Gut bacteria linked to levels of latent HIV

Photo Credit: Towfiqu Barbhuiya

Scientific Frontline: Extended "At a Glance" Summary: Gut Microbiota and Latent HIV Reservoirs

The Core Concept: The composition and metabolic activity of a patient's gut bacteria are strongly associated with the size of the latent HIV reservoir—the amount of dormant virus that remains in the blood despite effective antiretroviral therapy.

Key Distinction/Mechanism: While standard antiretroviral drugs effectively target active HIV, they cannot eliminate the dormant viral reservoir. This new research identifies that specific bacterial species (such as Faecalibacterium prausnitzii and Lachnospira sp000437735) correlate with smaller HIV reservoirs, whereas inflammation-associated species like Prevotella copri and heightened metabolic processes related to sugar breakdown and amino acid formation are linked to larger viral reservoirs.

Major Frameworks/Components: 

• Viral Reservoir Quantification: Utilizing blood sample analysis to measure the levels of intact HIV DNA remaining in the body.
• Microbiome Profiling: Employing whole-metagenomic sequencing to map the exact composition and functional capabilities of the gut bacteria.
• Metabolic Pathway Analysis: Identifying specific functional interactions, such as sugar breakdown and amino acid synthesis, that differentiate larger and smaller reservoirs.

Getting a glimpse of viral dances in the dark in the Sargasso Sea

Water samples were collected from the surface and in an area called the deep chlorophyll maximum near Bermuda in the Atlantic Ocean.
Photo Credit: Steven Wilhelm

Scientific Frontline: "At a Glance" Summary: Viral Activity in the Sargasso Sea

• Main Discovery: Researchers discovered that marine viruses exhibiting cyclical behavior are predominantly active at night, specifically targeting heterotrophic microbes that consume organic matter rather than the expected photosynthetic bacteria.
• Methodology: Scientists collected marine water samples from both the ocean surface and the deep chlorophyll maximum over a continuous 112-hour period, extracting surface water every four hours and deep water every twelve hours to track temporal microbial changes.
• Key Data: Among the more than 48,000 viral species identified in the samples, nearly 3,100 displayed diel (24-hour cyclical) behavior, with approximately 90% of these rhythmic viruses reaching their peak abundance during the night.
• Significance: The findings expose a previously unknown layer of complexity within marine microbial networks, shifting the understanding of how nocturnal viral infections influence carbon cycling and the broader ecological services provided by the world's oceans.
• Future Application: This high-resolution temporal data will be integrated into advanced ocean modeling systems to more accurately predict how marine ecosystems and carbon frameworks will respond to climate change variables, such as warming temperatures and increased water acidification.
• Branch of Science: Marine Microbiology, Virology, Oceanography
• Additional Detail: Concurrent advancements from the research team include the development of vConTACT3, a knowledge-guided machine learning tool that rapidly classifies fragmented viral genomes across a broad biological spectrum, significantly accelerating future virology research.

Viruses ‘eavesdrop’ on each other – but it can backfire

A colony of Bacillus subtilis grown on solid medium. These structured communities reflect how bacteria can organise & grow collectively.
Image Credit Elvina Smith

Scientific Frontline: Extended "At a Glance" Summary: Viral Eavesdropping and Arbitrium Systems

The Core Concept: Phages (viruses that infect bacteria) utilize chemical signals to communicate and can "eavesdrop" on the signals of other viral species, a process that can manipulate the eavesdropping virus into adopting a disadvantageous infection strategy.

Key Distinction/Mechanism: When infecting a host cell, phages must decide whether to replicate and kill the host (lysis) or remain dormant (lysogeny). They use chemical signals called peptides (part of the "arbitrium" system) to assess host availability; high peptide levels indicate scarce hosts (favoring dormancy), while low levels indicate abundant hosts (favoring lysis). However, cross-species eavesdropping can cause a listening virus to mistakenly choose dormancy, ultimately benefiting the signaling virus by eliminating competition.

