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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
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
January 15, 11:32 AM
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Study findings highlight the potential for targeting cross-reactive T cells for diagnosis or MS therapies. The results of preclinical research headed by a team at Karolinska Institutet have indicated how T cells that play a role in the immune system’s reaction to the common Epstein-Barr virus (EBV) can also cross-react with a protein in the brain, ultimately contributing to multiple sclerosis (MS). The team said the study provides new insight into the long-suspected link between EBV and MS. “Our results provide mechanistic evidence that immune responses to EBV can directly damage the brain in MS,” said Olivia Thomas, PhD, assistant professor at the Department of Clinical Neuroscience at Karolinska Institutet. “It is a complex neurological disease, and it may be that the molecular mechanisms vary between patients.” Thomas is first author of the team’s published paper in Cell, titled “Anoctamin-2-specific T cells link Epstein-Barr virus to multiple sclerosis.” MS is a chronic inflammatory disease in which the immune system attacks the central nervous system and causes nerve damage. “Multiple sclerosis (MS) causes neurological disability in young adults, with an estimated 2.8 million patients worldwide,” the authors wrote. “MS is characterized by inflammatory lesions in the central nervous system (CNS) and usually presents clinically with a relapsing-remitting phenotype.” It has long been known that everyone who develops MS has had an infection with the Epstein-Barr virus, a common virus that often infects young people, sometimes causing glandular fever but often without any obvious symptoms. Exactly how this virus contributes to MS has long been unclear. “Epstein-Barr virus (EBV) is the common cause of infectious mononucleosis (IM) and a prerequisite for MS,” the team continued. Through their newly reported studies, part of which the investigators analyzed blood samples from people with MS compared with those of healthy controls, the researchers have now shown that when the immune system fights EBV, T cells that normally attack the virus can also react to a protein in the brain called Anoctamin-2 (ANO2). “… cross-reactivity between EBV nuclear antigen 1 (EBNA1) and anoctamin-2 (ANO2) antibodies was previously demonstrated in persons with MS (pwMS),” they pointed out. This phenomenon is called molecular mimicry—immune cells mistaking the body’s own proteins for those of the virus. “Given the link between ANO2 antibodies and MS, we hypothesized that ANO2-specific T cells may also exist and cross-react with EBNA1 via molecular mimicry.” Through their study, the team was able to isolate T cells that react to both the EBV protein EBNA1 and ANO2 from people with MS, demonstrating that these cross-reactive T cells are significantly more common in people with MS than in healthy controls. “Here, we show that ANO2-specific CD4+ T cells are more frequent in pwMS,” they stated. “Notably, the proportion of pwMS with ANO2-reactive T cells was much higher (∼57% of untreated pwMS) than previously reported for ANO2 antibody seropositivity (∼15%), further reinforcing the potential relevance of ANO2 cellular immunity in neuroinflammation.” In addition, experiments in a mouse model showed that these cells can exacerbate MS-like symptoms and cause damage to the brain. According to the researchers, the results may help explain why some people develop MS after an EBV infection while others do not. The study builds on previous research showing that misdirected antibodies after EBV infection may play a role. “The discovery opens up new treatments that target these cross-reactive immune cells,” suggested Tomas Olsson, PhD, professor, who led the study together with Andre Ortlieb Guerreiro-Cacais, PhD, associate professor, both at the Karolinska Institutet. “Since several EBV vaccines and antiviral drugs are now being tested in clinical trials, the results may be of great importance for future preventive and therapeutic efforts.” The team said their study offers “… first mechanistic evidence that EBNA1 CD4+ T cells can target the MS autoantigen ANO2, thereby establishing a link between EBV infection and neuroinflammation.” In their discussion, they concluded, “In this study, we demonstrate that over half of pwMS have T cell responses to ANO2, which highlights the potential of targeting these cells for diagnosis or MS therapies, either by depletion or ANO2 immune tolerance.” Published in Cell (Jan. 13, 2026): https://www.cell.com/cell/fulltext/S0092-8674(25)01481-3
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Scooped by
Juan Lama
January 8, 12:47 PM
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Though Gilead Sciences made waves last June with a landmark FDA approval for its twice-yearly HIV preventative Yeztugo (lenacapavir), the first-in-class drug had previously been used as a long-acti | Though Gilead Sciences made waves last June with a landmark FDA approval for its twice-yearly HIV preventative Yeztugo (lenacapavir), the first-in-class drug had previously been used as a long-acting treatment for the viral infection. Now, Gilead has conducted an analysis of a phenomenon that can undermine all infectious disease therapies, including lenacapavir—HIV’s ability to evolve resistance to the breakthrough antiviral. After exposure to lenacapavir, HIV was able to shift the structure of its protein coating to avoid the drug’s effects, but this often came at a cost to the virus’s reproduction. The results, published