Lithium study yields insights in the fight against HIV

Ana Luiza Abdalla and Andrew Mouland in front of a flow cytometer at the Lady Davis Institute for Medical Research. The instrument was used to collect key data for the study
Photo Credit: Lucca Jones

Scientific Frontline: "At a Glance" Summary

• Main Discovery: Lithium treatment effectively prevents the reactivation of HIV in latent infected cells, keeping the virus dormant through a biological mechanism previously unidentified in this context.
• Methodology: Researchers utilized a novel fluorescence-based assay to distinguish between dormant and active virus in lab-grown human cells, testing lithium's efficacy while simultaneously disrupting the autophagy pathway to isolate the mechanism of action.
• Key Data: Experiments demonstrated that lithium's ability to suppress viral reactivation persisted even when the cell's autophagy (recycling) system was disabled, directly contradicting the prevailing hypothesis that autophagy was required for this effect.
• Significance: This finding supports the feasibility of a "functional cure"—strategies that keep the virus permanently dormant rather than eradicating it—and identifies a new biological target for maintaining HIV latency.
• Future Application: Development of new pharmaceutical agents that mimic lithium's viral suppression properties without causing the psychoactive side effects or toxicity associated with the drug's current clinical use.
• Branch of Science: Virology and Pharmacology
• Additional Detail: While lithium is an inexpensive and readily available drug, the authors explicitly warn against its current use by HIV patients due to significant side effects and the lack of human clinical trials for this specific indication.

Scientists unlock the genetic key to tackling disease in koalas

Photo Credit: David Clode

Scientific Frontline: "At a Glance" Summary

• Main Discovery: Researchers successfully predicted cancer susceptibility in koalas by analyzing specific inheritance patterns of the Koala Retrovirus (KoRV) within their genomes.
• Methodology: The study integrated whole genome sequencing with detailed life history and health records of over 100 koalas, spanning 46 family groups and four generations, to track viral transmission.
• Specific Mechanism: Bioinformatic analysis distinguished between lethal viral integrations in oncogenes, which caused lineage extinction, and beneficial integrations associated with increased longevity and offspring count.
• Key Statistic: KoRV-associated leukemia remains a critical threat to species survival, accounting for mortality in up to 60% of captive populations and 3% of wild koalas.
• Significance/Application: The derivation of Genetic Risk Scores (GRS) from this data allows conservationists to optimize breeding programs by selecting individuals with low disease risk, thereby improving long-term population health.

When a virus releases the immune brake: New evidence on the onset of multiple sclerosis

Fluorescence microscope image of a mouse brain. The protective myelin layer (red) surrounds the nerve cell extensions. Cells infected with a virus are visible in light blue. Such infections cause immune cells to invade the brain and attack the myelin layer.
Image Credit: Hyein Kim, University of Basel

Scientific Frontline: "At a Glance" Summary

• Discovery of Initiation Mechanism: Researchers have identified a specific biological sequence where the Epstein-Barr virus (EBV) triggers early multiple sclerosis (MS)-like damage by allowing self-reactive B cells to bypass immune checkpoints.
• Molecular Mimicry: The mechanism relies on a viral protein (Latent Membrane Protein 1) that mimics a crucial "approval" signal usually provided by other immune cells, preventing the programmed elimination of B cells that target the body's own proteins.
• Localized Pathogenesis: Experimental mouse models demonstrated that these "out-of-control" B cells capture myelin antigens and cause localized demyelinating lesions in the central nervous system, mirroring the earliest stages of MS.
• B Cell Direct Action: The study shifts the understanding of B cells from indirect influencers of inflammation to direct agents of lesion formation, suggesting they are the primary "spark" for chronic brain inflammation.
• Therapeutic Correlation: The findings explain the clinical efficacy of current B-cell depleting therapies and emphasize that MS risk is shaped by the timing and sequence of rare immune events rather than infection alone.
• Future Prevention: This discovery highlights the potential for preventive strategies, such as targeted vaccinations designed to inhibit severe EBV infections and prevent the subsequent invasion of the brain by pathogenic B cells.