Major Frameworks/Components:

• Arbitrium Communication Systems: The specific peptide-based chemical signaling networks used by phages to coordinate infection strategies.
• Lysis-Lysogeny Decision: The fundamental biological choice a virus makes upon infecting a cell, determining whether it will actively replicate and destroy the cell or integrate and lie dormant.
• Inter-Species Cross-Talk: The phenomenon where signals intended for intra-species coordination are intercepted by unrelated viral species.
• Viral Manipulation: The evolutionary dynamic where communication serves not just as cooperation, but as a mechanism for one species to suppress the competitive reproduction of another.

Study: Bumblebees are hosts for dangerous bee virus

Red-tailed bumblebees can act as hosts for a dangerous bee virus.
Photo Credit: Uni Halle / Patrycja Pluta

Scientific Frontline: Extended "At a Glance" Summary: Viral Transmission Dynamics in Multispecies Bee Communities

The Core Concept: Wild red-tailed bumblebees (Bombus lapidarius) act as the primary reservoir hosts for the acute bee paralysis virus (ABPV), carrying the pathogen with minimal harm while posing a fatal transmission risk to vulnerable honeybee populations.

Key Distinction/Mechanism: Historically, scientific consensus held that managed honeybees were the primary source of viral infections, spilling pathogens over into wild bee populations. This research fundamentally shifts that paradigm by demonstrating that wild bumblebees can serve as the key epidemiological reservoir for certain viruses, transmitting the pathogen back to honeybees via contaminated pollen and nectar at shared floral feeding sites.

Major Frameworks/Components: 

• Epidemiological Modeling: Utilization of the basic reproduction number (\(R_0\)) to quantify and estimate the specific viral spread potential from one insect to others of the same species.
• Multispecies Network Analysis: Observational tracking of shared floral visitation patterns among diverse bee species to map potential interspecies transmission nodes.
• Comprehensive Pathogen Screening: Molecular virus screening of 1,725 insects to determine host-specific viral prevalence and vector capabilities.
• Differentiated Host Profiling: Identification of distinct primary hosts for specific pathogens (e.g., honeybees as main carriers for deformed wing virus and black queen cell virus; red-tailed bumblebees for acute bee paralysis virus).

New compounds to inactivate a key protein in the influenza virus

These new molecules can inhibit neuraminidase, one of the proteins that coats the influenza virus and a key target in many first-line treatments for both seasonal and pandemic influenza.Image Credit:University of Barcelona (NC-ND)

Scientific Frontline: Extended "At a Glance" Summary: Sugar-Derived Aziridines for Influenza Inhibition

The Core Concept: Researchers have designed a novel family of antiviral molecules—sugar-derived aziridines based on the structure of oseltamivir (Tamiflu)—that effectively bind to and inhibit neuraminidase, a key surface protein required for the spread of the influenza virus.

Key Distinction/Mechanism: Unlike current first-line flu treatments which act as reversible inhibitors, these new compounds initially mimic the enzyme’s transition state and subsequently form a covalent chemical bond with a key amino acid in the active site. This creates an irreversible block, permanently deactivating the enzyme and halting viral replication.

Major Frameworks/Components:

• Neuraminidase (NA) Targeting: Focusing on the specific viral surface enzyme responsible for enabling newly formed virus particles to detach from and exit infected host cells.
• Aziridine Ring Substitution: The structural modification of replacing the alkene group in standard oseltamivir with a highly configured aziridine ring to act as the primary reactive agent.
• Covalent Inhibition: The chemical mechanism ensuring permanent deactivation of the viral enzyme, overcoming the limitations and reversibility of traditional antiviral drugs.
• Computational Structural Biology: The utilization of atomic-level 3D modeling and computational methods to observe transition states and design the precise molecular structure of the inhibitors.