in Science Translational Medicine on Jan. 7, suggest that while it may be difficult for lenacapavir-resistant strains of HIV to spread, surveillance for drug resistance and the pairing of lenacapavir with other antivirals could help prevent the virus from evolving resistance to the groundbreaking treatment. The new study adds to existing evidence that “resistances are rare” in HIV treated with lenacapavir, Jared Baeten, M.D., Ph.D., senior vice president and virology head at Gilead, told Fierce Biotech. “That has been the most reassuring thing,” he added. Before its headline-grabbing 100% efficacy rate in an HIV prevention trial and subsequent long-acting prophylactic approval, lenacapavir was approved in 2022 as Sunlenca for the treatment of HIV that resisted other antiviral therapies. The drug is the only approved HIV med that targets the virus’s protein capsid, which acts as a shield for the pathogen’s genetic material. “All drugs for HIV have the potential for the development of resistance,” Baeten said. Because lenacapavir uses a novel mechanism to target the virus, the goal of the new study was to establish whether and how HIV may evolve to evade the drug and, potentially, other future capsid inhibitors. To attack that question, Gilead scientists analyzed HIV samples taken during lenacapavir’s phase 3 Capella and phase 2 Calibrate trials, which studied the molecule’s use as an HIV treatment. In 40 samples, the team identified three primary changes to the virus’s capsid that enabled it to escape lenacapavir binding, the most common of which was a methionine amino acid that was swapped to an isoleucine. Though this change “resulted in high-level resistance” to lenacapavir, it also led to “extreme fitness cost, reducing replication capacity to below 20%” that of normal HIV, Manish Choudhary, Ph.D., and Jonathan Li, M.D., virologists at Brigham and Women’s Hospital and Harvard Medical School, noted in a Jan. 7 commentary on the new study. The mutation, called M66I, primarily arose in the Capella study, in which lenacapavir was given as a monotherapy to patients whose HIV didn’t respond to other treatments. But, even in some of these patients, the virus was still effectively suppressed because of the trade-off between drug resistance and virus replication, Baeten noted. And lenacapavir resistance didn’t translate to resistance to other classes of antivirals. Allison Agwu, M.D., an infectious disease specialist at Johns Hopkins University and former chair of the HIV Medicine Association, found it interesting that “the evolution of resistance can come at a fitness cost” to the virus, but she noted that HIV was able to tack on other mutations to compensate for those negative effects, she told Fierce Biotech. “It is important to continue to interrogate the evolution and consequences of resistance mutations” to lenacapavir, she added. Overall, the results will help “construct a fully active regimen” for patients with drug-resistant forms of HIV, Baeten said. For patients with less complicated forms of the virus, it’s important to avoid lenacapavir resistance in the first place, he said, which comes down to “maintaining adherence to the medicines.” “These findings highlight the importance of maintaining fully active companion drugs during HIV treatment, improving access to resistance testing and surveillance and accelerating development of next-generation capsid inhibitors,” Choudhary and Li wrote. Agwu agreed, highlighting that “infrastructure to support consistent and sustained drug access to avoid lapses” is critical for avoiding drug resistance. Gilead is trying to turn lenacapavir into a pipeline gift that keeps on giving, while also developing new capsid inhibitors and probing why exactly lenacapavir resistance hampers HIV’s ability to replicate, Baeten said. “We're not going to be done with HIV until the virus is done,” Baeten added, pointing to his video call background featuring Gilead’s pledge to end the HIV epidemic. “We are constantly thinking about how to stay further ahead.” Published Jan. 7, 2026: https://www.science.org/doi/10.1126/scitranslmed.aea0947
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Scooped by
Juan Lama
January 6, 12:08 PM
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The Centers for Disease Control and Prevention (CDC) has upende | The Centers for Disease Control and Prevention has upended the immunization schedule for children in the U.S., eliminating six of the 17 vaccines that were previously recommended to protect them from disease. The new schedule removes recommendations for flu and COVID vaccines for children. Also chopped were shots for rotavirus, meningitis, hepatitis A and hepatitis B. These shots can still be administered but only after consultation with a healthcare specialist. Additionally, immunization against respiratory syncytial virus (RSV)—the top cause for infant hospitalizations in the U.S., according to the CDC—is now limited to those at high risk and children whose mothers have not been vaccinated. The CDC also now advises that one dose of the HPV vaccine is as effective as two shots. Jim O’Neill, the acting director of the CDC, said in a press conference that the changes are effective immediately. They were determined through a “comprehensive scientific assessment” of the U.S. immunization schedule compared to other developed nations, according to a release from the Department of Health and Human Services (HHS). The U.S. previously recommended more childhood vaccines than any peer nation, according to the HHS, which pointed out that Denmark advises immunization against just 10 diseases. The changes come in response to a memorandum last month from President