20, 2026): https://doi.org/10.1093/gerona/glag008
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Scooped by
Juan Lama
January 19, 11:26 AM
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Numerous applications in research and medicine rely on reliable identification and quantification of virus-infected cells. Current methods either apply reporter viruses, that often differ from clinical isolates (e. g. cell tropism, immune evasion) or staining approaches, that prevent live-cell experiments and may introduce biases through manual counting. We present a deep learning model for the label-free identification of virus-infected cells on light microscopy images (VAIruScope). To overcome limitations, our pipeline enables an automated quantification of virus-infected cells based on the recognition of cytopathic effects. The method was applied to different cell models and four clinically relevant prototype viruses representing RNA- (influenza A virus), DNA- (human cytomegalovirus, herpes simplex virus-1) and retroviruses (human immunodeficiency virus-1). VAIruScope identified infected cells achieving classification accuracies of up to 96 %. As proof-of-concept, the method was validated using electron microscopy for a wild-type HSV-1. VAIruScope may be applicable to live-cell imaging to investigate infection dynamics. Prepring in bioRxiv (Jan. 15, 2026): https://doi.org/10.64898/2026.01.15.699499
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Scooped by
Juan Lama
April 8, 12:03 PM
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More than three-quarters of all cases of liver cancer worldwide are associated with chronic viral hepatitis but scientists have been limited in their ability to model how these viruses lead to cancer. In the new study, a Rockefeller team showed that mice infected with an engineered version of a rat virus develop liver inflammation, scarring, and ultimately cancer similar to that seen in humans with viral hepatitis-associated liver cancer. The new mouse model can be used to study how liver virus cause cancer.... Study published in J. Hepatology (March 2026): https://www.journal-of-hepatology.eu/article/S0168-8278(26)00085-1/fulltext
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Scooped by
Juan Lama
March 29, 1:33 PM
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Many viruses have adapted to persist in infected humans for life1,2. Variable host control of their ongoing abundance (viral load) can lead to clearance or disease3–5. Here we analysed the viral DNA load of 31 common viruses in human blood and saliva using whole-genome sequencing data from UK Biobank (n = 490,401), All of Us (n = 414,817) and Simons Foundation Powering Autism Research for Knowledge (SPARK; n = 12,519). Viral DNA load varied markedly with age, time of day and season; most viruses were also present at greater abundance in men than in women. Human genetic variation at dozens of loci associated with DNA load of seven viruses: Epstein–Barr virus (EBV, 45 loci), human herpesvirus (HHV)-7 (37 loci), HHV-6B, Merkel cell polyomavirus and three anelloviruses. Variation at the major histocompatibility complex (MHC) locus generated the strongest associations (P = 5.8 × 10–9 to 2.5 × 10–1459), which were specific to each virus. The HLA-B*08:01 allele also exhibited a host–virus genetic interaction with EBV subtype (P = 7.4 × 10–70). Other human genetic effects implicated genes encoding proteins that process peptides for antigen presentation, such as ERAP1 (HHV-7, P = 2.7 × 10–78) and ERAP2 (EBV, P = 4.6 × 10–111). Mendelian randomization analyses supported a strong causal effect of EBV DNA load on increased risk of Hodgkin’s lymphoma (P = 1.8 × 10–3), but not multiple sclerosis (P = 0.52). This suggests that higher chronic EBV load increases lymphoma risk, whereas associations of EBV infection with autoimmune conditions reflect host immune responses to particular viral epitopes. Analyses of biobank data show that human variation such as age, sex and genetics, particularly at the major histocompatibility complex locus, is associated with viral abundance and supports a causal link between abundance of Epstein–Barr virus and Hodgkin’s lymphoma. Published in Nature (March 25, 2026): https://doi.org/10.1038/s41586-026-10288-y
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Scooped by
Juan Lama
March 15, 10:53 AM
