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Roberta M. Kamin-Lewis

Roberta M. Kamin-Lewis Ph.D.

Academic Title: Associate Professor
Primary Appointment: Microbiology and Immunology
Location: HH 324
Phone: (410) 706-4686

Research Interests:

My research is focused on human host defense mechanisms with emphasis on mucosal immunity (immunity in the major tracts-GI, genital-urinary, oral cavity, etc) and HIV-1 vaccine development. The major route of HIV transmission worldwide is via heterosexual contact. Thus, there is an urgent need for the development of a preventative HIV-1 vaccine that will stimulate immunity in the genital tract. It has been observed that stimulation of immunity in one mucosal site (e.g. the intestine) can produce immunity in another mucosal site (e.g. the genital tract). This shared immunity among mucosal sites is due to the circulation of soluble antibodies and the circulation of B cells with so-called mucosal markers. To elicit mucosal immunity, the two most convenient routes of delivering a vaccine are intranasal or oral, with the latter targeting the gastrointestinal tract. We are interested in the oral delivery of a candidate HIV-1 vaccine. Our approach is to use attenuated Salmonella as a bacterial vector that targets the intestine. With oral delivery, it is necessary to confirm that the vaccine has elicited an immune response. In this regard, my lab is identifying and characterizing responses in recipients of a licensed vaccine for Salmonella typhi. These results will then be extended to studying responses in individuals given an HIV vaccine delivered by the Salmonella vector. In additional studies, we are studying parameters of immunity to a bacterium found in the oral cavity, Porphyromonas gingivalis. This bacterium is one of the causative agents of periodontal disease. Both Salmonella and the oral pathogen P. gingivalis are Gram negative organisms and thus can elicit a potent inflammatory response via a molecule on their outer membrane known as lipopolysaccharide--LPS. In this regard, we are also investigating the pathway of LPS in activating T cells and the role of LPS in modulating the expression a surface molecule that HIV-1 uses to enter cells?a receptor known as CCR5. Reported studies have shown that LPS can decrease the expression of this receptor on the surface of another blood cell type?the monocyte.


Devico AL, Fouts TR, Shata MT, Kamin-Lewis R, Lewis GK, Hone DM. 2002. Development of an oral prime-boost strategy to elicit broadly neutralizing antibodies against HIV-1. Vaccine. 20(15):1968-74.

Skurnick, JH., Palumbo, P., DeVico, A., Shacklett, BL, Valentine, FT, Merges, M, Kamin-Lewis, RM, Mestecky, JM, Denny, T, Lewis, GK, Lloyd, J, Praschunus, R, Baker, A, Nixon, DF, Stranford, S, Gallo, RC, Vermund, SH, Louria, DB. 2002 Correlates of Non-Transmission in United States Women at High Risk of HIV-1 Infection through Sexual Exposure. J Infect Dis. 185(4):428-38.

Reid, W., Sadowska, M, Denaro, F, Rao, S., Foulke Jr., J., Hayes, H., Fouts, R., Lewis,G. K., Kamin-Lewis, R.M., Wei, C., Ray, P., Gallo, R., Reitz, M. and Bryant, J. 2001. An HIV-1 transgenic rat that develops HIV-related pathology and immunologic dysfunction. Proc Natl Acad Sci U S A. 98(16):9271-6.

Kamin-Lewis R, Abdelwahab SF, Trang C, Baker A, DeVico AL, Gallo RC, Lewis GK. 2001. Perforin-low memory CD8+ cells are the predominant T cells in normal humans that synthesize the beta -chemokine macrophage inflammatory protein-1beta. Proc Natl Acad Sci U S A. 98(16):9283-8.