Donald Trump to the CDC to review the childhood vaccine schedule. “After an exhaustive review of the evidence, we are aligning the U.S. childhood vaccine schedule with international consensus while strengthening transparency and informed consent,” Robert F. Kennedy Jr., secretary of the HHS, said in a statement. “This decision protects children, respects families, and rebuilds trust in public health.” The schedule adjustments run counter to scientific evidence that backed the approval and CDC recommendations of the vaccines, which were vetted through an independent advisory board. The CDC action Monday emerged from a vastly less vigorous and science-based review, according to the American Medical Association (AMA). “When longstanding recommendations are altered without a robust, evidence-based process, it undermines public trust and puts children at unnecessary risk of preventable disease,” the AMA said in a statement. “We urge federal health leaders to recommit to a transparent, evidence-based process that puts children’s health and safety first and reflects the realities of our nation’s disease burden.” Trump’s nomination of RFK Jr.—a longtime anti-vaccine activist—to the HHS post less than a year ago signaled the potential for consequential changes in vaccine policy. One of RFK Jr.’s first acts after he was confirmed was to remove all 17 experts on the CDC’s Advisory Committee on Immunization Practices and replace them with his own selections. “Donald Trump and Secretary Kennedy have long embraced unfounded anti-vax conspiracies and debunked propaganda, and now they’ve weaponized their dangerous views against American kids,” Kayla Hancock, director of Public Health Watch, said in a statement. “RFK Jr.’s contempt for peer-reviewed science showing these vaccines are safe and effective has been turned into harmful action, and it’s no hyperbole to say innocent children could die as a direct result.” The HHS assessment was led by Tracy Beth Høeg, M.D., Ph.D., acting director for the Center for Drug Evaluation and Research, and Martin Kulldorff, Ph.D., chief science and data officer for the Assistant Secretary for Planning and Evaluation, in consultation with experts from the CDC, the FDA, the National Institutes of Health and the Centers for Medicare & Medicaid Services, according to an HHS document. The officials reviewed vaccine recommendations in 20 countries, the report said. “The data support a more focused schedule that protects children from the most serious infectious diseases while improving clarity, adherence, and public confidence,” O’Neill said. The CDC has kept intact its recommendation that all children be vaccinated against diphtheria, tetanus, whooping cough, haemophilus influenzae type b (Hib), pneumococcal conjugate, polio, measles, mumps, rubella and human papillomavirus, for which there is international consensus, as well as varicella (chickenpox).
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Scooped by
Juan Lama
January 3, 12:48 PM
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Mpox (formerly monkeypox) is caused by monkeypox virus (MPXV) and has prompted two recent global health emergencies. Clade IIb MPXV, a recently recognized subclade, has been associated with oral and genital lesions and transmission among men who have sex with men (MSM); however, mechanisms of genital pathogenesis and sexual transmission are not understood. We investigated several routes of MPXV Clade IIb virus infection (intranasal, oral, anal, and intraperitoneal) and found high and prolonged viral titres in the testes after IP inoculation still detectable at 21 days. The testes had significant changes to tissue architecture including loss of spermatogenesis, disorganization of spermatozoa, loss of Leydig cells, and breakdown of the seminiferous tubule membranes. Viral antigen positive cells were present in the interstitial spaces between the seminiferous tubules with macrophage infiltration also evident. This work provides insights into potential of sexual transmission for MPXV viruses as well as mechanisms of Mpox disease which may significantly impact long-term fertility or sex organ health of infected males. Author Summary Mpox (formerly monkeypox) is a painful disease similar to smallpox caused by the monkeypox virus (MPXV) which is an emerging/re-emerging virus. Recently the WHO has declared two global health emergencies due to human-to-human transmission of MPXV. Clade IIb MPXV is a newly recognized subclade that has been associated with genital lesions and sexual transmission/contact; however, how the virus causes disease in sex-organs or how it is passed from person-to-person is not understood. We investigated several routes of MPXV Clade IIb inoculation and found IP inoculation in male mice led to high and prolonged viral titres in testes. Additionally, the testes were significantly affected having loss of sperm and cellular organization. Evidence of inflammatory cell infiltration, specifically, macrophages, are suspected to be the cause of testes specific disease. This work provides insights into potential of sexual transmission for MPXV viruses as well as mechanisms of Mpox disease. Preprint (Dec. 16, 2025): https://doi.org/10.64898/2025.12.16.694558
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Scooped by
Juan Lama
December 26, 2025 12:59 PM