Cat Disease Challenges What Scientists Thought About Coronaviruses

Lychee had feline infectious peritonitis, a feline coronavirus. He was part of a clinical trial at the UC Davis School of Veterinary Medicine that cured him of the disease.
Photo Credit: Courtesy of University of California, Davis

Scientific Frontline: "At a Glance" Summary

• Main Discovery: Researchers at UC Davis discovered that the feline coronavirus responsible for Feline Infectious Peritonitis (FIP) infects a much broader range of immune cells than previously believed, including B and T lymphocytes, rather than being limited to a single cell type.
• Methodology: The team examined lymph node samples from cats with naturally occurring FIP, analyzing the presence of viral material and evidence of active viral replication within specific immune cell populations.
• Mechanism: The study confirmed that the virus actively replicates inside these critical immune cells—B lymphocytes (antibody producers) and T lymphocytes (infection fighters)—instead of merely leaving behind inert fragments.
• Key Finding: Traces of the virus were found to persist in immune cells even after antiviral treatment was concluded and the cats appeared clinically healthy, suggesting a mechanism for disease relapse or long-term immune disruption.
• Implication: Because some immune cells have multi-year lifespans, this persistence offers a valuable model for understanding human long COVID and chronic post-viral syndromes, providing a rare opportunity to study viral reservoirs in immune tissues inaccessible in human patients.

First ancient human herpesvirus genomes document their deep history with humans

Laboratory technician and one of the authors in the contamination-controlled ancient DNA laboratory at the University of Tartu extracting tiny amounts of DNA from centuries-old skeletons.
Photo Credit: Courtesy of University of Tartu

For the first time, scientists have reconstructed ancient genomes of Human betaherpesvirus 6A and 6B (HHV-6A/B) from archaeological human remains more than two millennia old. The study, led by the University of Vienna and University of Tartu (Estonia) and published in Science Advances, confirms that these viruses have been evolving with and within humans since at least the Iron Age. The findings trace the long history of HHV-6 integration into human chromosomes and suggest that HHV-6A lost this ability early on. 

HHV-6B infects about 90 percent of children by the age of two and is best known as the cause of roseola infantum – or "sixth disease" – the leading cause of febrile seizures in young children. Together with its close relative HHV-6A, it belongs to a group of widespread human herpesviruses that typically establish lifelong, latent infections after an initial mild illness in early childhood. What makes them exceptional is their ability to integrate into human chromosomes – a feature that allows the virus to remain dormant and, in rare cases, to be inherited as part of the host's own genome. Such inherited viral copies occur in roughly one percent of people today. While earlier studies had hypothesized that these integrations were ancient, the new data from this study provide the first direct genomic proof. 

Virology: In-Depth Description

Image Credit: Scientific Frontline / AI generated

Virology is the branch of biological science dedicated to the study of viruses—submicroscopic, parasitic particles of genetic material contained in a protein coat—and virus-like agents. Its primary goal is to understand the structure, classification, and evolution of these pathogens, their mechanisms of infection and exploitation of host cells, and their interactions with host organism physiology and immunity.

Receptors in mammary glands make livestock and humans inviting hosts for avian flu

Microscope-captured images of a mammary gland of a pig show the presence of influenza receptors. In the image on the left, receptors for avian influenza A are colored orange. In the image on the right, receptors for the type of influenza A that typically infects mammals are purple.
Image Credit: Dr. Tyler Harm/Iowa State University

An ongoing outbreak of highly pathogenic avian influenza has affected more than 184 million domestic poultry since 2022 and, since making the leap to dairy cattle in spring 2024, more than 1,000 milking cow herds. 

A new study led by Iowa State University researchers shows that the mammary glands of several other production animals – including pigs, sheep, goats, beef cattle and alpacas – are biologically suitable to harbor avian influenza, due to high levels of sialic acids.

“The main thing we wanted to understand in this study is whether there is potential for transmission among these other domestic mammals and humans, and it looks like there is,” said Rahul Nelli, the study’s lead author and a research assistant professor of veterinary diagnostic and production animal medicine.

New Method Uncovers How Viruses Evade Immune Responses — and How We Might Fight Back

Co-first authors Erin Doherty (left) and Jason Nomburg (right)
Photo Credit: Courtesy of Innovative Genomics Institute

Viruses and their hosts — whether bacteria, animals, or humans — are locked in a constant evolutionary arms race. Cells evolve defenses against viral infection, viruses evolve ways around those defenses, and the cycle continues.

