Global Virus Network opens international headquarters at University of South Florida
Global Virus Network
Tampa, FL (March 9, 2026) — The Global Virus Network (GVN) marked the opening of its International Headquarters on March 5 at the University of South Florida (USF) Institute for Translational Virology and Innovation (ITVI), a GVN Center of Excellence. The Global Virus Network represents eminent human and animal virologists from more than 90 Centers of Excellence and Affiliates across over 40 countries working to advance research, collaboration and pandemic preparedness.
The ribbon-cutting formalizes a strategic partnership that positions USF Health as the permanent home of GVN’s global scientific network and expands its capacity to coordinate research, surveillance and response to emerging viral threats. GVN selected USF in 2024 to host its International Headquarters.
“We are proud that the Global Virus Network has chosen to establish its International Headquarters at USF, connecting our students, researchers and clinicians with leading virologists and institutions around the world,” said Moez Limayem, PhD, president of the University of South Florida. “USF is deeply committed to supporting GVN’s global mission, and we are excited to host this international hub for virology and pandemic preparedness. This partnership reflects USF Health’s leadership in global health and advances our mission to drive high-impact research and scientific collaboration.”
Founded fifteen years ago following lessons learned from the HIV/AIDS pandemic, the GVN was created to unite the world’s foremost virologists in a permanent, independent scientific network focused on understanding and confronting viral diseases. The network now includes Centers of Excellence and Affiliates across six continents, working collaboratively to improve how the world detects, studies and responds to viral outbreaks.
“The establishment of the Global Virus Network’s International Headquarters at USF Health reflects the strength of the scientific and clinical ecosystem we are building here in Tampa,” said Charles J. Lockwood, MD, MHCM, executive vice president of USF Health and dean of the USF Health Morsani College of Medicine. “By bringing together world-leading virologists with clinicians, this partnership accelerates the path from discovery to real-world impact, improving how we detect, understand and respond to viral diseases that threaten global health.”
The headquarters is housed within the USF Health Institute for Translational Virology and Innovation, founded and directed by Robert C. Gallo, MD, who is also co-founder and international scientific director of GVN and best known for his pioneering discovery of human retroviruses, including HIV as the cause of AIDS.
“This is a very important and meaningful day for the Global Virus Network and for me personally,” Dr. Gallo said. “When we founded GVN fifteen years ago, our goal was simple but ambitious: to unite the world’s leading virologists into a consequential scientific network dedicated to confronting viral threats. We could not have found a better home for GVN than USF Health. The partnership ensures that the network has the stability and environment needed to expand its global mission in pandemic preparedness and translational virology.”
Mathew Evins, chief executive officer and managing executive of the Global Virus Network, said the headquarters represents a focal point for global scientific collaboration.
“The COVID-19 pandemic underscored the need for independent, globally connected scientific infrastructure that exists between outbreaks, not just during crises,” Evins said. “As we cut this ribbon, we are establishing a permanent hub for collaboration, a place where scientists strengthen surveillance, accelerate research and improve the world’s ability to respond to viral threats. Pandemic preparedness requires sustained international cooperation, and this partnership provides the foundation for that work.”
The establishment of GVN’s International Headquarters at USF reinforces a shared commitment to scientific rigor, long-term preparedness and global collaboration in confronting current and future viral threats.
“What we open today is more than a headquarters,” Dr. Gallo said. “It is a foundation for the future, for scientific discovery, global partnership and protecting public health worldwide.”
To view this story on the GVN website, click here.
Click here for images of event and International HQ
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About the Global Virus Network
The Global Virus Network (GVN) is a worldwide coalition comprising 90+ Virology Centers of Excellence and Affiliates across 40+ countries, whose mission is to facilitate pandemic preparedness against viral pathogens and diseases that threaten public health globally. GVN advances knowledge of viruses through (i) data-driven research and solutions, (ii) fostering the next generation of virology leaders, and (iii) enhancing global resources for readiness and response to emerging viral threats. GVN provides the essential expertise required to discover and diagnose viruses that threaten public health, understand how such viruses spread illnesses, and facilitate the development of diagnostics, therapies, and treatments to combat them. GVN coordinates and collaborates with local, national, and international scientific institutions and government agencies to provide real-time virus informatics, surveillance, and response resources and strategies. GVN's pandemic preparedness mission is achieved by focusing on Education & Training, Qualitative & Quantitative Research, and Global Health Strategies & Solutions. The GVN is a non-profit 501(c)(3) organization. For more information, please visit www.gvn.org.