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Some 5000 years ago, the corpse of a man known as Ötzi, “the Iceman,” froze in the Alps along what’s now the Austrian-Italian border. The resulting mummy, known for his preserved clothing, weaponry, and tattooed skin, most likely succumbed to an arrowhead lodged in his shoulder. But before Ötzi’s death, he also endured broken bones, intestinal parasites, and soot-blackened lungs. Now, scientists may add another ailment to that list: the cancerous human papillomavirus, HPV16. In a paper posted to the bioRxiv preprint server, researchers report that Ötzi and a 45,000-year-old Homo sapiens fossil from western Siberia both contain stretches of DNA from the cancer-causing virus. The results, which have yet to undergo peer review, could help pin down when and how modern humans first encountered the virus. “This is a very nice finding,” says Ville Pimenoff, a computational geneticist at the University of Oulu who wasn’t involved with the work. It adds to evidence that “Homo sapiens was basically infected by these viruses for all of its existence.” Hundreds of human papillomaviruses, or HPVs, make themselves at home in and on our bodies. Most cause no trouble, but about a dozen can lead to genital and throat cancers, constituting roughly 5% of cancers worldwide. Those infections—and the cancers they spur—can be quashed by vaccines available since 2006. But there’s some concern that in response to widespread vaccination, other HPV types move into the vacated niches. A 2023 study of more than 3000 Finnish teens found that 8 years after immunizations, the highly cancerous types of HPV targeted by the vaccines mostly remained absent, but the diversity of other types increased. Pimenoff, who led the Finnish study, says the results show the importance of understanding the full diversity of HPV lineages—as well as how the virus has evolved over time. In another study published in 2017, he and his colleagues traced back HPV16, the culprit underlying many cervical cancers. They found that HPV diversified alongside early hominins and that modern humans seem to have encountered one of today’s dominant variants of HPV16 some 60,000 years ago, possibly by mating with infected Neanderthals. The new preprint fills in an important gap by detecting HPV in ancient human fossils. To search for the virus within past members of our own species, a team led by molecular biologist Marcelo Briones of the Federal University of São Paulo (UNIFESP) downloaded publicly available DNA sequences collected from Ötzi and a fossil known as Ust-Ishim, which eroded from a western Siberian riverbank in 2008. Although only the shaft of a femur bone was discovered, radiocarbon dating showed the Ust-Ishim man lived 45,000 years ago. Mixed in with those individuals’ DNA, Briones and colleagues identified tens of thousands of segments that matched portions of the HPV16 genome. But because ancient DNA segments are short and DNA only encodes four letters (the nucleotides A, T, C, G), it’s possible these matches were due to random luck—in other words, statistical noise, not a true biological signal that the ancient genomes bore the virus. To test for this, the team also generated and analyzed mock sequences to see how likely it would be for random sequences to return a pattern similar to what Briones and colleagues saw in the ancient DNA. The results suggest the sequences do, in fact, come from viruses, says study first author Juliana Yazigi, a bioinformatics student at UNIFESP. “We’re pretty confident there’s a signal there. … We have the oldest evidence of HPV.” Moreover, the identified viruses most closely matched the HPV type an earlier study suggested came from Neanderthals. To be present within Ötzi and Ust-Ishim—individuals separated by some 40,000 years and 5000 kilometers—this HPV16 variant must have been circulating within our species for a long time. So long, Briones thinks, that it’s more likely our species transmitted the cancer-causing HPV16 to Neanderthals rather than the other way around. Supporting this scenario, in a previous project applying the same approach to Neanderthal fossils, Briones’s team found the low-risk HPV12—not the highly cancerous HPV16. In pushing back direct evidence for HPV16 in our species, University of Arizona virologist Koenraad Van Doorslaer says the new findings are “potentially challenging the idea that HPV was [due to] this Neanderthal interbreeding event.” “Is this gonna make better vaccines, better treatments, better cures? Probably not,” he adds. “But not all science should be about that. It should just be about learning cool things.” Preprint availble in bioRxiv (Dec. 13, 2025): https://doi.org/10.64898/2025.12.14.694221
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Scooped by
Juan Lama
December 20, 2025 12:39 PM
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The recent global outbreaks of mpox highlight the urgent need for both fundamental research and antiviral development. However, studying the mpox virus (MPXV), with its large and complex genome, remains challenging due to the requirement for high-containment facilities. Here, we describe a strategy for de novo assembly of MPXV clade IIb genomes in bacterial artificial chromosomes using transformation-associated recombination cloning. Leveraging CRISPR-Cas9 and Lambda Red recombination, we engineer replication-defective MPXV particles with dual deletions of OPG96 (M2R) and OPG158 (A32.5 L)—genes essential for virion assembly, that are capable of recapitulating key stages of the viral life cycle. We apply this system to screen a compound library and identify G243-1720, a potent anti-poxvirus inhibitor with broad activity in vitro and in vivo. G243-1720 blocks the formation of extracellular enveloped virions and cell-cell spread. Resistance mutation selection, crystallographic analysis, analytical ultracentrifugation, and mass photometry reveal that, despite its distinct chemical structure, G243-1720 shares a mode of action with tecovirimat, both functioning by affecting dimerization of protein OPG57 (F13). Our findings underscore the potential of G243-1720 as a promising broad-spectrum anti-poxvirus lead compound and demonstrate the utility of replication-defective MPXV particles as a reliable platform for viral biology studies and antiviral development. The recent global mpox outbreaks underscore the critical need for antiviral development, hindered by the complexity of the MPXV genome. Using yeast TAR cloning, CRISPR-Cas9, and Lambda Red recombination to engineer replication-defective MPXV, the authors offer a platform for therapeutic research and identify G243-1720, a compound with a tecovirimat-like mechanism, as a promising anti-poxvirus compound. Published in Nature Communications (Dec. 15 2025): https://doi.org/10.1038/s41467-025-67487-w