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As the U.S. flu season winds down, health officials say the flu vaccine didn’t work very well with one of its worst effectiveness rates in more than a decade. A new strain that dominated the early winter was not well matched to the vaccine, leading to an intense early onslaught of flu. The Centers for Disease Control and Prevention on Friday posted data that showed a continued decline in doctor's office and hospital visits for flu symptoms through last week. The number of states reporting high flu activity dropped to 16, many of them in a belt stretching from Colorado to Virginia. “The winter respiratory virus season is slowly coming to a close, and we’re all very grateful for that,” said Dr. William Schaffner, a Vanderbilt University vaccine expert. This season's vaccines were around 25% to 30% effective in preventing adults from getting sick enough from the flu that they had to go to a doctor’s office, clinic or hospital, according to a CDC report this week. Children who were vaccinated were about 40% less likely to get treatment at a doctor’s office or hospital. Officials generally are pleased if a flu vaccine is 40% to 60% effective. Judging from past CDC research, this season saw one of the lowest effectiveness rates in the last two decades. Flu infections surged in late December and were especially intense in some parts of the country. New York City health officials called it the most intense season in 20 years. Relatively low flu vaccination rates did not help, but experts also blamed the new flu strain that was causing most infections. The new strain belonged to a category of flu virus, called A H3N2. This new version, subclade K, seemed to spread more easily — though it did not necessarily cause more severe illness. The vaccine available for this season was built to address a different version of H3N2, and the new strain's explosion is a likely explanation for why the vaccine was less effective, Schaffner said. CDC scientists estimate there have been at least 27 million illnesses, 350,000 hospitalizations and 22,000 deaths from flu so far this season. At the same point last year, the estimates were at least 40 million illnesses, 520,000 hospitalizations, but about the same number of deaths. At least 101 children have died so far this season. For those whose vaccination status is known, about 85% were not fully vaccinated against flu. The flu vaccine may not protect everyone from getting sick, but it can prevent people from becoming severely ill and dying. That's why getting a flu shot remains worthwhile, Schaffner said. CDC data suggests adult vaccination rates are up slightly this season, to 46.5%, following an unusually bad season last year that set a record for the most child deaths this century. An estimated 48% of U.S. kids were vaccinated against flu around the end of last month. That's about the same as last year, but down from the 52% vaccinated at this point in 2024, according to CDC data. Starting in 2010, the government recommended annual flu vaccinations for Americans 6 months and older. In January, however, the Trump administration stopped broadly recommending flu shots for all children, saying instead that it’s up to parents and family doctors to decide. Meanwhile, work is already underway for next winter’s flu season. Last month, the World Health Organization announced its recommendations for which virus strains to address in the vaccines for the 2026-27 northern hemisphere flu season. The vaccines should be built to handle subclade K, the organization said. This week, a U.S. Food and Drug Administration advisory committee endorsed the WHO recommendations. CDC Report in MMWR (March 12, 2026): https://www.cdc.gov/mmwr/volumes/75/wr/mm7509a2.htm
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Juan Lama
March 12, 12:06 PM
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Emerging research from the University of Virginia (UVA) has unveiled a startling connection between severe viral respiratory infections and an increased risk for lung cancer development months or even years post-infection. This groundbreaking study, spearheaded by Dr. Jie Sun and colleagues at UVA’s Beirne B. Carter for Immunology Research and Comprehensive Cancer Center, elucidates how severe cases of COVID-19, influenza, and pneumonia induce long-lasting alterations in lung immune cell behavior, effectively “reprogramming” the pulmonary immune landscape to favor tumor growth. Their findings illuminate critical implications for clinical surveillance paradigms, vaccination policies, and future cancer prevention strategies. The investigation began with an acknowledgement of the longstanding gap in understanding the long-term oncogenic consequences of viral lung injuries. Researchers utilized both murine models and retrospective human clinical data to assess how severe respiratory viral infections modulate lung immunity and impact carcinogenesis. Results from murine studies demonstrated that mice afflicted with severe pulmonary infections exhibited a marked propensity to develop lung