About

Andrew Broadbent is an Assistant Professor in the Department of Animal and Avian Sciences at the University of Maryland, College Park. His research aims to advance understanding of the molecular basis underpinning the replication and pathogenesis of avian viruses, with a focus on viruses with segmented RNA genomes such as avian influenza virus (AIV), infectious bursal disease virus (IBDV), and avian reovirus (ARV). His work seeks to improve the control of animal viruses by enhancing vaccine efficacy, designing future vaccines, and identifying gene targets for engineering more resistant animals. Additionally, his research models disease pathogenesis and immunosuppression to identify host and viral factors influencing disease outcomes, and to understand how immunosuppression impacts the evolution and transmission of zoonotic infectious diseases. Broadbent's lab also investigates viral replication mechanisms, host-cell antiviral responses, and the potential utility of viruses as vaccine vectors and in oncolytic viral therapy. His approach employs a combination of in vitro cell culture, primary tissues, in vivo studies, and molecular biology, immunological, and bio-imaging techniques to address these questions.

Research topics

• Virology
• Biology
• Pathology
• Medicine
• Political Science
• Immunology
• Physics
• Fishery
• Crystallography
• Optics

Selected publications

• The C-terminus of infectious bursal disease virus VP3 encodes a predicted intrinsically disordered region, which promotes the formation of cytoplasmic puncta and modulates their physical properties

  mBio · 2026-01-12

  articleOpen accessSenior author

  ABSTRACT The virus factories (VFs) of infectious bursal disease virus (IBDV) are biomolecular condensates formed through liquid-liquid phase separation (LLPS). A major component of the IBDV VF is the nonstructural protein VP3, but the molecular basis underlying VF formation remains poorly understood. Here, we demonstrate that VP3 was necessary but not sufficient for phase-separated biomolecular condensates to form. Using live-cell imaging of cells transfected with fluorescent reporter-tagged proteins, our data suggested that the minimal components required to form these structures were VP3, the viral polymerase (VP1), and viral RNA (vRNA). Furthermore, using protein modeling and molecular dynamics simulations, we determined that the 36 amino acid carboxy (C)-terminus of VP3 forms a highly dynamic intrinsically disordered region (IDR). When this was removed, puncta were significantly less numerous ( P < 0.0001), smaller ( P < 0.0001), and more irregular in shape than puncta formed in the presence of wt VP3, demonstrating that the VP3 C-terminal IDR promoted their formation. Moreover, by fluorescence recovery after photobleaching, the VP3ΔC puncta had a significantly reduced mobile fraction (0.29) as compared to full-length VP3 puncta (0.70) ( P < 0.001), demonstrating that the VP3 C-terminal IDR modulated their physical properties. In summary, our data reveal that VP3 forms part of a higher-order complex with VP1, and likely vRNA, to drive LLPS and the formation of IBDV VFs, and that the VP3 C-terminus encodes an IDR that is essential for modulating the physical properties of the resultant structures. IMPORTANCE Liquid-liquid phase separation (LLPS) is a phenomenon of growing interest in cell biology. It is a part of the replication cycles of diverse viruses, but our understanding of the molecular basis that underpins the mechanism of phase separation is incomplete. We previously demonstrated that the virus factories of the birnavirus IBDV, a major agricultural pathogen, are biomolecular condensates formed through LLPS. In this study, we discovered that VP3 was necessary but not sufficient for condensates to form, and the minimal components of these structures were VP3, VP1, and likely vRNA. We also discovered that the C-terminal 36 amino acid region of IBDV VP3 encoded a highly dynamic intrinsically disordered region that promoted the formation of the cytoplasmic puncta and modulated their physical properties. This work contributes to a more detailed understanding of birnavirus replication at the molecular level and to the study of LLPS as a phenomenon.