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Scooped by
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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Scooped by
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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Scooped by
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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Scooped by
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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Scooped by
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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Scooped by
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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Scooped by
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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Scooped by
Juan Lama
January 9, 12:13 PM
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GSK’s bepirovirsen met the main goal of two Phase 3 studies, achieving functional cure rates for patients with chronic hepatitis B infection after six months of treatment. This antisense oligonucleotide therapy could provide a treatment alternative to antiviral drugs that patients must take for life. An experimental GSK drug in development for treating chronic hepatitis B now has results from two pivotal studies showing the therapy brought levels of the virus low enough to allow the immune system to then control the infection without further medication. This outcome amounts to a functional cure, where the virus can no longer be detected in the blood. Without reporting specific figures, GSK said Wednesday the drug, bepirovirsen, led to statistically significant and clinically meaningful functional cure rates, meeting the main goal of the studies. With the preliminary data in hand, the company is now preparing regulatory submissions for the drug globally. Hepatitis B virus can cause both acute and chronic liver disease. The infection becomes chronic when the immune system is unable to clear the virus. More than 250 million people worldwide are estimated to have chronic hepatitis B infection, which can lead to liver cancer. Standard treatment is antiviral therapies, such as Gilead Sciences’ Vemlidy, that must be taken chronically and achieve low functional cure rates. Gilead reported $783 million in global Vemlidy sales for the first nine months of 2025, a 12% increase compared to the same period in the prior year. Bepirovirsen is an antisense oligonucleotide designed to target RNA to inhibit the production of proteins associated with hepatitis B virus infection and replication. In addition to inhibiting the replication of viral DNA, GSK says this drug also suppresses the level of hepatitis B surface antigen in the blood and stimulates the immune system to increase the chances of a durable response to the therapy. The preliminary data reported Wednesday are from two Phase 3 studies that enrolled more than 1,800 total patients from 29 countries. The treatment period was 24 weeks. GSK said the functional cure rates were significantly higher with the study drug plus standard of care antivirals compared to standard therapy alone. The company added that if approved, bepirovirsen could become the first finite, six-month therapy for chronic hepatitis B infection. Full clinical trial results will be submitted for presentation at an upcoming scientific meeting and published in a peer-reviewed journal. “Today’s result supports our plans to progress bepirovirsen as a treatment and also continue its development as a backbone in future sequential therapies,” GSK Chief Scientific Officer Tony Wood said in a prepared statement. “We’re pleased by this major advance in our expanding hepatology pipeline, aimed to transform outcomes in liver disease.” Bepirovirsen came from the labs of Ionis Pharmaceuticals. In 2010, Ionis began a drug discovery partnership with GSK that included infectious diseases. After bepirovirsen posted positive Phase 2 results in 2019, GSK licensed the hepatitis B virus program, making the big pharma company responsible for further development and regulatory submissions for the drug worldwide. In its 2024 annual report, Ionis said it had received more than $105 million in payments to date from the collaboration. In a note sent to investors, Leerink Partners analyst Mani Foroohar wrote that bepirovirsen’s positive data readout was largely expected, given the program’s successful Phase 2 results. The firm is waiting for detailed data before it can place a value on the asset. He added that while chronic hepatitis B represents a large, underserved market, the commercial opportunity will depend on the positioning of antisense oligonucleotide/siRNA therapies in this market. Foroohar said Ionis could receive up to $150 million in remaining milestone payments plus royalties from sales of bepirovirsen.