tumors and suffered higher mortality rates following cancer establishment when compared to uninfected controls. This phenomenon suggested a causative link between intense lung inflammation and an immunological milieu conducive to cancer progression. In parallel analysis, the team accessed large-scale patient datasets revealing a statistically significant association between hospitalization for severe COVID-19 and an elevated incidence of lung cancer, quantified at a 1.24-fold increased risk independent of traditional risk factors like smoking and pre-existing comorbidities. This correlation underscored the real-world clinical relevance of the murine findings and raised urgent questions about post-infection cancer monitoring protocols. Notably, mild COVID-19 cases did not present this increased risk, implying that the severity of immune perturbation is the critical determinant in carcinogenic priming. Mechanistically, the study pinpointed drastic shifts in lung-resident innate immune cells—specifically neutrophils and macrophages—that are ordinarily responsible for pathogen clearance and tissue homeostasis. Following severe viral infection, these cells adopt dysfunctional phenotypes characterized by sustained pro-inflammatory cytokine production and extracellular matrix remodeling. This aberrant activation fosters a chronic inflammatory microenvironment rich in reactive oxygen species and growth factors, creating fertile ground for malignant transformation and tumor growth. Additionally, perturbations to the epithelial lining of alveoli were observed, further compromising the lung’s integrity and enhancing vulnerability to oncogenic insults. A significant and hopeful facet of Sun’s research is the protective effect consistent vaccination confers against these detrimental alterations. Vaccinated individuals, by priming adaptive immunity and curbing viral replication, mitigate the chaotic immune activation and lung injury associated with severe infection. The data suggest that vaccines serve a dual protective role: preventing acute disease hospitalization and abrogating the long-term immune scarring responsible for increased cancer susceptibility. This finding advocates for intensified vaccination efforts not only for infectious disease control but also for cancer prevention in vulnerable populations. The clinical ramifications of these discoveries are profound. Dr. Jeffrey Sturek, a UVA physician-scientist who collaborated on the study, emphasized the need to rethink post-viral infection surveillance akin to long-established cancer risk assessments derived from smoking history. Patients recovering from severe viral pneumonia could benefit from more rigorous and routine lung cancer screening protocols, perhaps integrating low-dose computed tomography scans for early tumor detection. The insights call for personalized medicine approaches that integrate viral infection history into oncological risk stratification models. Beyond clinical implications, the study expands our fundamental understanding of how acute infectious insults can prime chronic disease pathways. It reveals a novel paradigm where immune memory of viral trauma contributes to malignancy, broadening the landscape of cancer etiology beyond genetic and environmental factors. Such knowledge opens avenues for innovative therapeutic interventions aimed at restoring immune cell function and reversing pro-tumor inflammatory imprints in post-infection lungs. UVA’s Beirne B. Carter Center continues to lead in dissecting the complex interplay between infection, immunity, and cancer, building on prior work elucidating immune cell plasticity in disease. The Center’s integrative approach, combining immunology, oncology, and infectious disease expertise, uniquely positions it to translate these findings into targeted therapies. Their efforts are complemented by the UVA Comprehensive Cancer Center’s national leadership in cancer research, recognized through the prestigious National Cancer Institute designation. Publication of this multidisciplinary research in the high-impact journal Cell not only solidifies its scientific rigor but also ensures wide dissemination among the biomedical community. The work was supported by multiple National Institutes of Health grants and UVA institutional awards, highlighting the collaborative investment in addressing pressing health challenges arising from global pandemics and endemic respiratory diseases. Dr. Sun and colleagues stress the urgency for the medical community to incorporate viral infection histories into routine cancer risk evaluation and to champion vaccination as a multifaceted health safeguard. With millions affected worldwide by severe COVID-19 and influenza annually, proactive measures based on this research could markedly reduce lung cancer morbidity and mortality. The authors anticipate that ongoing research will further clarify molecular pathways involved, fostering development of precision medicine interventions to disrupt the cancer-promoting sequelae of viral lung infections. Published in Cell (March 11, 2026): https://www.sciencedirect.com/science/article/abs/pii/S0092867426002205