  PublisherDOI

• Evaluating how infectious bursal disease virus (IBDV) infection influences influenza H3N8 challenge in chickens

  Journal of General Virology · 2026-03-10

  articleOpen accessSenior author

  Infectious bursal disease virus (IBDV) causes an endemic immunosuppressive disease in chickens. Prior exposure to IBDV influences the pathogenesis and shedding of chicken strains of influenza A virus (IAV), but its effect on waterfowl strains is poorly understood. To address this, we inoculated 14-day-old specific pathogen-free chickens with low pathogenicity avian influenza strain A/Mallard/Alberta/156/01 (H3N8) and compared the replication, shedding, pathogenesis, transmission and intra-host evolution between immunocompetent chickens and chickens that had IBDV-mediated immune dysregulation due to a prior infection with strain F52/70 at 2 days of age. The IAV replicated in the upper respiratory tract, and the virus was shed from the oropharyngeal cavity, but there was no shedding from the cloaca and no transmission to sentinel chickens. IAV replication in chickens was associated with amino acid substitutions in the polymerase complex and HA. Prior IBDV infection had no significant effect on IAV pathogenicity, replication or shedding and had a modest effect on IAV diversity, increasing the number of amino acid substitutions from an average of 2.50 substitutions per sample ( sd ±1.83) in the Mock/IAV group to 4.75 ( sd ±1.81) in the IBDV/IAV group ( P <0.01). Taken together, our data suggest that IBDV is unlikely to play a major role in the spillover or spread of waterfowl IAV strains in chicken flocks, although it could expand IAV diversity. This information is useful for informing preventative measures for controlling IAV in poultry flocks.

  PublisherDOI

• Molecular characterization of infectious bursal disease virus (IBDV) strains of genogroup A2B1 circulating in Delaware, Maryland, and Virginia from 2018 to 2023

  Microbiology Spectrum · 2026-04-16

  articleOpen accessSenior author

  ABSTRACT Infectious bursal disease virus (IBDV) causes a major immunosuppressive disease in chickens. In this study, we characterized the IBDV strains circulating in Delaware, Maryland, and Virginia (Delmarva) from 2018 to 2023. The sequence of the hypervariable region (HVR) of the VP2 capsid encoded by segment A, and a region of the VP1 polymerase gene encoded by segment B was obtained from 53 and 34 bursal samples, respectively. Phylogenetic analysis revealed that all the sequences belonged to genogroups A2 and B1, typical of US variant strains. An amino acid signature was identified in the HVR consensus sequence compared with the type-strain Delaware E (Del-E) consisting of amino acid substitutions S215N, S317R, G322E, and E323D. Strains with this signature were previously identified in 2007, in 25% of Delmarva IBDV sequences, and classified as clade two variants. Here, we found this signature had increased in prevalence and was present in 34/53 (64%) of the sequences from 2018 to 2023, including 13/17 (76%) of the sequences from 2023. The signature significantly reduced the virus neutralization titer of serum antibodies raised against Del-E ( P < 0.05), suggesting that the substitutions could drive immune escape. Additionally, we detected amino acid substitutions in and around a key region of VP1 that correlates with virulence (residues 145–147), suggesting that different IBDV isolates could vary in pathogenic potential. Finally, 2/78 (2.5%) of the IBDV-positive bursal samples were also positive for avian reovirus (ARV), demonstrating that coinfection with multiple immunosuppressive viruses occurs in the field. These findings highlight the importance of ongoing IBDV surveillance. IMPORTANCE Infectious bursal disease virus (IBDV) causes a major immunosuppressive disease of poultry. Recently, new strains have emerged and spread in several countries. Ongoing surveillance in the US flocks is therefore critical to determine if any exotic strains of IBDV are circulating. The Delmarva region is a major US poultry-producing area; however, despite its importance, the last reported molecular characterization of IBDV isolated strains was in 2007. Here, we updated the molecular epidemiology of IBDV in the region and uncovered an amino acid signature in the consensus sequence of the capsid hypervariable region comprised of amino acid substitutions S215N, S317R, G322E, and E323D that drives viral escape from neutralizing antibody responses. These findings highlight the importance of ongoing IBDV surveillance and will help to better inform vaccine antigen selection to improve IBD control.