Local immune coordination in the lung reveals a new layer of defense

Clusters of immune cells in the influenza-infected lung of a mouse. B cells are shown in cyan, T cells in magenta, and green areas indicate regions with low oxygen levels. Oxygen is particularly scarce at the edges of the cell clusters.
Image Credit: University of Basel, Jean De Lima

Scientific Frontline: "At a Glance" Summary: Local Immune Coordination in the Lung

• Main Discovery: Researchers identified a previously unappreciated subtype of helper T cells that migrate to the lungs during infection and produce the protein HIF-1α to orchestrate a localized, coordinated immune defense.
• Methodology: The team utilized advanced imaging techniques to map immune cell positioning in the lungs of influenza-infected mice and employed a specific mouse model to selectively deactivate the HIF-1α molecule at precise moments post-infection.
• Key Data: Deactivating HIF-1α in targeted T cells reduced the release of the signaling molecule IL-21, triggering a collapse of the local immune network and a subsequent decline in lung macrophages, natural killer cells, and antibody-producing B cells.
• Significance: The findings demonstrate that temporary lung immune hubs act as advanced command centers for broad immune protection, establishing a critical layer of localized respiratory defense that operates independently of the initial systemic immune response.
• Future Application: This discovery offers a biological foundation for designing inhalable vaccines to build immune defenses directly at viral entry sites and presents new strategies for tissue-targeted immunotherapies.
• Branch of Science: Immunology, Pulmonology, Virology, Oncology.
• Additional Detail: The coordinated response of HIF-1α driven T cells was also observed in a mouse model of lung cancer, indicating that their localized protective role extends beyond fighting viral infections to actively combating tumor cells.

Promising active substance against hepatitis E identified

Researchers have discovered a compound that prevents hepatitis E viruses from replicating. 
Photo Credit: © RUB, Marquard

Scientific Frontline: Extended "At a Glance" Summary: Bemnifosbuvir as a Treatment for Hepatitis E

The Core Concept: Bemnifosbuvir is a synthetic nucleotide/nucleoside analogue, currently in clinical trials for hepatitis C, that has been identified as a highly effective inhibitor of the hepatitis E virus (HEV).

Key Distinction/Mechanism: The drug functions by providing "false building blocks" that mimic the natural structural components of viral genetic material. When the hepatitis E virus attempts to copy its genome, it incorporates these synthetic molecules, which successfully halts viral replication while leaving healthy host cells unharmed.

Major Frameworks/Components:

• Nucleotide/Nucleoside Analogues: The foundational pharmacological framework utilizing synthetic molecules structured similarly to DNA/RNA components to disrupt viral synthesis.
• Fluorescent Reporter Virus Screening: An in vitro screening methodology utilizing a modified virus carrying a fluorescent molecule, allowing researchers to visually monitor and quantify viral replication and its active inhibition.
• Preclinical Validation: The methodological progression from cellular assays to animal models to confirm both the compound's safety profile and its direct efficacy against HEV-induced liver inflammation.

What Is: Zoonotic Spillover

Scientific Frontline: Extended "At a Glance" Summary: Zoonotic Spillover

The Core Concept: Zoonotic spillover is the successful transmission of a pathogenic entity—such as a virus, bacterium, or parasite—from a non-human animal reservoir into a human population. This rare but consequential event occurs when a pathogen successfully crosses the strict biological boundary between species.

Key Distinction/Mechanism: Unlike regular endemic transmission, a zoonotic spillover is dictated by the "Spillover Barrier Model." A pathogen must overcome a hierarchical series of formidable biological and ecological obstacles. Spillover only succeeds when specific vulnerabilities across these barriers perfectly align in both space and time, allowing the pathogen to bind to human cellular receptors and evade immediate immune destruction.