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Juan Lama
February 19, 12:09 PM
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A virus that is big enough to be seen under an ordinary light microscope co-opts its host’s systems with the help of potentially purloined genes. Scientists report that a type of giant virus multiplies furiously by hijacking its host’s protein-making machinery — long-sought experimental evidence that viruses can co-opt a system typically associated with cellular life. The researchers found that the virus makes a complex of three proteins that takes over its host’s protein-production system, which then churns out viral proteins instead of the host’s own. Virologists had already suspected that viruses could perform such a feat, says Frederik Schulz, a computational biologist at the Lawrence Berkeley National Laboratory in California, who was not involved with the work. But the new findings, published in Cell on 17 February, are an important confirmation. Compared with other viruses, he says, this one “has a more powerful toolbox to really replace what the host is doing”. Big microbe Giant viruses, which are so named for their massive genomes, might seem exotic, but they are decidedly commonplace. They tend to infect single-celled organisms called protists — a group that includes amoebae and protozoa — that “are all over the place”, says Eugene Koonin, an evolutionary biologist at the US National Center for Biotechnology Information in Bethesda, Maryland. The giant DNA virus used in this study, Acanthamoeba polyphaga mimivirus, has a genome that is about five times larger than those of poxviruses, which have the biggest genomes of any virus that infects humans. Mimivirus is giant in another way too: it is large enough to be seen under a light microscope. To understand whether the virus affects its host’s protein-assembly line, the researchers isolated viral proteins that interact with host organelles called ribosomes. These structures translate RNA molecules into proteins. Viral imitation The scientists identified three viral proteins that seemed likely to be involved in hijacking host protein production. They then genetically engineered the viruses to lack these proteins and found that viruses that were missing any one of the three multiplied 1,000–100,000 times more slowly than those that did have these proteins. “It turns out that, yes, they were absolutely required for infection,” says Maximilian Fels, a virologist at Harvard Medical School in Boston, Massachusetts, and a co-author of the study. The mimivirus genome includes genes for three viral products that shut down protein synthesis in the host and redirect it towards making viral proteins. #giantvirusThe authors found that the three viral proteins form a complex that is similarly shaped to one produced by the host that attaches to the ribosome and affects which proteins are made. When mimivirus infects a host, its protein cluster replaces the host’s, and viral RNA molecules gain preferential access to the ribosome, depriving the host RNA molecules of access to the cellular machinery. The researchers also exposed the host cells to stressful conditions by adding harmful chemicals or depriving the cells of nutrients. Even in these stressed cells, which would typically respond by halting most protein production, the virus could still multiply. But it did not multiply as quickly if it was missing any one of the three crucial proteins. Gene thieves Individual viruses are so simple and have such bare-bone structures that they do not qualify as cells. So how did Acanthamoeba polyphaga mimivirus come to have proteins that can replace part of its host cell’s function? Scientists say that it’s possible that mimivirus ‘stole’ useful genes from its hosts early in its evolutionary history, and then evolved to use them. “These large viruses that have large DNA genomes are gene thieves,” says Nels Elde, an evolutionary geneticist at the University of Utah in Salt Lake City. “They collect host genes almost like trading cards.” The authors of the new paper hypothesize that mimivirus and other giant viruses are so large because they’ve taken a lot of genetic machinery on board. This might allow the viruses to thrive in a wider range of environments than can viruses with smaller genomes.
