About

Adam Bailey, M.D., Ph.D., is an Assistant Professor in the Department of Pathology & Laboratory Medicine at the University of Wisconsin-Madison. He earned his B.A. in Molecular Biology from Colgate University in 2009, where he conducted research on Reoviruses under Dr. Geoff Holm and participated in an NIH-exchange program studying Influenza A Virus pathogenesis at the National Institutes of Health. Adam joined the Medical Scientist Training Program at the University of Wisconsin-Madison School of Medicine and Public Health in 2010, completing his Ph.D. in Molecular Pathology in 2015 with research on primate Pegiviruses and Arterivirus in Dr. David O’Connor's laboratory. He earned his M.D. from the University of Wisconsin-Madison in 2017 and completed his residency in Clinical Pathology at Washington University in St. Louis in 2020. During his time at Washington University, he contributed to advances in viral diagnostics and total-laboratory automation in the clinical microbiology laboratory and conducted post-doctoral research in Dr. Michael Diamond's lab, focusing on SARS-CoV-2 diagnostics, animal models of viral pathogenesis, and in vitro systems of infection. Adam also developed independent research lines on viral hemorrhagic fever, earning the NIH Director’s Early Independence Award in 2020. Since joining the Department of Pathology & Laboratory Medicine at UW-Madison as an Associate Professor in 2021, he helps direct clinical laboratories at the University of Wisconsin Hospital and leads a research laboratory focused on viral pathogenesis, zoonosis, and medical countermeasures.

Research topics

• Medicine
• Biology
• Internal medicine
• Virology
• Immunology
• Microbiology
• Intensive care medicine
• Pathology
• Biochemistry
• Anesthesia
• Emergency medicine
• Cardiology
• Molecular biology
• Genetics
• Anatomy

Selected publications

• Elucidating the enigmatic biology of arteriviruses through receptor discovery

  Journal of Virology · 2026-03-30

  articleOpen access1st authorCorresponding

  Family) that infect a variety of mammals. Arterivirus infections can manifest in a variety of ways, ranging from viral hemorrhagic fever to persistent sub-clinical infection. A perplexing feature of arterivirus biology is the unusual network of small glycoproteins that decorate the virion surface. How these glycoproteins mediate viral entry into target cells remains poorly understood, but it is widely accepted that the arterivirus entry process is novel. This review highlights recent advances in the characterization of arterivirus entry receptors and examines unique features of arterivirus biology-including disease, persistence, tropism, evolution, and cross-species transmission-through the lens of receptor utilization.

  PublisherDOI

• Time for a New Yellow Fever Vaccine

  The Journal of Infectious Diseases · 2026-03-07

  article1st authorCorresponding
  PublisherDOI

• Dataset for 'Multiple LDLR family members act as entry receptors for Yellow Fever virus'

  Mendeley Data · 2026-03-16

  datasetOpen access

  Using CRISPR-Cas9 screen, we identified LRP4 as an entry receptor for Yellow Fever virus. By screening the whole LDLR family members, we further identified LRP1, and VLDLR also act as receptors for Yellow Fever virus. Data were generated by NGS, flow cytometry, qRT-PCR, H&E staining, Bio-Layer Interferometry. There are 5 main Figures and 10 Extended Data Figures. Data were obtained from multiple cell lines including 293T, Vero, HepG2, HAP1, K562 and Raji cells. C57BL/6J mice, AG129 mice and hFGR mice were also used in this project.

  PublisherDOI

• Integrated phenotypic screening and chemical proteomics identifies ETF1 ligands that modulate viral translation and replication

  Proceedings of the National Academy of Sciences · 2026-01-28

  articleOpen access

  Emerging and reemerging viruses pose a significant threat to global health. Although direct-acting antivirals have shown success, their efficacy is limited by the rapid emergence of drug-resistant viral variants. Hence, there is an urgent need for additional broad spectrum antiviral therapeutic strategies. Here, we identify by phenotypic screening a set of stereochemically defined photoreactive small molecules (photo-stereoprobes) that stereoselectively suppress SARS-CoV-2 replication in human lung epithelial cells. Structure-activity relationship-guided chemical proteomics identified the eukaryotic translation termination factor 1 (ETF1) as a target of the photo-stereoprobes, and this interaction was recapitulated with recombinant purified ETF1. We found that the photo-stereoprobes modulate programmed ribosomal frameshifting mechanisms essential for SARS-CoV-2 infection without causing ETF1 degradation, thus distinguishing the photo-stereoprobes from other known ETF1-directed small molecules. We finally show that the photo-stereoprobes also inhibit the replication of additional viruses with noncanonical ribosomal frameshifting mechanisms. Our findings identify a mechanistically distinct class of ETF1 ligands that implicate host translation termination processes as a potential drug target for antiviral development.

