Adam Bailey
University of Wisconsin-Madison, WI·Microbiology & Immunology
Viruses that infect animals reveal general rules about how any virus enters a cell, avoids being cleared by the immune system, and makes its host sick. Three projects here use animal virus systems and small-animal models to attack three such puzzles: how a neglected family of RNA viruses gets into cells and crosses the placenta, why one yellow fever vaccine strain is safe while its parent strain kills, and how a virus that infects roughly one in seven people worldwide manages to persist for years without causing disease.
- Fields
Microbiology & Immunology
Medicine & Clinical Research
Biology
- Topics
arterivirus
neonatal Fc receptor
FcRn
- Grants
- 3 known grants, through Mar 2031
What they work on
- Map which parts of the neonatal Fc receptor (FcRn), a molecule that normally ferries antibodies across barriers, arteriviruses need for cell entry, by building chimeric FcRn molecules combining virus-permissive and virus-resistant versions from different species.
- Identify which of the 7 to 11 surface glycoproteins on arterivirus particles engage FcRn, by generating chimeric arteriviruses carrying glycoprotein combinations from different viruses, and screen for host factors that can substitute for FcRn during entry.
- Track arterivirus infection in live mice using lactate dehydrogenase-elevating virus engineered to express the light-producing enzyme nanoluciferase, identifying infected tissues over time and the macrophage subpopulations that support replication.
- Test whether arteriviruses hijack FcRn's normal role in placental antibody transport to transmit from mother to fetus, by comparing vertical transmission in FcRn-knockout and wild-type mice.
- Determine how two mutations in the yellow fever virus NS2B gene abolish disease in hamsters, relating them to induction of type I interferon, the cell's first antiviral alarm, and identifying the innate immune factors blocked by virulent but not vaccine-strain virus.
- Determine how yellow fever virus causes severe gut damage without infecting gut cells, mapping the anatomical distribution of gastrointestinal and vascular damage in hamsters and testing whether the viral protein NS1 acts as the responsible toxin.
- Identify the lymphocyte subsets and effector functions behind partial control of mouse-adapted pegivirus, using immune-gene-knockout mice and timed lymphocyte depletion, and insert an immunogenic peptide into the virus to test whether it hides antigens from the immune system.
- Test whether complete clearance of mouse-adapted pegivirus can be transferred from elite-controller mice by moving spleen cells into lymphocyte-deficient Rag-knockout recipients, then removing or purifying individual lymphocyte subsets to find which is sufficient.
More about the research
The first project concerns arteriviruses, an understudied family of RNA viruses distantly related to coronaviruses that infect many mammals, with some able to infect human cells. Each virus particle carries an unusually large set of surface glycoproteins, 7 to 11 depending on the virus, unlike any known machinery for fusing with a cell membrane. The macrophage protein CD163 is a required receptor but is not sufficient on its own; the lab recently identified the neonatal Fc receptor (FcRn), a molecule that normally shuttles antibodies across barriers including the placenta, as an additional entry factor. Aim 1 maps the interaction from both sides: chimeric FcRn molecules that mix pieces from arterivirus-permissive and arterivirus-resistant versions in different species will localize the critical domains and residues, chimeric viruses carrying glycoprotein combinations from different arteriviruses will identify the viral partners, and screens will look for host factors that can substitute for FcRn. Aim 2 moves into mice using lactate dehydrogenase-elevating virus (LDV), a mouse arterivirus that causes lifelong virus in the blood. A version engineered to express nanoluciferase, a light-producing enzyme, will allow whole-body imaging of which tissues are infected over time; the team will then identify which macrophage subpopulations within those tissues support infection and whether persistent infection blocks recovery of those cells. FcRn-knockout mice will test whether arteriviruses exploit FcRn's normal role in the placenta to pass from mother to fetus.
Why it matters
Arteriviruses are considered "pre-emergent" because some can already infect human cells; learning which host and viral molecules they need could help anticipate or block a jump into people, and explain how they damage macrophages and cross the placenta. The yellow fever work aims to define what makes the 17D vaccine safe and what drives the fatal phase of disease, with implications for safer vaccines and treatments for a disease that kills tens of thousands a year. The pegivirus studies probe why the immune system fails to clear a virus that persists in roughly 15% of people, a model of "failed immunity" relevant to other chronic infections.
Known grants
From NIH and NSF research grants. Labs often have other funding we can't see.
Closest labs
Cynthia McMillen
University of Pittsburgh, PA·Microbiology & Immunology·Early-career
Compare mother-to-offspring transmission of four Oropouche virus strains (BeAn19991, BeH759021, LET2083, AM0088) from four genetically distinct lineages, to test whether genomic reassortment underlies changes in tissue targeting and virulence.
Zhongde Wang
Utah State University, UT·Microbiology & Immunology
Create a humanized-NTCP Syrian hamster using CRISPR gene editing to change the two codons in the hamster NTCP entry receptor that encode the amino acid residues required for hepatitis B virus infection.
Anita McElroy
University of Pittsburgh, PA·Microbiology & Immunology
Determine the route by which Rift Valley fever virus spreads from a peripheral site to the central nervous system, using mouse models in which virus is injected into the footpad to mimic a mosquito bite.
The school
University of Wisconsin-Madison: 91 labs on PI Pages, $1.9B a year on research, 854 research doctorates a year.
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