One important weapon that cells use in the fight against viruses is a set of tiny molecular “alarm signals” made of nucleotides: the same chemical building blocks that make up DNA and RNA. When a virus infects a cell, these nucleotide messengers activate powerful immune defenses. To survive, viruses must find ways to shut these signals down. In a new study published in the journal Cell Host & Microbe, IGI researchers reveal that viruses have evolved a surprisingly large and diverse set of enzymes specifically designed to destroy these immune alarm signals, helping them hide from or disable the host’s antiviral defenses.

Severe impact of avian flu on southern elephant seals

Elephant seals on Lagoon Island near Ryder Bay, Adelaide Island.
Photo Credit: Steve Gibbs, BAS

New research reveals 47% decline in breeding female elephant seals at sub-Antarctic island of South Georgia following a highly pathogenic avian influenza outbreak. 

Scientists from the British Antarctic Survey (BAS) have documented the severe impact of highly pathogenic avian influenza (HPAI) on southern elephant seals at South Georgia, revealing a 47% decline in breeding females between 2022 and 2024. 

The research, published today in the journal Communications Biology, shows that the world’s largest population of southern elephant seals – which accounts for over half of the global population of breeding age – has suffered unprecedented losses following the arrival of HPAI H5N1 at the remote sub-Antarctic island in late 2023. 

New study finds higher hantavirus risk in drier, underdeveloped areas

A study of the long-term risk of contracting hantavirus across large geographic areas provides public health officials with information about populations most at risk for contracting hantavirus and the potential drivers of disease risk. Humans become infected with hantavirus when they inhale the airborne particles of feces and urine of disease-carrying rodents.
Photo Credit: Zoshua Colah

In a recent study of the contiguous United States, Los Alamos National Laboratory researchers found that the risk of disease from hantavirus is higher in drier, underdeveloped geographic areas with more socioeconomic vulnerability and increased numbers of unique rodent species. This is the first study to examine the combined effects of multiple variables — including socioeconomic, environmental, land use and rodent species — to determine which are most likely to predict the risk of people contracting hantavirus.

“We ran each of these variables separately — looking at where people are most at risk given just the environmental variables, just the land-use variables, etc. — and then we combined them all,” said Morgan Gorris, a scientist at Los Alamos and lead author on the study published in Transboundary and Emerging Diseases. “This gave us a map of where people are most at risk of being exposed to hantavirus and contracting hantavirus pulmonary syndrome (HPS).”

Newly Discovered Host Mechanism in Coronaviruses

Cell culture cells expressing a kinase activity reporter (green) after infection with the human coronavirus HCoV-229E (red). Cell nuclei are stained blue.
Image Credit: © Molekulare und medizinische Virologie

The discovery could serve as a starting point for antiviral strategies.

A research team at Ruhr University Bochum, Germany, has identified a previously unknown cellular mechanism crucial to the replication of coronaviruses: c-Jun N-terminal kinase (JNK) is activated during infection with human coronavirus HCoV-229E and mediates the phosphorylation of the viral nucleocapsid (N) protein, an integral step in the virus cycle. These results aid in better understanding virus-host interactions and may open new approaches to exploring antiviral strategies in the long term. The team led by Dr. Yannick Brüggemann and Professor Eike Steinmann reports its findings in the journal npj Viruses.

New antivirals could help prevent cold sores by changing cell structures

Pin1 inhibitors suppress HSV-1 replication by inhibiting viral protein synthesis and preventing nucleocapsid egress from the nucleus.
Illustration Credit: Takemasa Sakaguchi/Hiroshima University

A class of antivirals called Pin1 inhibitors could reduce or stop outbreaks of herpes simplex virus 1 (HSV-1), the common infection behind oral herpes, according to new research published in Antiviral Research.

HSV-1 causes sores around the mouth, commonly called cold sores or fever blisters. Most people are infected with HSV-1 in childhood, and between 50% and 90% of people worldwide have HSV-1. After the initial infection, HSV-1 remains in the body and can reactivate throughout a person’s life. While HSV-1 infections are usually mild, they can be serious and even deadly for people with suppressed immune systems. Finding new, more effective antivirals for this common illness is essential. 