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Scooped by
Juan Lama
January 8, 12:26 PM
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Gene therapy ‘switch’ may offer non-addictive pain relief. New approach targets pain signals while leaving the rest of the brain untouched. More than 50 million Americans live with chronic pain. Drugs are currently available; however, close to 80% of the 600,000 deaths attributed to drug use in 2019 were related to opioids with about 25% of those deaths caused by opioid overdose. In addition, nearly half of Philadelphians who responded to a 2025 Pew survey reported knowing someone with opioid use disorder (OUD) and one-third knew someone who had died as the result of an overdose. Taken together, novel approaches to pain management are a large, unmet need. Now, a gene therapy opens a new avenue for targeting pain centers in the brain while eliminating the risk of addiction from narcotics treatments. This work is published in Nature in the paper, “Mimicking opioid analgesia in cortical pain circuits.” “To our knowledge, this represents the world’s first CNS-targeted gene therapy for pain, and a concrete blueprint for non-addictive, circuit-specific pain medicine,” says Gregory Corder, PhD, assistant professor of Psychiatry and Neuroscience at University of Pennsylvania Perelman School of Medicine. “The goal was to reduce pain while lessening or eliminating the risk of addiction and dangerous side effects,” he said. “By targeting the precise brain circuits that morphine acts on, we believe this is a first step in offering new relief for people whose lives are upended by chronic pain.” Uncovering how opioids alter nociceptive neural dynamics to produce pain relief is essential for developing safer and more targeted treatments for chronic pain. By imaging brain cells that act as pain trackers, the researchers revealed new insights into how morphine eases suffering. They suggest that “a population of cingulate neurons encodes spontaneous pain-related behaviors and is selectively modulated by morphine.” The team built a mouse-model behavioral platform driven by AI that tracks natural behaviors, creates a readout of pain levels, and helps gauge how much treatment is needed to alleviate the pain. More specifically, they “identified a persistent shift in cortical activity patterns following nerve injury that reflects the emergence of an unpleasant, affective chronic pain state” and that “morphine reversed these neuropathic neural dynamics and reduced affective–motivational behaviors without altering sensory detection or reflexive responses, mirroring how opioids alleviate pain unpleasantness in humans.” This readout allowed the team to design a targeted gene therapy that mimics morphine’s beneficial effects but avoids its addictive ones while delivering an “off switch” specifically for pain felt in the brain. They targeted opioid-sensitive neurons in the cingulate using a synthetic μ-opioid receptor promoter to drive inhibition. When activated, this switch provides durable pain relief without affecting normal sensation or triggering reward pathways that can lead to addiction. They note that it recapitulated the analgesic effects of morphine during chronic neuropathic pain and offers a new strategy for precision pain management that targets a key nociceptive cortical opioid circuit. The team is moving forward with Michael Platt, PhD, professor in the department of psychology at the University of Pennsylvania, on the next phase of work toward clinical trials. “The journey from discovery to implementation is long, and this represents a strong first step,” Platt said. “Speaking both as a scientist and as a family member of people affected by chronic pain, the potential to relieve suffering without fueling the opioid crisis is exciting.” Published in Nature (January 7, 2026): https://doi.org/10.1038/s41586-025-09908-w
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Scooped by
Juan Lama
January 3, 1:13 PM
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Highlights
• Structures of HSV-1 helicase-primase and replication fork complexes determined
• Inhibitors cause the helicase-primase complex to pause on DNA
• Conserved polymerase FYNPYL motif interacts with viral helicase
• Structures inform mechanisms of drug selectivity and targeting
Summary
Herpesviruses are widespread double-stranded DNA viruses that establish lifelong latency and cause various diseases. Although DNA-polymerase-targeting antivirals are effective, increasing drug resistance underscores the need for alternatives. Helicase-primase inhibitors (HPIs) are promising antivirals, but their mechanisms of action are poorly defined. Furthermore, how the helicase-primase (H/P) complex and DNA polymerase coordinate genome replication is not well understood for herpesviruses. Here, we report cryo-electron microscopy (cryo-EM) structures of the herpes simplex virus 1 H/P complex bound to HPIs, showing that these lock the H/P complex in an inactive state. Single-molecule assays reveal that HPIs cause H/P complexes to pause in unwinding activity on DNA. The structure of an HPI-bound replication fork complex, comprising the H/P complex (UL5, UL52, and UL8) and the polymerase holoenzyme (UL30 and UL42), reveals a previously uncharacterized interface bridging these complexes. These findings provide a structural framework for understanding herpesvirus replisome assembly and advancing inhibitor development.