  PublisherOA PDFDOI

• 1331 A Comparative Histopathology Model for Studying Viral Hemorrhagic Fevers

  Laboratory Investigation · 2026-03-01

  articleSenior author
  PublisherDOI

• Multiple LDLR family members act as entry receptors for yellow fever virus

  Nature · 2025-10-29 · 12 citations

  article
  PublisherDOI

• Systematic analysis of SARS-CoV-2 infection of an ACE2-negative human airway cell

  UNC Libraries · 2025-05-17

  articleOpen access
  PublisherDOI

• Mesenteric ischemia and bacterial translocation precipitate the intoxication phase of yellow fever

  bioRxiv (Cold Spring Harbor Laboratory) · 2025-03-05 · 1 citations

  preprintOpen accessSenior authorCorresponding

  ABSTRACT Yellow fever (YF) is classically conceptualized as a hepatotropic disease; indeed, the liver is the primary site of yellow fever virus (YFV) replication. However, circumstantial evidence suggests that extra-hepatic disease may be important for the ∼30% of YF cases that progress to the severe “intoxication” phase of the disease. Using a Syrian hamster-adapted (HA)-YFV, we worked backwards from observations in humans to examine early events that precipitate the intoxication phase of YF. HA-YFV caused severe disease in ∼80% of infected animals characterized by lethargy and weight loss that progressed to widespread petechiae and death by day 6. Clinical chemistry, coagulation testing, histology, immunohistochemistry, and in-situ hybridization were consistent with a cascade of hepatocyte-specific virus replication causing liver damage and a defect in clotting factor synthesis. Despite a lack of extra-hepatic HA-YFV replication, severe pathology was observed in the intestines and pancreas. Histopathological analysis over the time-course of HA-YFV infection revealed an ischemic pattern in these tissues, culminating in fibrinoid/coagulative necrosis of these organs. Further investigation showed that ischemia-induced erosion of the gut epithelial barrier serves as an entry point for luminal bacteria that spread systemically via the portal system. Thus, the intoxication phase of YF is a sepsis-like syndrome caused by translocation of bacteria from a damaged gastrointestinal tract. Evaluation of human YF cases for these previously overlooked disease features confirmed this overarching mechanism: bacteria were identified in the portal vein and liver parenchyma of fatal YF cases along with elevations in plasma markers of bacteremia and a bacteria-driven inflammatory response. Importantly, blood concentrations of the gastrointestinal damage marker intestinal fatty acid binding protein (I-FABP) were significantly elevated in fatal YF cases relative to non-fatal cases, suggesting that I-FABP measurements could be useful in prognosis and treatment decision making. Our findings tie together several recent and historically unexplained observations surrounding the highly-lethal intoxication phase of YF in humans: a high AST/ALT ratio, “black vomit,” pancreatitis, and paradoxical neutrophilia. A better appreciation for the drivers of mesenteric ischemia, and preemption of bacterial sepsis, may improve outcomes in cases of severe YF.

  PublisherOA PDFDOI

• Here we go again: More diseases dubiously attributed to pegivirus infection

  PLoS Pathogens · 2025-10-28 · 1 citations

  articleOpen access1st authorCorresponding
  PublisherDOI

• Yellow Fever Hepatitis: Rediscovering Villela Bodies, a Neglected Histopathologic Clue