Researchers focused on an enzyme called peptidyl-prolyl cis-trans isomerase NIMA-interacting 1, or Pin1, that regulates protein stability, function, and cellular structure. When this enzyme is dysregulated, it can play a role in a variety of conditions, including obesity, cancer, heart failure, and more. Viruses, such as cytomegalovirus (CMV) and SARS-CoV-2, are known to affect Pin1, and Pin1 inhibitors have been developed to reduce the impact of these viruses. 

Researchers find key to stopping deadly infection

When rotavirus enters a cell without the FA2H enzyme, it becomes trapped in pockets called endosomes (indicated by red arrows). This prevents the virus from infecting the rest of the cell.
Image Credit: Ding Lab/WashU Medicine

Rotavirus causes severe dehydrating diarrhea in infants and young children, contributing to more than 128,500 deaths per year globally despite widespread vaccination efforts. Although rotavirus is more prevalent in developing countries, declining vaccination uptake in the United States has resulted in increasing cases in recent years.

New research from Washington University School of Medicine in St. Louis has identified a key step that enables rotavirus to infect cells. The researchers found that disabling the process in tissue culture and in mice prevented infection. This discovery opens up new avenues for therapeutic intervention to treat rotavirus and other pathogens that rely on the same infection mechanism.

“Rotavirus kills infants and children, young people who never had a chance at life,” said Siyuan Ding, an associate professor of molecular microbiology at WashU Medicine. “That’s why we want to develop effective therapeutics, even though we already have vaccines that we can use. Not all kids receive the vaccine, and this virus is very infectious. Once a child has the virus, there’s currently no treatment; we can only manage the symptoms.”

Sudan Ebola virus can persist in survivors for months

Image Credit: AI Generated

More than half of survivors of the Sudan Ebola virus still suffer serious health problems two years post-infection and the virus can persist in semen and breast milk for months after recovery, according to the first study examining the virus’s long-term effects.

The study, led by researchers at Washington State University, found 57.5% of the survivors of an outbreak in Uganda from 2022–23 reported ongoing and debilitating health issues that interfered with their daily lives. The detection of traces of the virus in semen and breast milk also raised concerns about the potential for sexual and mother-to-child transmission. The findings were recently published in the journal BMC Medicine.

“This is the first time anyone has been able to closely follow Sudan Ebola survivors over the long term, and the results show the virus continues to affect people’s lives well after an outbreak ends,” said lead researcher Kariuki Njenga, a professor in the WSU College of Veterinary Medicine’s Paul G. Allen School for Global Health and senior scientist at WSU Global Health – Kenya. “Just as concerning is the fact we detected the virus in semen and breast milk, which shows there is a risk survivors could pass on Ebola months after recovery.”

How mosquito-borne viruses breach the brain’s defenses

Stem cell-derived blood-brain barrier cells.
Image Credit: Pablo Alvarez/Li Lab 

Mosquito-borne viruses can cause more than fevers and joint pain. In severe cases, they invade the brain, leading to seizures, encephalitis, lasting memory loss and sometimes death. But thanks to a new UCLA study, researchers have uncovered how some of these viruses breach the brain’s defenses — and point toward ways of keeping them out.

The research, published in Cell Reports, focuses on Sindbis virus, a relatively mild pathogen that scientists use as a safe stand-in for more dangerous mosquito-borne viruses such as chikungunya. 

Using a stem cell-based model of the human blood-brain barrier, developed with collaborators from Florida State University, the UCLA team compared two closely related Sindbis strains — one brain-invading and one not — and found that small changes in viral surface proteins called glycoproteins dictate whether the virus can cross.

The team discovered that the invasive strain grips just one or two specific proteins on blood-brain barrier cells, turning those proteins into doorways that let the virus inside. By contrast, the non-invasive strain spreads its efforts across many receptors and is far less successful.

Koala stress linked to disease threat

Many koalas in the study were successfully treated for Chlamydia before being released back into the wild.
Photo Credit: Currumbin Wildlife Hospital

Researchers have revealed a clear relationship between stress and increased disease risk in koalas in South East Queensland and on the New South Wales North Coast.

A study led by Dr Michaela Blyton at The University of Queensland measured and tracked the level of koala retrovirus (KoRV) in groups of captive and wild koalas.