Published in Cell (December 29, 2025): https://www.cell.com/cell/fulltext/S0092-8674(25)01376-5
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Scooped by
Juan Lama
December 30, 2025 12:23 PM
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Since 2021, highly pathogenic avian influenza viruses (HPAIV) belonging to H5N1 clade 2.3.4.4b have caused high mortality in North American wild birds and poultry. In 2025, a new D1.1 genotype caused two human deaths and host-switched to dairy cattle. However, the evolutionary origins and dynamics of D1.1 have not been fully characterized. Here, our phylogenetic analysis of 17,516 H5N1 genome sequences uncovers how D1.1 introduced a major shift in the antigenic diversity and ecology of the H5N1 epizootic in North America. D1.1 is the first major H5N1 genotype to (a) emerge in the Pacific flyway and spread west-to-east faster than any prior genotype; (b) antigenically shift via reassortment with the North American N1 segment, displacing the previously fixed Eurasian N1; and (c) transmit to a broader range of host species than any H5N1 genotype to date, introducing mammalian adaptations. Preprint in bioRxiv (Dec. 23, 2025): https://doi.org/10.64898/2025.12.19.695329
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Scooped by
Juan Lama
December 22, 2025 11:20 AM
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Whale breath collected by drones is giving clues to the health of wild humpbacks and other whales. Scientists flew drones equipped with special kit through the exhaled droplets, or "blows", made when the giants come up to breathe through their blowholes. They detected a highly infectious virus linked to mass strandings of whales and dolphins worldwide. The sampling of whale "blow" is a "game-changer" for the health and well-being of whales, said Prof Terry Dawson of King's College London. "It allows us to monitor pathogens in live whales without stress or harm, providing critical insights into diseases in rapidly changing Arctic ecosystems," he said. The researchers used drones carrying sterile petri dishes to capture droplets from the exhaled breath of humpback, fin and sperm whales, combined with skin biopsies taken from boats. They confirmed for the first time that a potentially deadly whale virus, known as cetacean morbillivirus, is circulating above the Arctic Circle. The disease is highly contagious and spreads easily among dolphins, whales, and porpoises causing severe disease and mass deaths. It can jump between species and travel across oceans, posing a significant threat to marine mammals. The researchers hope this breakthrough will help spot deadly threats to ocean life early, before they start to spread. "Going forward, the priority is to continue using these methods for long-term surveillance, so we can understand how multiple emerging stressors will shape whale health in the coming years," said Helena Costa of Nord University, Norway. The study, involving King's College London and The Royal (Dick) School of Veterinary Studies in the UK, and Nord University in Norway is published in BMC Veterinary Research.
