Research interests

The incidence of HIV-1 infection is slowing globally, thanks to broadening implementation of antiretroviral treatment to infected individuals and programs targeting populations at risk of infection with prophylaxis.  However, UNAIDS reports indicate that more than half of HIV-1 infected adults in sub-Saharan Africa are women of childbearing age.  The availability of antiretroviral treatment to pregnant HIV-1 infected women has reduced the rates of mother-to-child transmission and simultaneously increased the rates of children born uninfected with HIV, but not unexposed.

Epidemiologic studies of these HIV-1 exposed uninfected (EU) infants consistently report that these infants have increased morbidity and mortality during the first 2 years of life compared to unexposed infants, even in research settings of improved quality of medical care, infant growth monitoring and nutritional counseling. While early reports found minimal differences in morbidity and mortality between HIV-1 EU compared to HIV-1 unexposed infants, recent studies noted appreciable increases in morbidity and mortality in EU infants:  2-3 fold higher mortality rates and 20-30% more sick clinic visits and hospitalization. Reduced placental transfer of maternal antibody may explain vulnerability during infancy. However, persistent morbidity beyond the neonatal period was noted in EU infants and it is not clear why EU infants have continued elevated risk throughout the first year of life. The main focus of my research aims to uncover the mechanisms contributing to the infant vulnerabilities.  One hypothesis we are exploring is that in utero HIV-1 exposure alters the TCR repertoire in infants and leaved a durable imprint on the developing immune system. We are interested in evaluating the role of maternal viral load, immune activation and plasma cytokine environment on the neonatal immune repertoire present at birth by measuring cord blood TCR diversity through amplification of the CDR3 region followed by sequence analysis of expanded clones.