About USF Health
USF Health is dedicated to making life better through research, education and patient care. It is the partnership of the USF Health Morsani College of Medicine, the College of Nursing, the College of Public Health, the Taneja College of Pharmacy, the School of Physical Therapy and Rehabilitation Sciences, the Biomedical Sciences Graduate and Postdoctoral Programs and USF Health’s multispecialty physicians’ group, the largest on Florida’s west coast. In 2025, U.S. News & World Report ranked the USF Health Morsani College of Medicine as the No. 1 medical school in Florida and in the highest tier nationwide for research. U.S. News also ranked the USF College of Public Health and the USF College of Nursing’s Master of Science program No. 1 in the state. Together with Tampa General Hospital, USF Health forms one of the nation’s premier academic health systems, with more than 1,000 physicians and providers caring for more than one million patients each year. USF Health is part of the University of South Florida, a top-ranked research university and member of the Association of American Universities (AAU). USF serves approximately 50,000 students and generates nearly $10 billion in annual economic impact for Florida. For more information, visit health.usf.edu.
Recent pandemic viruses jumped to humans without prior adaptation, UC San Diego study finds
Large-scale evolutionary analysis shows most zoonotic viruses emerge without prior adaptation, while passing through a laboratory leaves detectable genetic signatures, offering a new tool to interpret outbreak origins
University of California - San Diego
A new University of California San Diego study published in Cell challenges a long-standing assumption about how animal viruses become capable of sparking human epidemics and pandemics. Using a phylogenetic, genome-wide analysis across multiple viral families, researchers report that most zoonotic viruses — infectious pathogens that spread from animals to humans, including the cause of COVID-19 — do not show evidence of special evolutionary adaptation before spilling over into humans.
“This work has direct relevance to the ongoing controversy around COVID-19 origins,” said Joel Wertheim, PhD, senior author and professor of medicine in the Division of Infectious Diseases and Global Public Health at UC San Diego School of Medicine. “From an evolutionary perspective, we find no evidence that SARS-CoV-2 was shaped by selection in a laboratory or prolonged evolution in an intermediate host prior to its emergence. That absence of evidence is exactly what we would expect from a natural zoonotic event — and it represents another nail in the coffin for theories invoking laboratory manipulation.”
The prevailing model of zoonotic emergence has often assumed that viruses must first acquire adaptive mutations before they can sustain human-to-human spread. To test that assumption, the research team analyzed viral genomes from outbreaks caused by influenza A virus, Ebola virus, Marburg virus, mpox virus, SARS-CoV and SARS-CoV-2. They focused on the evolutionary period immediately preceding human outbreaks, where any substantial pre-spillover adaptation should leave a detectable imprint.
Across these diverse viruses, the investigators found a strikingly consistent pattern: selection pressures before zoonotic emergence were indistinguishable from those acting during routine circulation in animal reservoirs. In other words, there was no evolutionary signal suggesting that these viruses were being “pre-adapted” for humans prior to their outbreaks. Instead, measurable changes in selection typically appeared only after sustained transmission began in people.
“From a broad epidemiological standpoint, our findings challenge the idea that pandemic viruses are evolutionarily special before they reach humans,” Wertheim said. “Rather than requiring rare, finely tuned adaptations in animals, many viruses may already possess the basic capacity to infect and transmit between humans. What matters most is human exposure to a diverse array of animal viruses.”
The study relies on a sophisticated phylogenetic framework that measures changes in the intensity of natural selection across entire viral genomes. By comparing rates of different types of mutations, the researchers were able to detect whether natural selection was intensified, relaxed or unchanged across key evolutionary transitions. Importantly, the team validated their approach using known examples of and artificially selected viruses propagated in cell culture or in laboratory animals, which produced clear and reproducible evolutionary signatures distinct from natural transmission.
Those controls proved critical when examining one historical outlier: the reemergence of H1N1 influenza A virus in 1977. Unlike other zoonotic events analyzed, the 1977 H1N1 strain showed both unusually limited genetic divergence from 1950s viruses and a clear shift in selection consistent with viruses that propagated in cell culture or in laboratory animals.
“The 1977 influenza story is, in many ways, even more compelling than what we found for COVID-19,” Wertheim said. “Our results provide new molecular evidence supporting the long-suspected idea that the H1N1 pandemic was sparked by a laboratory strain — possibly in the context of a failed vaccine trial.”
Historical records and prior genetic analyses have suggested that the 1977 H1N1 virus appeared almost unchanged after a 20-year absence, a pattern difficult to reconcile with natural evolution. The new findings add another layer, showing that the virus also experienced selection similar to that seen in laboratory-adapted influenza strains and live-attenuated vaccines.
