Undergraduate
Brown University, Sc.B., Biology, 1993

Medical School
New York University School of Medicine, Ph.D., 2000, M.D. 2001

Residency
Children’s Hospital and Regional Medical Center/University of Washington, 2001-03

Fellowship
Children’s Hospital and Regional Medical Center/University of Washington, 2003-06

Prevention of mother-to-child-transmission of HIV-1 infection

Etiology of mastitis: Breastfeeding accounts for nearly half of mother-to-child transmission of HIV-1 (MTCT). Safe and affordable alternatives to breastfeeding are not available for the majority of infants born to HIV-1 infected women. Numerous studies support the role of mastitis in increasing breastfeeding transmission, likely from the increase in breast milk HIV-1 load associated with inflammation of the lactating breast. Clinical mastitis, characterized by pain, redness and swelling, occurs in up to one-third of lactating women. Subclinical mastitis, without symptoms, but with an increased breast milk sodium ([Na+]), is even more prevalent and has also been associated with increases breast milk HIV-1 RNA and MTCT. There are no published studies elucidating the etiologies of subclinical mastitis, nor mastitis in HIV-1 infected women. Veterinary studies of mastitis implicate a broad range of bacteria, mycobacteria, fungi, mycoplasmas and herpes group viruses. We hypothesize that mastitis, especially subclinical mastitis, in HIV-1 infected women is also caused by a variety of organisms. In addition, that mastitis increases milk HIV-1 load within the breast, independent of the blood, presumably by immune stimulation of latently infected cells. By identifying the infectious agents associated with high levels of HIV-1 in breast milk, treatment and prophylaxis strategies can be developed that may reduce HIV-1 transmission to breastfeeding infants. Studies are in progress to examine associations between breast milk virus, cells and [Na+] and blood virus; and, to determine the infectious etiologies of mastitis in HIV-1 infected women.


Evaluation of HIV-1 specific immunization of infants by breastfeeding from infected mothers during nevirapine chemoprophylaxis: Considerable data indicate that HIV-1 specific humoral immunity can protect from infection and that cellular immunity modulates HIV-1-associated immune depletion. We hypothesize that when HIV-1 infection of infants is prevented by administration of nevirapine to breastfeeding infants, sufficient exposure to virus will result in HIV-1 specific immunization. We are evaluating whether HIV-1 specific primed-T cell and IgA responses in infants can be induced by repeated exposure to virus in maternal breast milk. If currently available drug regimens provide simultaneous prophylaxis of breastfeeding infants from HIV-1 infection and allow induction of HIV-1-specific immune responses, this would provide a rationale for studies to evaluate the protective effect of these immune responses after the prophylaxis is discontinued. If protective immunity can be induced during a short period of chemoprophylaxis while breastfeeding, this would provide the basis for a novel strategy for the immunization of infants in countries where breastfeeding remains their primary source of nutrition, and of HIV-1 infection.


Human Herpes Virus 8 and Kaposi's Sarcoma

Natural history of primary HHV-8 infection in Ugandan children: Human Herpesvirus 8 (HHV-8) causes Kaposi’s sarcoma (KS), the most common cancer in Uganda. This study addresses several fundamental but poorly understood aspects of HHV-8 epidemiology and pathobiology. The natural history of primary HHV-8 will be studied in a cohort of 30 children followed prospectively from birth to 3 years of age in Kampala, Uganda. HHV-8 acquisition of these children will be determined by weekly testing using highly sensitive and specific DNA-based (polymerase chain reaction, PCR) methods. The mothers of these children will be co-infected with HIV and HHV-8 in order to observe the greatest number of primary HHV-8 infections in the children, and to examine the effect of HIV infection on acute HHV-8 infection. The timing of HHV-8 acquisition will be used to describe the clinical presentation, viral replication patterns and immune responses that occur with primary HHV-8 infection. The mothers and young siblings of these children will also be sampled to evaluate the association between HHV-8 acquisition and exposure to HHV-8 shedding in the saliva of household contacts. This design allows the study of factors related both to HHV-8 transmission as well as acquisition. Such information is central to the rational development of interventions to diagnose, prevent and treat HHV-8 related disease.

Gantt S, Clavijo P, Bai XM, Esko J and Sinnis P (1997) Cell adhesion to a motif shared by the malaria circumsporozoite protein and thrombospondin is mediated by its glycosaminoglycan-binding region and not by CSVTCG. J. Biol. Chem. 272(31): 19205-13.

Gantt S, Myung JM, Briones MRS, Li WD, Corey EJ, Omura S, Nussenzweig V and Sinnis P (1998) Proteosome inhibitors block development of Plasmodium. Antimicrob. Agents Chemother. 42(10): 2731-8.

Kappe S, Bruderer T, Gantt S, Fujioka H, Nussenzweig V and Menard R (1999) Conservation of a gliding motility and cell invasion machinery in apicomplexan parasites. J. Cell Biol. 147(5): 937-44.

Gantt S, Persson C, Abagyan R, Rose K, Birkett AJ and Nussenzweig V (2000) Antibodies against TRAP do not inhibit Plasmodium sporozoite infectivity in vivo. Infect. Immun. 68(6): 3667-3673.

Thathy V, Fujioka H, Gantt S, Nussenzweig R, Nussenzweig V and Menard R (2002) Levels of circumsporozoite protein in the Plasmodium oocyst determine sporozoite morphology. EMBO J. 21(7):1586-96.

Benson C, Gantt S, Zerr DM, Qin X and Abe P (2005) Use of 16S ribosomal DNA polymerase chain reaction to identify Haemophilus influenzae type b as the etiology of pericarditis in an infant. Pediatr. Infect. Dis. J. Mar;24(3):287-8.

Gantt S, Shetty AK, Seidel KD, Matasa K, Musingwini G, Woelk G, Zijenah LS, Katzenstein DA and Frenkel LM (2007) Laboratory Indicators of Mastitis are Not Associated with Elevated HIV-1 DNA or Predictive of HIV-1 RNA Concentrations in Breast Milk. J. Infect. Dis. 196(4):570-6. PMID: 17624843

Gantt S, Carlsson J, Shetty AK, Seidel KD, Qin X, Mutsvangwa J, Musingwini G, Woelk G, Zijenah LS, Katzenstein DA and Frenkel LM (2008) Cytomegalovirus and Epstein-Barr Virus in Breast Milk are Associated with HIV-1 Shedding but Not With Mastitis. AIDS. 22(12):1453-60. PMID: 18614868



Book chapters

Gantt S and Frenkel LM, (2006) Antiviral Therapies, in Gellis and Kagan's Current Pediatric Therapy, 18th Ed., Burg FD, et al., Editors, Saunders.