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Juan Lama
February 17, 12:11 PM
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Mucosal surfaces are primary entry sites for many infectious pathogens, yet parenteral vaccination alone often fails to elicit effective mucosal immunity. Mucosally delivered vaccines offer a promising strategy for reinforcing frontline defences and inducing localized, pathogen-specific immune responses. Recent studies indicate that mucosal vaccines elicit tissue-resident memory T and B cells, along with robust local antibody secretion, to prevent infection and transmission. However, achieving sterilizing immunity at mucosal sites proves challenging owing to the complex immune environments consisting of epithelial barriers, varying mucus composition, pH differences and hormonal influences. In this Review, we outline how specialized immune-inductive and effector mechanisms across distinct mucosal compartments contribute to protective immunity and discuss emerging strategies to harness multilayered mucosal immunity to develop safe, effective vaccines that elicit durable protection. Many clinically relevant pathogens enter the body through mucosal surfaces, yet conventional parenteral immunization is insufficient to elicit robust mucosal immunity. This Review examines the unique anatomical and immunological features of the mucosal surfaces of the body and how this knowledge can be used to develop protective mucosal vaccines. Published in Nat. Reviews Immunology (February 16, 2026): https://doi.org/10.1038/s41577-026-01273-7
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Juan Lama
February 15, 9:08 AM
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Staff members at the United States’s premier infectious-disease research institute have been instructed to remove the words “biodefense” and “pandemic preparedness” from the institute’s web pages, according to e-mails Nature has obtained. The directive comes amid a broader shake-up at the US National Institute of Allergy and Infectious Diseases (NIAID), one of 27 institutes and centres at the National Institutes of Health (NIH). The NIAID is expected to deprioritize the two topics in an overhaul of its funded research projects, according to four NIAID employees who spoke to Nature on the condition of anonymity, because they are not authorized to speak to the press. NIH director Jay Bhattacharya explained the restructure at an event with other top agency officials on 30 January. “It’s a complete transformation of [the NIAID] away from this old model” that has historically prioritized research on HIV, biodefence and pandemic preparedness, he said. The institute will focus more on basic immunology and other infectious diseases currently affecting people in the United States, he added, rather than on predicting future diseases. About one-third of the NIAID’s US$6.6-billion budget currently funds projects involving emerging infectious diseases and biodefence. The research studies pathogens of concern and monitors their spread, and develops medical countermeasures against threats from radiation exposure, chemicals and infectious diseases. Nahid Bhadelia, director of Boston University’s Center on Emerging Infectious Diseases in Massachusetts, says the decision to deprioritize these areas will leave people in the United States more vulnerable to pathogens that are constantly evolving in wildlife around the world and spilling into human populations, sometimes sparking outbreaks. “Just because we say we’re going to stop caring about these issues doesn’t make the issues go away — it just makes us less prepared,” she says. A spokesperson for the NIH, the world’s largest public funder of biomedical science, based in Bethesda, Maryland, says, “NIAID’s new vision sharpens its focus on the interconnected pillars of infectious diseases and immunology, expanding opportunities for research that address the most pressing challenges to Americans’ health today.” The spokesperson declined to respond to Nature's queries about the agency’s specific plans to restructure the institute. Political heat
The NIAID is currently under the leadership of acting director Jeffery Taubenberger, after its previous director, infectious-disease physician Jeanne Marrazzo, was fired by the administration of US President Donald Trump after less than two years into the post. Her predecessor, Anthony Fauci, held the job for 38 years. Fauci and the institute have been scrutinized by Trump and other Republican politicians as a result of public-health measures used during the COVID-19 pandemic — such as lockdowns and school closures — which they say resulted in people losing trust in the country’s health agencies. (During the pandemic, Fauci offered recommendations on how to prevent the spread of the virus, but neither Fauci nor the NIAID set policy for public-health measures.)