Major Frameworks/Components:

• The Three Layers of Biological Barriers: The zoonotic reservoir layer (host density and distribution), the environmental and vector layer (pathogen persistence in abiotic conditions), and the recipient spillover host layer (human exposure, susceptibility, and cellular infection dynamics).
• Viral Shedding Dynamics: Pathogens are often excreted in discrete temporal and spatial "pulses" triggered by demographic shifts or environmental stress.
• Epidemiological Transmission Models:
• SIR (Susceptible-Infectious-Recovered): Seasonal epidemic cycles driven by natural host population fluctuations.
• SIRS (Susceptible-Infectious-Recovered-Susceptible): Cyclical circulation driven by waning immunity within a reservoir.
• SILI (Susceptible-Infectious-Latent-Infectious): Persistent infections triggered by stress-induced viral reactivation.

Exposing A Hidden Anchor For HIV Replication

In a major advance, UD professor Juan Perilla (right) and doctoral student Juan S. Rey and their collaborators have revealed a known player’s hidden role in helping HIV mature into an infectious force.
Photo Credits: Evan Krape, Jeffrey C. Chase

Scientific Frontline: "At a Glance" Summary

• Main Discovery: The viral protein integrase performs a critical, previously unknown structural function by forming gluey filaments that line the HIV capsid interior to anchor the RNA genome, a process required for the virus to mature into an infectious state.
• Methodology: The team combined high-resolution cryo-electron microscopy (cryo-EM) imaging of frozen samples with high-performance computing and atom-by-atom molecular modeling to visualize the 3D structure of the protein filaments and their interaction with capsid hexamers.
• Key Data: The viral capsid measures approximately 120 nanometers in width (roughly 1/800th of a human hair), and during the acute infection phase, a single host cell can produce as many as 10,000 new HIV particles.
• Significance: This study provides the first direct evidence of integrase's structural role in viral organization, demonstrating that without the specific filament-capsid interaction, HIV particles fail to properly pack their genetic material and cannot infect host cells.
• Future Application: These findings reveal a novel vulnerability in the HIV life cycle, offering a specific target for the development of next-generation antiretroviral drugs and inhibitors distinct from existing FDA-approved treatments.
• Branch of Science: Virology, Structural Biology, and Biochemistry.
• Additional Detail: Experiments using specialized inhibitors known as ALLINIs successfully disrupted the oligomerization of integrase assemblies, confirming that breaking the integrase-capsid bond directly correlates with a loss of viral infectivity.

Building Immunity Against Avian Flu Risks

Plate test used to quantify infectious viral particles or neutralizing antibodies. Each hole corresponds to one viral particle.
Photo Credit: CDC

Scientific Frontline: "At a Glance" Summary

• Main Discovery: Researchers identified that specific cross-reactive antibodies acquired from seasonal influenza exposure or vaccination target the conserved "stem" region of the avian influenza A (H5N1) virus, providing a baseline level of protection against the disease.
• Methodology: The team analyzed immune responses across different population cohorts by comparing antibody levels in individuals vaccinated with an adjuvanted H1N1 vaccine during the 2009 pandemic against those receiving standard seasonal shots, while also examining the influence of birth year on immune imprinting.
• Key Data: Individuals who received the AS03-adjuvanted H1N1 vaccine exhibited a nearly fourfold increase in cross-reactive antibodies compared to a 30% increase from standard seasonal vaccines, and those born before 1965 showed naturally higher antibody levels due to childhood exposure to H1 or H2 subtypes.
• Significance: The study reveals that these antibodies do not prevent the virus from entering cells but instead inhibit its ability to detach and spread to neighboring cells, essentially trapping the virus and potentially reducing disease severity.
• Future Application: Findings support the strategic deployment of adjuvanted influenza vaccines to broaden population immunity, which could lower the antigen dose required for specific H5N1 vaccines and increase global vaccination capacity during a pandemic.
• Branch of Science: Immunology and Virology
• Additional Detail: The research underscores the concept of "immune imprinting," where the specific influenza subtype a person is exposed to in early childhood permanently shapes their immune system's ability to recognize and combat related viral strains later in life.

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).”