  PublisherDOI

• Prior infection with IBDV prolonged the shedding of a mallard H3N8 influenza A virus (IAV) challenge from the oropharyngeal cavity of some chickens and increased the number of amino acid substitutions in the IAV samples

  bioRxiv (Cold Spring Harbor Laboratory) · 2025-01-01

  preprintOpen accessSenior authorCorresponding

  Abstract Infectious bursal disease virus (IBDV) is endemic worldwide and causes immunosuppression in chickens. We hypothesized that a previous history of IBDV in chickens would render them more susceptible to infection by influenza A viruses (IAVs) from aquatic waterfowl reservoirs. To model this, we inoculated 14 day old specific pathogen free (SPF) chickens with a low pathogenicity avian influenza (LPAI) virus strain from a mallard (A/Mallard/Alberta/156/01 (H3N8)) and compared replication and shedding between immunocompetent chickens and chickens that had immune dysregulation due to a prior IBDV infection with strain F52/70 (genogroup A1B1) at 2 days of age. The mallard IAV strain replicated in the upper respiratory tract of the chickens, and virus was shed from the oropharyngeal cavity, but there was no shedding from the cloaca, and no transmission to sentinel chickens. Replication of the mallard IAV in the chicken host was associated with amino acid substitutions in the polymerase complex and HA. IBDV infection increased the average fold change of IAV replication in the trachea of chickens, prolonged the shedding of infectious IAV from 5 to 6 days in some chickens, increased the number of amino acid substitutions detected in the IAV population from 13 to 30, and significantly increased the number of mutations per IAV sample from 2.50 (SD +/- 1.83) in the Mock/IAV group to 4.75 (SD +/- 1.81) in the IBDV/IAV group (p < 0.01). Taken together, IBDV infection prolonged the shedding of the mallard IAV in some chickens and changed IAV intra-host evolution. Author summary Spillover of IAVs from wild aquatic waterfowl into poultry populations occur frequently, which increases the risk of human infection as people have more contact with poultry than wild birds. Poultry flocks may have other co-morbidities that may influence the spread of IAV. Our data demonstrate that prior IBDV infection increased the average fold change of a mallard H3N8 LPAI virus in the trachea of inoculated chickens, prolonged the shedding of infectious IAV from the oropharyngeal cavity, and significantly increased the average number of amino acid substitutions per IAV sample. We hypothesize that IBDV infection could increase the amount of IAV shed into the environment and broaden the diversity of the IAV population shed. We conclude that controlling the spread of wild aquatic waterfowl strains of IAV in chickens should involve a holistic approach, including the control of co-morbidities and immunosuppressive diseases that could exacerbate their spread.

  PublisherDOI

• A veterinary virapalooza: a summary of the 2024 American Society for Virology (ASV) Veterinary/Zoonotic Virology Satellite Symposium and online H5N1 panel discussion

  Journal of Virology · 2025-05-13

  reviewOpen access1st authorCorresponding

  The year 2024 saw veterinary/zoonotic virology take center stage once more as the American Society for Virology (ASV) hosted a satellite symposium on the subject in June and an online panel discussion in December. The symposium comprised six talks from experts on viruses of economic importance to agriculture and of public health importance. The viruses in question spanned foot and mouth disease virus (FMDV), African swine fever virus (ASFV), Marek's disease virus (MDV), severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), and influenza A viruses (IAVs), and topics covered fundamental virology, applied virology, epidemiology, and surveillance. The goal was to emphasize that improving the control of animal viral diseases requires an integrated, holistic approach involving academia, government, and industry labs undertaking research on basic virology, vaccinology, epidemiology, and surveillance. Moreover, the symposium aimed to highlight career opportunities in the agricultural/veterinary sector for those with virology training. Six months following the symposium, the ASV held an online panel discussion on the ongoing H5N1 IAV situation in poultry, cattle, and people to provide more up-to-date information to its membership. A summary of the talks and discussions is presented here.