“We wanted to see what happened to their KoRV loads over time and how it related to chlamydial infection and levels of the stress hormones cortisol and corticosterone in their feces,” Dr Blyton said.

“Virus load likely weakens the immune system, so those with a higher KoRV load are more at risk of diseases such as Chlamydia which can cause blindness, infertility and death.

“Poor quality or disappearing habitat may increase stress and the koalas with higher average cortisol levels had higher average KoRV loads.

Influenza A viruses adapt shape in response to environmental pressures

Colorized transmission electron micrograph of influenza A virus particles, colorized red and gold, isolated from a patient sample and then propagated in cell culture. Influenza A can infect both humans and animals, including birds and pigs. More specifically, this image features the H3N2 influenza strain, isolated from a patient in Victoria, Australia, in 1975. Notable for forming both spheric
Image Credit: National Institute of Allergy and Infectious Diseases

Influenza A virus particles strategically adapt their shape—to become either spheres or larger filaments—to favor their ability to infect cells depending on environmental conditions, according to a new study from National Institutes of Health (NIH) scientists. This previously unrecognized response could help explain how influenza A and other viruses persist in populations, evade immune responses, and acquire adaptive mutations, the researchers explain in a new study published in Nature Microbiology.

The study, led by intramural researchers at NIH’s National Institute of Allergy and Infectious Diseases (NIAID), was designed to determine why many influenza A virus particles exist as filaments. The filament shape requires more energy to form than a sphere, they state, and its abundance has been previously unexplained. To find the answer, they developed a way to observe and measure real-time influenza A virus structure during formation.

UQ team finds relative of deadly Hendra virus in the US

A northern short-tailed shrew
Photo Credit: RPN

Researchers at The University of Queensland have identified the first henipavirus in North America. 

Dr Rhys Parry from the School of Chemistry and Molecular Biosciences said Camp Hill virus was confirmed in shrews in the US state of Alabama.

“Henipaviruses have caused serious disease and death in people and animals in other regions,” Dr Parry said

“One of the most dangerous is the Hendra virus, which was first detected in Brisbane, Australia and has a fatality rate of 70 per cent.

“Another example is Nipah virus which has recorded fatality rates between 40 and 75 per cent in outbreaks in South-East Asia, including in Malaysia and Bangladesh.

“The discovery of a henipavirus in North America is highly significant, as it suggests these viruses may be more globally distributed than previously thought.”

Better prediction of epidemics

The curve calculated using a “reproduction matrix” (turquoise) reflects the actual infection rate (black) much more accurately than previous models (yellow and blue).
Graphic Credit: Empa

The reproduction number R is often used as an indicator to predict how quickly an infectious disease will spread. Empa researchers have developed a mathematical model that is just as easy to use but enables more accurate predictions than R. Their model is based on a reproduction matrix that takes into account the heterogeneity of society.

"Your friends have more friends than you do", wrote the US sociologist Scott Feld in 1991. Feld's so-called friendship paradox states that the friends of any given person have more friends on average than the person themselves. This is based on a simple probability calculation: Well-connected people are more likely to appear in other people's social circles. "If you look at any person's circle of friends, it is very likely that this circle contains very well-connected people with an above-average number of friends," explains Empa researcher Ivan Lunati, head of the Computational Engineering laboratory. A similar principle served Lunati and his team as the basis for a new mathematical model that can be used to more accurately predict the development of case numbers during an epidemic.

Study explains why some osteoporosis drugs may protect against Covid-19

Drugs already in-use for other conditions could help in the fight against Covid-19 and its variants
Photo Credit: Courtesy of University of York

Researchers have provided the molecular explanation for why some osteoporosis drugs offer protection against Covid-19.

Drugs already in-use for other conditions could help in the fight against Covid-19 and its variants

The study, by researchers at the University of York, builds on work conducted by Harvard Medical School that compared more than 450,000 users of a class of drugs, called bisphosphonates, with non-users during the months leading up to the pandemic in 2020. 

The Harvard study showed that those who used drugs, such as alendronate and zoledronate, had lower odds of testing for SARS-CoV-2 infection, Covid-19 diagnosis and Covid-19-related hospitalization, but the study didn’t explain why this was the case.