To restore trust, Bhattacharya, Taubenberger and Taubenberger’s senior adviser, John Powers, outlined a “new vision” for the institute in a commentary1 published in Nature Medicine on 16 January. “NIAID’s work clearly neither prevented the pandemic nor prevented Americans from experiencing among the highest levels of all-cause excess mortality in the developed world during that time,” they wrote. “Given the increasing prevalence of allergic and autoimmune disorders and the burden of common infections in the population over the past few decades, the NIAID must focus research on these conditions with a greater sense of urgency.” New direction The instructions to agency staff members to rebrand the institute’s language are only the first step towards implementing this new vision, according to the NIAID employees. NIH principal deputy director Matthew Memoli has ordered more changes, including the review of the portfolio of grants funding biodefence and pandemic preparedness, in the coming weeks and months, they say. If funds are allocated to other topics, “that’s a very big deal”, Bhadelia says. Few other US agencies have the budget or infrastructure to fund basic research into these topics, says Gigi Gronvall, a biosecurity specialist at the Johns Hopkins Bloomberg School of Public Health in Baltimore, Maryland. Taubenberger hinted during the 30 January event that a reallocation is coming. “To better prepare for the future [we need to] better deal with what we’re facing today,” he said. “Maybe a better way to look at this is ‘people preparedness’. One way for people to be prepared is to be healthier, eat better and exercise, so you’re less likely to get sick or have a poor outcome,” Powers added. This priority is important, Bhadelia says, but “the new vision is remarkable not for what’s included — but what’s excluded. It almost paints a picture of ‘one or the other’. In reality, these things interact with each other”. For example, people with chronic conditions are at greater risk during a pandemic, she says. Gronvall adds that this approach is “full of hubris”. “We know that there are groups of viruses that are more likely to cause illness, epidemics and pandemics,” she says, so it makes sense to study them. For example, Bhadelia adds, the anticipatory basic research that the NIAID has funded helped make it possible to develop COVID-19 vaccines in record time, which “allowed us to reduce mortality” from the pandemic. The restructure is also expected to target the NIAID division focusing on HIV/AIDS research, which oversees a $1.5-billion portfolio of projects developing therapeutics and vaccines against the virus. The division’s 33 branches will likely be consolidated, one NIAID employee tells Nature. But it’s not clear whether the total number of projects or amount of money the division doles out will be impacted, the employee adds. Almost 20% of the NIH’s 2024 workforce of 21,000 have been laid off or have left voluntarily since Trump took office last January. The NIH spokesperson declined to say whether there will be further layoffs of NIAID staff members as part of the restructure. “Everyone is worried about what comes next,” an institute employee says.
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Juan Lama
February 10, 11:51 AM
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Incidence patterns of post-acute sequelae, characterised by persistence or delayed onset after the acute phase of an infection, are not well documented after infectious disease outbreaks. Nipah virus was first detected in the 1998-1999 Malaysia outbreak and remains a significant public health concern due to its high epidemic potential and recurrent outbreaks in South Asia. We conducted a systematic review on the prevalence, incidence, duration, and characteristics of post-acute sequelae in survivors of Nipah virus infection. We searched PubMed and Web of Science for studies published up to November 17, 2025. We included 8 articles, and extracted prevalence for 34 potential neurological, psychiatric or non-specific post-acute sequelae. The pooled prevalence of total residual neurological deficits was 24% (95% CI 9-49) among total survivors of Nipah infection, and 45% (95% CI 11-85) among the subset of survivors with acute Nipah encephalitis (5 articles). In the single controlled study, total residual neurological deficits, fatigue and daytime somnolence were significantly more prevalent in Nipah infection survivors than population-based controls. We estimated that 10% (95% CI 4-20) of Nipah infection survivors also experience late-onset or relapsing neurological symptoms after initial recovery. These findings demonstrate a substantial long-term disease burden following Nipah virus infection, which should be accounted for in mathematical modelling studies. However, the estimates are mainly based on data from the Malaysia/Singapore outbreak and may not be generalisable to the Bangladeshi and Indian setting, where current outbreaks occur and are caused by a different viral strain. Further limitations relate to subjective outcome assessment and heterogeneous populations of total Nipah infection survivors, which could have biased our estimates. Preprint inmedRxiv ( Feb. 09, 2026): https://doi.org/10.64898/2026.02.03.26345343
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Juan Lama
February 4, 12:35 PM
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A panzootic caused by highly pathogenic avian influenza (HPAI) A(H5N1) virus, clade 2.3.4.4b, has affected many animal species around the world since 2021. In March 2024, genotype B3.13 of this virus was identified in dairy cattle in the United States, following a spillover event from wild birds. Mammary gland lesions were a key finding in infected cows, with infectious virus detected in their milk. Raw milk is sold legally in retail establishments in multiple US states, including California. In November 2024, HPAI A(H5N1) virus, clade 2.3.4.4b, genotype B3.13, was detected in raw milk sold commercially in California and then in bulk milk tanks. The affected product later was recalled. We describe an 8-mo-old cat with a history of severe illness after consuming this raw milk before it was recalled. The cat was euthanized and submitted for postmortem examination and diagnostic workup. Autopsy and histopathology revealed icterus, nasal discharge, hydrothorax, gliosis, and necrotizing pneumonia, hepatitis, and salpingitis, among other lesions. Immunohistochemistry for influenza A virus revealed intralesional immunolabeling in many organs. Molecular detection was positive for HPAI A(H5N1) virus, clade 2.3.4.4b, genotype B3.13. To our knowledge, HPAI A(H5N1) virus has not been reported previously in cats after consuming raw milk purchased from a retail establishment, nor has salpingitis been associated with HPAI A(H5N1) virus infection in a mammal. Hepatic damage and icterus were prominent findings in our case rather than primary involvement of the CNS.