  PublisherDOI

• The C terminus of infectious bursal disease virus (IBDV) VP3 encodes a predicted intrinsically disordered region (IDR), which promotes the formation of cytoplasmic puncta and modulates their physical properties

  bioRxiv (Cold Spring Harbor Laboratory) · 2025-01-18

  preprintOpen accessSenior authorCorresponding

  Abstract The virus factories (VFs) of infectious bursal disease virus (IBDV) form through liquid-liquid phase separation (LLPS). A major component of the IBDV VF is the nonstructural protein VP3. Here, we predicted the full-length structure of the VP3 monomer and homodimer and employed molecular dynamics simulations to characterize their behavior. We identified the 36 amino acid carboxy(C)-terminus as a highly dynamic intrinsically disordered region (IDR). We then compared the cytoplasmic puncta that were made in the presence of the wild type (wt) VP3 with those made with a VP3 that lacked the C-terminus (VP3ΔC). Using live-cell imaging with fluorescent reporter tagged proteins, we found that VP3ΔC puncta were significantly less numerous (p<0.0001), smaller (p<0.0001), and more irregular in shape than puncta formed in the presence of wt VP3, demonstrating that the VP3 C terminal IDR promoted their formation. Moreover, by fluorescence recovery after photobleaching (FRAP), the VP3ΔC puncta had a significantly reduced mobile fraction (0.29) as compared to full-length VP3 puncta (0.70) (p<0.001), demonstrating that the VP3 C terminal IDR modulated their physical properties. However, the VP3ΔC puncta still exhibited liquid-like fusion events in the cytoplasm and were sensitive to treatment with aliphatic diols. Moreover, VP3 did not form puncta when expressed alone, and the removal of the C terminus did not abolish puncta formation completely. We propose that VP3 forms part of a higher order complex with other biomolecules to drive LLPS, and that the VP3 C terminal IDR modulates the physical properties of the resultant LLPS structures. Importance LLPS is a phenomenon of growing interest in cell biology. It is a part of the replication cycles of diverse viruses, but our understanding of the molecular basis that underpins the mechanism of phase separation is incomplete. We previously demonstrated that the birnavirus IBDV, a major agricultural pathogen, exploits LLPS in the formation of its VFs. Here, we have characterized the C-terminal 36 amino acid region of IBDV VP3 bioinformatically and by molecular dynamics simulations and found that it encodes a highly dynamic intrinsically disordered region (IDR). Furthermore, we found this region to promote the formation of cytoplasmic puncta and modulate their physical properties. This work contributes to a more detailed understanding of birnavirus replication at the molecular level, and to the study of LLPS as a phenomenon.

  PublisherDOI

• Virology—the path forward

  Journal of Virology · 2024-01-03 · 9 citations

  articleOpen access

  In the United States (US), biosafety and biosecurity oversight of research on viruses is being reappraised. Safety in virology research is paramount and oversight frameworks should be reviewed periodically. Changes should be made with care, however, to avoid impeding science that is essential for rapidly reducing and responding to pandemic threats as well as addressing more common challenges caused by infectious diseases. Decades of research uniquely positioned the US to be able to respond to the COVID-19 crisis with astounding speed, delivering life-saving vaccines within a year of identifying the virus. We should embolden and empower this strength, which is a vital part of protecting the health, economy, and security of US citizens. Herein, we offer our perspectives on priorities for revised rules governing virology research in the US.

