The failure of about 50% of children born of HIV-seropositive women to exhibit evidence of having acquired HIV infection during at least the first few years of life points to some as yet undefined role of the maternal immune system in preventing vertical virus transmission during gestation or parturition. Although the contribution of maternal HIV-specific antibodies to protection of the infant cannot be excluded, the fact that HIV is highly cell- associated makes it probable that T cell-mediated immune responses directed specifically against HIV-infected cells can effect a reduction in maternal virus load, thereby reducing fetal risk. By characterizing such responses as to fine specificity and magnitude, and by correlating them with the presence or absence of infection in the newborn, it may be possible to devise immunization protocols that will potentiate preexisting HIV-specific cell-mediated immunity during pregnancy thus further decreasing the vertical transmission rate. Significant progress has been made in the identification and synthesis of amino acid sequences of viral epitopes that serve as T cell recognition sites and an increasing number of such peptides are being shown to be capable of triggering. In vitro, secondary T cell responses specific for variety of different viruses, including HIV. This project will utilize recombinant vaccinia virus containing the env gene of HIV to induce and maintain gp120-specific lines and clones of T cells originating from peripheral blood lymphocytes of HIV-seropositive pregnant women. A series of gp120 peptides will be synthesized and used to probe the fine specificity of these T cells at the clonal level in order to uncover potential differences in maternal immunologic responsiveness that would be predictive of vertical HIV transmission. Similarly, infants born to HIV-seropositive mothers will be monitored prospectively for a gain or loss of T cell responsiveness to these same peptides in an attempt to correlate fine specificity with the appearance, course and nature of HIV- induced disease.

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University of Maryland Baltimore
United States
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