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Juan Lama
January 27, 11:58 AM
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Neuraminidase inhibitors (NAIs) and cap-dependent endonuclease inhibitors (CENIs) represent two classes of antiviral drugs recommended for early treatment of patients with seasonal influenza A virus (IAV) infections. However, only limited human data, particularly on combination antiviral treatment, are available to inform optimal dosing regimens against novel IAVs, including highly pathogenic avian influenza A(H5N1) virus, associated with severe disease. Clade 2.3.4.4b A(H5N1) viruses have caused outbreaks in avian and mammalian species worldwide, highlighting the need to assess antiviral drug efficacy against these strains. We challenged ferrets with a D1.1 genotype A(H5N1) virus and treated infected animals with the NAI oseltamivir phosphate (OST) and the CENI baloxavir acid (BXA), alone or in combination, with treatment onset commencing pre- or post-symptom onset (24- or 48-hours post-inoculation (p.i.), respectively). When administered pre- or post-illness onset, BXA, but not OST, monotherapy provided significant reduction of clinical signs and significantly decreased infectious viral levels (in both respiratory and extrapulmonary specimens) compared with mock-treated animals. Combination OST/BXA treatment, when administered pre- or post-symptom onset, resulted in significant improvements in both metrics versus OST monotherapy. These data support continued investigation of antiviral treatment modalities that include both NAI and CENI for patients with mild and severe A(H5N1) disease. Combination treatment with two antiviral drugs (oseltamivir and baloxavir) effectively limits clade 2.3.4.4b A(H5N1) influenza virus replication and disease severity in ferrets. Published January 26, 2026: https://doi.org/10.1038/s42003-026-09607-w
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Juan Lama
January 23, 12:11 PM
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When scientists sent bacteria-infecting viruses to the International Space Station, the microbes did not behave the same way they do on Earth. In microgravity, infections still occurred, but both viruses and bacteria evolved differently over time. Genetic changes emerged that altered how viruses attach to bacteria and how bacteria defend themselves. The findings could help improve phage therapies against drug-resistant infections. In a new study, terrestrial bacteria-infecting viruses were still able to infect their E. coli hosts in near-weightless "microgravity" conditions aboard the International Space Station, but the dynamics of virus-bacteria interactions differed from those observed on Earth. Phil Huss of the University of Wisconsin-Madison, U.S.A., and colleagues present these findings January 13thin the open-access journal PLOS Biology. Interactions between phages -- viruses that infect bacteria -- and their hosts play an integral role in microbial ecosystems. Often described as being in an evolutionary "arms race," bacteria can evolve defenses against phages, while phages develop new ways to thwart defenses. While virus-bacteria interactions have been studied extensively on Earth, microgravity conditions alter bacterial physiology and the physics of virus-bacteria collisions, disrupting typical interactions. However, few studies have explored the specifics of how phage-bacteria dynamics differ in microgravity. To address that gap, Huss and colleagues compared two sets of bacterial E. coli samples infected with a phage known as T7 -- one set incubated on Earth and the other aboard the International Space Station. Analysis of the space-station samples showed that, after an initial delay, the T7 phage successfully infected the E. coli. However, whole-genome sequencing revealed marked differences in both bacterial and viral genetic mutations between the Earth samples versus the microgravity samples. The space-station phages gradually accumulated specific mutations that could boost phage infectivity or their ability to bind receptors on bacterial