  PublisherOA PDFDOI

• Reassortant strains of infectious bursal disease virus (IBDV) belonging to genogroup A3B1 predominate in British broiler chicken flocks

  bioRxiv (Cold Spring Harbor Laboratory) · 2024-04-24

  preprintOpen accessSenior authorCorresponding

  Abstract As part of ongoing epidemiological surveillance for infectious bursal disease virus (IBDV), the hypervariable region (HVR) of the VP2 capsid gene encoded by segment A, and a region of the VP1 polymerase gene, encoded by segment B, were sequenced from 20 IBDV-positive bursal samples obtained in 2020 and 2021, from 16 commercial British broiler farms. Of the 16 farms, none contained very virulent (vv) strains belonging to genogroup A3B2, but 5/16 (31%) contained strains of genogroup A3B1, demonstrating birds were infected with reassortant strains containing a vv segment A and a non-vv segment B. In addition, 3/16 (19%) farms contained vaccine or classical strains belonging to genogroup A1B1, and 8/16 (50%) were co-infected with both genogroup A1B1 and A3B1 strains. Therefore, a total of 13/16 (81%) of the farms contained genogroup A3B1 reassortant viruses, the majority of which 8/13 (62%)) were found to be co-infected with genogroup A1B1 strains. Moreover, of the flocks containing reassortant strains, 5/13 (38%) had HVR mutations Q219L, G254D, D279N, and N280T, consistent with a recently described Western European clade, but 8/13 had other mutations or no mutations, demonstrating that multiple clades were present in the samples. Taken together, vv strains were not detected in the British broiler flocks we sampled, whereas reassortant strains predominated, which belonged to different clades, and were frequently found in samples that were also infected with genogroup A1B1 strains.

  PublisherOA PDFDOI

• Reassortant Strains of Infectious Bursal Disease Virus (Ibdv) Belonging to Genogroup A3b1 Predominate in British Broiler Chicken Flocks

  SSRN Electronic Journal · 2024-01-01

  preprintOpen accessSenior author
  PublisherDOI

• Correction for Rasmussen et al., “Virology—the path forward”

  Journal of Virology · 2024-02-09 · 4 citations

  erratumOpen access

  7: "elevating SARS-CoV-1 to a select agent in 2009" should read "elevating SARS-CoV-1 to a select agent in 2012."The CDC proposed adding SARS-CoV-1 to the Select Agent registry in a federal notice on 13 July 2009 (https://www.federalregister.gov/documents/2009/07/13/E9-16536/posses sion-use-and-transfer-of-select-agents-and-toxins-proposed-addition-of-sars-associ ated).This notice of proposed rulemaking explicitly states that compliance with the proposed amendment would require anyone possessing SARS-CoV-1 to obtain current or amended registration with the HHS Select Agent Program and acknowledged that registration is a time-consuming and potentially costly process.Contemporaneous sources demonstrate that the research impact was anticipated in 2009 (https://absa.org/wpcontent/uploads/2017/01/090911DHHS_SARS_Select_Agent_Comments.pdf and https:// www.cidrap.umn.edu/sars/cdc-proposes-list-sars-virus-select-agent) and had already had a negative impact on SARS-CoV-1 research (S.

  PublisherOA PDFDOI

Frequent coauthors

• Paddy Horner

  Sexual Health Clinic

  38 shared

• Gillian Wills

  Imperial College London

  38 shared

• Myra O. McClure

  Imperial College London

  38 shared

• David C. Parker

  University of Alabama at Birmingham

  37 shared

• Alan Winston

  Imperial College London

  37 shared

• Rosy Reynolds

  University of Bristol

  37 shared

• David Brown

  Environment Agency

  36 shared

• Salik Nazki

  University of Oxford

  29 shared

Labs

• Andrew Broadbent LabPI

Education

• PhD, Microbiology & Immunology

  Imperial College London

  2010

• MSc, Parasitology

  London School of Hygiene and Tropical Medicine

  2006

• VetMB, Veterinary Medicine

  University of Cambridge

  2005

• MA, Pathology

  University of Cambridge

  2002

Awards & honors

• Excellence in Extension Award
• Excellence in Instruction Award
• Excellence in Research Award