Beyond settling historical debates, the authors argue that their work has important implications for how scientists interpret future outbreaks. By establishing what “normal” zoonotic emergence looks like at the genomic level, the framework provides a benchmark for distinguishing natural spillovers from scenarios involving laboratory handling or prolonged artificial selection.
“This doesn’t mean lab accidents don’t happen,” Wertheim emphasized. “But it does mean that if a virus had been extensively passaged in a lab before an outbreak, we would expect to see it in the evolutionary record. In nearly all pandemics we’ve studied, that signal simply isn’t there.”
Looking ahead, the researchers see potential applications in outbreak forensics, viral surveillance and pandemic preparedness.
“Our goal is not just to understand the past, but to be better prepared for the future,” Wertheim said. “By clarifying how pandemics actually begin, we can focus attention where it belongs — on surveillance, prevention and reducing the opportunities for the constant barrage of viral spillover.”
Link to full study: https://authors.elsevier.com/sd/article/S0092-8674(26)00171-6
Additional co-authors on the study include: Jennifer L. Havens and Jonathan E. Pekar from UC San Diego; Sergei L. Kosakovsky Pond and Jordan D. Zehr from Temple University; Edyth Parker and Kristian G. Andersen from Scripps Research Institute; and, Michael Worobey from the University of Arizona.
The study was funded, in part, with federal funds from the National Institute of Allergy and Infectious Diseases National Institutes of Health, National Institutes of Health (NIH-NIAID) and National Science Foundation (NSF). Jennifer L. Havens acknowledges support from NIH (grant R01AI153044). Sergei L. Kosakovsky Pond and Jordan D. Zehr acknowledge support from NIH (AI183870, GM151683, GM144468) and the NSF (grant DBI/2419522). Jonathan E. Pekar acknowledges support from NIH-NIAID (T15LM011271) and the UC San Diego Merkin Fellowship. Michael Worobey acknowledges support from NIH-NIAID (contract no. 75N93021C00015). Edyth Parker and Kristian G. Andersen acknowledge support from the NIH (grant U01AI151812). Kristian G. Andersen also acknowledges support from the NIH (grant U19AI135995). Joel O. Wertheim acknowledges support from NIH-NIAID (R01AI135992).
Jonathan E. Pekar, Michael Worobey, Kristian G. Anderson, and Joel O. Wertheim have received consulting fees and/or provided compensated expert testimony on SARS-CoV-2 and the COVID-19 pandemic.
Journal
Cell
Scientists trace crop viruses back to the last Ice Age
American Phytopathological Society
Long before humans cultivated crops or sailed between continents, a group of plant viruses was already evolving among wild plants in Eurasia. According to a new international study published in Plant Disease, the ancestors of modern tymoviruses likely emerged before the last Ice Age, reshaping scientists’ understanding of the vast evolutionary history of plant disease.
Tymoviruses infect dicot plants and are typically spread by leaf-eating beetles, although they can also be transmitted through seeds or direct plant contact. In parts of Eurasia and the Americas, these viruses infect both wild and crop plants, causing serious diseases in economically important crop plants, including several cultivated oilseed and vegetable brassica species and solanaceous crops such as potato, tomato, tobacco, and eggplant. They also infect legumes in Africa, Southeast Asia, and Australia. Because these viruses affect both cultivated plants and wild species, their spread has implications for both agriculture and natural ecosystems.
Led by Adrian J. Gibbs, Emeritus Faculty at the Australian National University, an international team of researchers conducted phylogenetic analysis and genomic sequencing of 109 tymoviruses and reconstructed their evolutionary relationships to estimate when and where this group of viruses first emerged. The newly sequenced tymovirus isolates mostly came from historical virus culture collections. The results suggest that the most recent common ancestor of all known tymoviruses existed before the last Ice Age, with some viral lineages likely reaching the Americas approximately 15,000 years ago. In contrast, the few tymoviruses that are now found on more than one continent appear to have spread globally much more recently—primarily during the past two centuries, coinciding with the expansion of international trade and agricultural exchange.
The analysis also revealed important clues about how these viruses adapt over time. Genes responsible for viral replication and protective structure showed strong evidence of stabilizing evolutionary pressure, while the genes responsible for movement between plant cells appear to evolve more rapidly. This flexibility may help the viruses adapt to new plant hosts, including economically significant crops.