  Archives of Pathology & Laboratory Medicine · 2025-09-25

  articleOpen access

  To the Editor.—In 2024, Brazil experienced the largest and most severe dengue epidemic of the 21st century, with numerous cases and high mortality rates, more than 10 years after the emergence of chikungunya and Zika in Brazil. In addition, oropouche fever spread to areas outside of the Amazon region, and now, in early 2025, there is an ongoing yellow fever (YF) outbreak in the state of São Paulo, in southeastern Brazil, so far mostly affecting nonhuman primates.1Among arboviruses, YF is the prototype viral hemorrhagic fever, with a mortality rate of approximately 35%. YF is endemic to sub-Saharan Africa and South America, particularly the Amazon River basin. In Brazil, urban transmission of YF has not occurred since 1942, but every 7 to 10 years, new epizootics and outbreaks arise in areas where forest and city meet, affecting susceptible, unvaccinated individuals. Data from the São Paulo State Health Department show 696 YF cases reported in São Paulo between 2017 and 2019, with 232 deaths (33.3%). In 2020 and 2021, one case was reported each year, with no deaths. In 2022 and 2023, 2 cases were reported each year, with a case fatality rate of 50%.1Throughout medical history, autopsies have been a powerful tool for elucidating the etiology and pathogenesis of infectious diseases, playing a crucial role in the COVID-19 and mpox epidemics. During the YF epidemic, our autopsy service conducted 85 autopsies on suspected or confirmed cases of severe YF.2,3 The goal of these autopsies was to determine the cause of death in cases with atypical presentation; clarify lethal outcomes in liver transplant recipients; and diagnose YF vaccine–associated viscerotropic disease (commonly abbreviated as “YEL-AVD”), based on the Brighton criteria.2,3The pathology of YF has been extensively documented in autopsy studies from the late 19th and early 20th centuries. Liver pathology has remained a central focus, notably in the studies of Councilman4 and Rocha-Lima,5 who described the characteristic mid-zonal hepatitis with eosinophilic corpuscles (Councilman bodies).4,5 Torres6 and Cowdry and Kitchen7 later described nuclear inclusions in YF liver tissue, more clearly observed in primates. These inclusions exhibited various morphologic features, with diseased hepatocytes showing prominent nucleoli at the margins of steatotic and apoptotic degeneration, although YF virus virions are not present in these inclusions, as determined by electron microscopy.6,7A distinctive histopathologic feature of the liver in YF is the presence of “ochre bodies” in hematoxylin-eosin–stained sections, located in the cytoplasm of hepatocytes and Kupffer cells, observed within Councilman bodies themselves, or seen as cell-free material in the lobular interstitium and hepatic sinusoids. These ochre bodies were described in an article published in the Archives of Pathology in 1941 by the Brazilian pathologist Eudoro Libânio Villela, and were found in YF late-stage cases, occurring after the 8th to 10th day of symptom onset.8 Later named Villela bodies (VBs), alongside Councilman bodies, these have become recognized as key features of YF histopathology.9From the 1990s onward, VBs were rarely cited.9 However, revisiting the work of Villela, we have linked a granular pattern of positivity for YF Envelope antigen in immunohistochemical reactions to VBs.2,3,9 Initially interpreted as hemosiderin or bile pigments, VBs do not stain with Prussian blue (for hemosiderin) or Hall stain (for bilirubin) and exhibit specific staining properties, such as orange-ochre in Sudan III dye, black in Del Río Hortega and Fontana-Masson stains, and fuchsia in Ziehl-Neelsen stain.8 The Figure (A through E) shows VBs stained with hematoxylin-eosin and fuchsin, along with their ultrastructure.Villela bodies are thought to represent a ceroid pigment resulting from lipid peroxidation in lysosomes, potentially containing YF virus antigenic fragments. In our autopsies—often from cases with extended evolution due to state-of-the-art care provided by our institution—VBs were frequently observed.2,3,9 Although liver biopsy is contraindicated in the acute phase of hemorrhagic fever, rare reports also describe VBs in liver biopsy specimens from YF cases.9 It remains to be seen whether VBs appear with other arboviruses, such as dengue virus.Villela bodies have a similar histologic appearance and histochemical affinity to ceroid pigment found in the liver in other diseases. However, their distribution in liver tissue is an important diagnostic clue. In YF, the ceroid pigmentation of VBs is found within hepatocytes, Kupffer cells, within Councilman bodies, and as cell-free material in the interstitium, mainly in hepatic zones 2 and 3 (Figure, A through E). This is different from the distribution of ceroid pigment found in other diseases, such as within perivenular hepatocytes of elderly people as part of the normal aging process, or within scattered hepatocytes in the liver parenchyma in patients with Dubin-Johnson, Gilbert, and telomere-shortening syndromes, or in patients with long-term phenobarbital use. Ceroid pigment may also be found in Kupffer cells, to varying degrees, near foci of chronic inflammatory reaction in chronic viral hepatitis, resolving hepatitis, drug-induced liver injury, acute fatty liver of pregnancy, and steatohepatitis.10With the emergence and re-emergence of arboviral diseases in Brazil and the Americas, understanding the histopathology of tissue lesions caused by these agents is crucial. The timely and accurate identification and reporting of findings across varied clinical presentations places diagnostic pathology at the forefront of epidemic preparedness. Autopsy plays a central role in this, not only in diagnosis but also in uncovering mechanisms of pathogenesis, as seen during the COVID-19 pandemic and mpox epidemic. Integrating clinical and epidemiologic data with macroscopic and histologic analyses is vital, combining accessible histochemical stains with advanced techniques like multiplex immunohistochemistry and transcriptomics. The rediscovery of findings such as VBs highlights autopsy’s enduring value in understanding arboviral diseases and addressing global health challenges.2,3,9The authors wish to thank all health workers who provided care to patients with severe yellow fever, to the Hospital das Clínicas da Faculdade de Medicina da Universidade de São Paulo (FMUSP)–Yellow Fever Crisis Committee, and to all medical residents, technicians, and professors from the Pathology Department - FMUSP who participated in the autopsy procedures.

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Frequent coauthors

• Jens H. Kuhn

  42 shared

• David H. O’Connor

  University of Wisconsin–Madison

  39 shared

• Michael Diamond

  Washington University in St. Louis

  36 shared

• Peter B. Jahrling

  23 shared

• Michael Lauck

  Promega (United States)

  21 shared

• Thomas C. Friedrich

  University of Wisconsin–Madison

  18 shared

• Tony L. Goldberg

  University of Wisconsin Health

  18 shared

• James Brett Case

  Washington University in St. Louis

  16 shared

Labs

• Bailey LaboratoryPI