cells. Meanwhile, the space-station E. coli accumulated mutations that could protect against phages and enhance survival success in near-weightless conditions. The researchers then applied a high-throughput technique known as deep mutational scanning to more closely examine changes in the T7 receptor binding protein, which plays a key role in infection, revealing further significant differences between microgravity versus Earth conditions. Additional experiments on Earth linked these microgravity-associated changes in the receptor binding protein to increased activity against E. coli strains that cause urinary tract infections in humans and are normally resistant to T7. Overall, this study highlights the potential for phage research aboard the ISS to reveal new insights into microbial adaption, with potential relevance to both space exploration and human health. The authors add, "Space fundamentally changes how phages and bacteria interact: infection is slowed, and both organisms evolve along a different trajectory than they do on Earth. By studying those space-driven adaptations, we identified new biological insights that allowed us to engineer phages with far superior activity against drug-resistant pathogens back on Earth." Published January 2026: https://doi.org/10.1371/journal.pbio.3003568
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Juan Lama
January 19, 11:46 AM
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Highly pathogenic avian influenza H5N1 viruses of clade 2.3.4.4b have caused widespread avian mortality and sporadic mammalian infections, raising concerns about their potential for efficient replication in the human population. Efficient replication in the human upper respiratory tract is considered a key barrier to transmission. Here, we demonstrate that an H5N1 virus isolated from bovine milk in Texas in 2024 (H5N1Tex/24) replicates as efficiently as the 2009 pandemic H1N1 virus (H1N1HH4/09) in well-differentiated human nasal epithelial cells. These cells express both avian- and human-type influenza receptors, indicating receptor adaptation is unnecessary for entry. H5N1Tex/24 replicates effectively at 33 degrees Celsius, reflecting nasal cavity temperature, whereas earlier avian H5N1 strains require 37 degrees Celsius, suggesting that H5N1Tex/24 has acquired another key adaptive feature to the human upper respiratory tract. H5N1Tex/24 remains sensitive to interferon-λ (IFN-λ) despite inducing low cytokine levels. Notably, no known mammalian-adaptive mutations such as PB2-E627K were detected. These findings suggest that H5N1Tex/24 possesses intrinsic traits enabling efficient replication in the human upper airways, a critical step toward potential airborne transmission, underscoring the need for vigilant surveillance. Preprint in bioRxiv (January 17, 2026): https://doi.org/10.64898/2026.01.16.699876
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Juan Lama
January 16, 1:23 PM
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Genome editing enzymes have vast therapeutic potential. However, achieving sufficient delivery in vivo remains a major challenge, because editing machinery is confined to the subset of transfectable cells in a tissue. Here, we tested the possibility that genome editing could be amplified in vivo by programming transfected cells to produce and transfer editing enzymes in lipid vesicles to neighboring cells. Our data show that this NANoparticle-Induced Transfer of Enzyme (NANITE) strategy tripled editing efficiency in cultured cells relative to non-spreading controls. Furthermore, a single intravenous injection of the NANITE plasmid into mice induced ~3-fold higher levels of liver editing at the Ttr locus relative to non-spreading controls, with corresponding reductions in serum transthyretin levels. Amplifying therapeutic enzymes in situ offers a nonviral and non-infectious strategy to overcome low delivery efficiencies and reduce effective dose requirements. Published in bioRxiv (January 13, 2026): https://doi.org/10.64898/2026.01.13.699115
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