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Scooped by
Juan Lama
December 17, 2025 11:46 AM
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Scientists are deploying an array of technologies that are making a vaccine against all varieties of influenza seem more achievable. In February 2014, the World Health Organization (WHO) tried to predict which strains of influenza were going to pose the biggest threat in that year’s Northern Hemisphere flu season. It failed. On the basis of surveillance data on which strains were circulating, the WHO selected four that would become the foundation of that year’s vaccine. One was an H3N2 virus strain that was the most prevalent of that particular subtype, at that moment. But by the time the vaccine was making its way into people’s arms that autumn, a different version of the virus had taken over — and the vaccine was only 6% effective at protecting against it. That year’s Northern Hemisphere flu season was more severe than the five that had preceded it, and lasted weeks longer than any in the previous decade.This problem of antigenic drift — when gene mutations cause components of the influenza virus to change, and it evolves away from the vaccines designed to keep it in check — could be reduced by the development of a universal flu vaccine. A shot that provides broad coverage against a wide array of strains could improve efficacy significantly from the 40–60% reduction in risk that flu vaccines typically achieve. It would also eliminate the need for WHO’s twice-yearly meetings to predict which viral strains to guard against, the subsequent scramble to manufacture the vaccine and the need for people to be vaccinated year after year. Some strategies to improve the effectiveness of the flu vaccine and reduce the need for annual shots have made it into early clinical trials. A major thrust of these efforts is to coax the immune system to respond to a part of the flu virus that it normally pays little attention to. Ordinarily, the immune system produces antibodies that focus on a particular part of haemagglutinin, a protein on the surface of the virus that allows it to enter cells. Antibodies clamp to haemagglutinin and block the virus from attaching. Haemagglutinin has 18 subtypes: H1 to H18. And, unfortunately, haemagglutinin can evolve rapidly, changing its shape so that antibodies can no longer bind to it. “What we’re trying to do is trick the immune system into attacking a part of the influenza virus that it typically doesn’t attack,” says Florian Krammer, a vaccinologist at the Icahn School of Medicine at Mount Sinai, New York. Haemagglutinin is a stalk, rising from the virus surface, topped by a ball-shaped head. The immune system focuses most of its efforts here. “The head domain sticks out of the virus, so it’s very easy for B-cell receptors, which in the end become antibodies, to recognize that part,” Krammer says. “The stalk is a little bit more hidden.” Krammer treats this as a challenge, and is trying to amplify the immune response to the haemagglutinin stalk. A second protein called neuraminidase, which helps the virus spread to other cells, has 11 subtypes. Although viruses with any combination of these haemagglutinin and neuraminidase subtypes can infect people, the two currently circulating in humans are H1N1 and H3N2. Krammer and his colleagues create new versions of the virus by taking H1 stalks and replacing the heads with those from other subtypes, such as H14 or H8. Apart from newborn babies, most people have been either infected with or vaccinated against flu — or both — and so have a pre-existing immune response. When presented with a chimaera protein (say, an H1 stalk and an H8 head) the immune system recognizes the part it has seen before (the stalk)and reacts to that. “That weakens the response to the head and strengthens the response to this stalk,” Krammer says. And a stronger reaction to the stalk should, in turn, make it harder for the virus to evade the immune response. The stalk plays a crucial part in allowing the virus to fuse with the host cell, and undergoes a series of structural changes during fusion. Any mutation that interferes with those changes renders the virus ineffective, meaning the stalk can’t evolve in response to the immune system as readily as the head can. The stalk also doesn’t vary much between virus strains, so immunity against this part provides broader protection. In 2020, Krammer and his colleagues tested a vaccine in a small phase I clinical trial3. They showed that it induced a large number of antibodies to target an H1 stalk. Although the COVID-19 pandemic put the work on hold, it has since resumed. The next step will be to try the same with an H3 stalk, and to combine the two to see whether the result generates a broad antiviral response. “It’s going slowly, but it’s going,” Krammer says. At Duke University in Durham, North Carolina, microbiologist Nicholas Heaton is also trying to get the immune system to look beyond the haemagglutinin head. His aim is to get it to notice other sites on the virus at which antibodies can bind, known as epitopes. “Normally, the immune system would focus on that haemagglutinin head domain. It’s obsessed with it,” Heaton says. “If you remove it, then you say, out of everything that’s left, what do you like? And so you get these responses to other epitopes.” Heaton and his colleagues used gene editing to create more than 80,000 variations of haemagglutinin with different changes to a specific part of the head domain, but with the same stalk4. The variety of head-domain epitopes meant that the immune system focused its attention on the stalk, leading to a significant increase in stalk antibodies when tested in ferrets and mice. But Heaton didn’t want to create a new immune response at the expense of the old one. He, therefore, also used conventional methods to create a virus particle that elicited the typical haemagglutinin-head-focused response, and then mixed the two types to achieve broader immunity. The variant epitopes also seem to induce some immunity, and many might help to inhibit the virus. The stalk-binding antibodies don’t actually neutralize the virus, Heaton says, but they can help the immune system to recognize it and clear it faster, theoretically lowering the viral burden and thus the severity of the infection. “People who would have stayed out of work for two days won’t even feel sick,” Heaton says. People who might have died could instead experience just a few days of illness. “Those are the types of shifts that we think would be accomplished by lower peak viral burden and faster clearance of the virus.”.....
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