Ph.D., University of Colorado, 1983.
Postdoctoral Fellow, Harvard University, Cancer Biology.
Dr. Overbaugh's laboratory has a long-standing interest in understanding the mechanisms of HIV transmission and pathogenesis. A major hypothesis for the studies in her lab is that the variants of HIV-1 that are transmitted are a selected subset of all the viruses that evolve during the course of infection. Thus, an overarching goal of Dr. Overbaugh's research is to determine whether some variants are more transmissible and others are more pathogenic in the host and to define the mechanisms underlying these differences. Her lab has shown that there is a genetic bottleneck in the sequences that are transmitted, leading to selection of just one or a few HIV variants in a new host. Her lab's studies have shown that people already infected by HIV can become re-infected/superinfected with HIV from another source partner. Her laboratory is exploring the immune responses in individuals who become superinfected to determine if they have deficits in immunity that may explain their susceptibility to re-infection, which has implication for defining immune correlates of vaccine protection. Her lab is exploring similar question in the context of mother-infant transmission, where the infant is infected in the presence of maternal HIV-specific antibodies.
Much of the HIV research in the lab is focused on populations in Africa because this is where the AIDS epidemic is most severe. Studies include analyses of antiretroviral drug resistance, which has become increasingly important as HIV treatments become available in Africa. The laboratory is part of a larger team, comprising researchers in both Seattle and Kenya (The Nairobi HIV/STD Project), that is studying the molecular epidemiology of HIV transmission. The project is also examining the efficacy of various intervention strategies to limit the spread of HIV, particularly those that may be practical to implement in Africa and other parts of the developing world.
Dr. Overbaugh has served as Chair of the NIH study section on HIV Molecular Biology (1998-2000), and as a member of various NIH review panels. She has served as a member of the NIH Office of AIDS Research Advisory Council and as an Editor for the Journal of Virology.
Honors and Awards
2011, Fellow, American Academy of Microbiology
2010, MERIT Award, National Institutes of Health (NIH), Early & Reinfection in High Risk Women
2008, McDougall Mentoring Award, FHCRC
2007, Women & Minority Faculty Medicine Mentoring Award, University of Washington School of Medicine
1999-2009, MERIT Award, National Institutes of Health (NIH), Early Infection in Women Exposed Mucosally to HIV-1
1999-2004, Elizabeth Glaser Scientist, Pediatric AIDS Foundation
1993-1998, Scholar, Leukemia Society of America
1994-1998, Associate Professor, University of Washington, School of Medicine, Microbiology
Disruption of Thiamine Uptake and Growth of Cells by Feline Leukemia Virus Subgroup A.. Journal of virology. 87(5):2412-9.. 2013.
HIV-1 maternal and infant variants show similar sensitivity to broadly neutralizing antibodies, but sensitivity varies by subtype.. AIDS (London, England). 27(10):1535-44.. 2013.
Evidence for Efficient Vertical Transfer of Maternal HIV-1 Envelope-Specific Neutralizing Antibodies but No Association of Such Antibodies with Reduced Infant Infection.. Journal of acquired immune deficiency syndromes (1999).. 2013.
Endothelial activation biomarkers increase after HIV-1 acquisition: plasma vascular cell adhesion molecule-1 predicts disease progression.. AIDS (London, England). 27(11):1803-1813.. 2013.
Antibody-dependent cell-mediated virus inhibition (ADCVI) antibody activity does not correlate with risk of HIV-1 superinfection.. Journal of acquired immune deficiency syndromes (1999).. 2013.
HIV-1 superinfection occurs less frequently than initial infection in a cohort of high-risk Kenyan women.. PLoS pathogens. 9(8):e1003593.. 2013.
Loss to Follow-Up as a Competing Risk in an Observational Study of HIV-1 Incidence.. PloS one. 8(3):e59480.. 2013.
Breast milk cellular HIV-specific interferon γ responses are associated with protection from peripartum HIV transmission.. AIDS (London, England). 26(16):2007-16.. 2012.
A Combination of Broadly Neutralizing HIV-1 Monoclonal Antibodies Targeting Distinct Epitopes Effectively Neutralizes Variants Found in Early Infection.. Journal of virology. 86(19):10857-61.. 2012.
Long-term Virologic Response and Genotypic Resistance Mutations in HIV-1 Infected Kenyan Children on Combination Antiretroviral Therapy.. Journal of acquired immune deficiency syndromes (1999).. 2012.
Cervicovaginal HIV-1 Neutralizing IgA Detected among HIV-1-Exposed Seronegative Female Partners in HIV-1-Discordant Kenyan Couples.. AIDS (London, England). 26(17):2155-2163.. 2012.
Antiretroviral Treatment Interruptions Predict Female Genital Shedding of Genotypically Resistant HIV-1 RNA.. Journal of acquired immune deficiency syndromes (1999).. 2012.
Low-frequency nevirapine resistance at multiple sites may predict treatment failure in infants on nevirapine-based treatment.. Journal of acquired immune deficiency syndromes (1999).. 2012.
Cellular immune responses and susceptibility to HIV-1 superinfection: a case-control study.. AIDS (London, England). 26(5):643-6.. 2012.
HIV-1 superinfection in women broadens and strengthens the neutralizing antibody response.. PLoS pathogens. 8(3):e1002611.. 2012.
The Antibody Response against HIV-1.. Cold Spring Harbor perspectives in medicine. 2(1):a007039.. 2012.
Valacyclovir Suppressive Therapy Reduces Plasma and Breast Milk HIV-1 RNA Levels During Pregnancy and Postpartum: A Randomized Trial.. The Journal of infectious diseases. 205(3):366-75.. 2012.
Genital Inflammation Predicts HIV-1 Shedding Independent of Plasma Viral Load and Systemic Inflammation.. Journal of acquired immune deficiency syndromes (1999). 61(4):436-40.. 2012.
Antiretroviral Treatment Interruptions Predict Female Genital Shedding of Genotypically Resistant HIV-1 RNA.. Journal of acquired immune deficiency syndromes (1999). 60(5):511-8.. 2012.