Beyond the scientific findings, the study represents an important collaboration across both geography and generations. The research team includes scientists from South America, Europe, the Middle East, and Australasia, combining expertise in modern genomic sequencing and virus population genetics with decades of historical research on plant viruses. The study’s lead author, Adrian J. Gibbs, published one of the earliest studies describing an Andean tymovirus in 1966, while other contributors have worked on Andean potato viruses since the 1970s.
Understanding how these viruses originated and spread helps researchers anticipate future risks in a world in which plants, seeds, and agricultural products move between continents faster than ever before. The study shows that while the evolutionary roots of some crop viruses stretch back to a world shaped by glaciers and prehistoric ecosystems, human activity in recent centuries has played a major role in shaping their modern distribution. This broader perspective provides valuable information for scientists studying virus evolution and for plant health and biosecurity authorities responsible for protecting crops and ecosystems from emerging diseases.
Read “A Phylogeny of the Tymoviruses, Sensu Stricto, and Its Global Interpretation in Space and Time” to learn more—published in Plant Disease.
Plant Disease, published by The American Phytopathological Society, is the leading international journal for rapid reporting of research on new, emerging, and established plant diseases. The journal publishes papers that describe translational and applied research focusing on practical aspects of disease diagnosis, development, and management in agricultural and horticultural crops.
Journal
Plant Disease
Article Title
A Phylogeny of the Tymoviruses, Sensu Stricto, and Its Global Interpretation in Space and Time
How viruses mess with our brains
A team from the UNIGE and the HUG reviewed 900 scientific articles to better understand the impact of viruses on memory, attention, and concentration.
What impact does a viral infection have on our memory, attention, and concentration? The COVID-19 pandemic has reignited interest in this question, which has now been extended to other infections such as HIV, herpes, and hepatitis. A team from the University of Geneva (UNIGE) and Geneva University Hospital (HUG) reviewed over 900 scientific articles exploring the links between the immune system and cognitive functions. This analysis, published in Neuroscience & Biobehavioral Reviews, has identified several biological markers associated with cognitive decline in the context of infection. It also provides a solid foundation for future research.
Despite decades of research, the effects of viral infections on cognitive functions—such as memory, concentration, and attention—remain poorly understood. Most studies rely on comprehensive screening tools, applied individually to each disease. However, the emergence of the SARS-CoV-2 virus, along with the frequency and persistence of post-infectious cognitive sequelae, has reignited interest in this area of research.
In a new study, a team from UNIGE and HUG compiled and analysed the results of 931 scientific articles examining the links between the immune system and cognitive functions across various viral infections, including SARS-CoV-2, HIV, herpes, and hepatitis. ''Our goal was to take a cross-disciplinary approach to move beyond the fragmented perspective that prevails in this field,'' explains Julie Péron, associate professor at the Laboratory of Clinical and Experimental Neuropsychology, Faculty of Psychology and Educational Sciences, and at the Interfaculty Center for Affective Sciences, UNIGE, as well as a consulting neuropsychologist in the Neurology Service, Department of Clinical Neurosciences, HUG."
Several Biological ''Signatures'' Identified
This analysis confirms that persistent inflammation—initially a natural response by the body to an attack—could be linked to memory and concentration problems. More importantly, it highlights certain biological markers of the immune system associated with variations in cognitive performance. ''High levels of white blood cells called 'activated monocytes' and pro-inflammatory cytokines—proteins that enable the immune system to communicate—are correlated with a decline in episodic memory and information processing speed, '' says Anthony Nuber-Champier, a PhD student at the Laboratory of Clinical and Experimental Neuropsychology, Faculty of Psychology and Educational Sciences, and at the Interfaculty Center for Affective Sciences, UNIGE, as well as the lead author of the study."
Conversely, certain markers, such as activated CD4+ T cells—also white blood cells—or anti-inflammatory cytokines, seem to be associated with better preservation of cognitive abilities. ''However, immune responses vary from person to person. What appears to be decisive is the balance between these different inflammatory signals in maintaining long-term cognitive stability,'' the researcher points out.
A Solid Foundation for Future Research
These findings contribute to a better understanding of the cognitive disorders observed after certain infections and lay the groundwork for further investigation. They also confirm the conclusions of several clinical studies conducted in the context of long COVID, including the COVID Cog and Trajectory projects, in which UNIGE and HUG are actively involved. Funded by the Swiss National Science Foundation (SNSF), these projects aim to identify neuropsychological and neuropsychiatric deficits in post-COVID-19 patients.
Journal
Neuroscience & Biobehavioral Reviews
Method of Research
News article
Subject of Research
Not applicable
Article Title
Immune-cognitive relationships across viral infections: A transnosological systematic review
