Abstract
BackgroundCell mediated immunity, including efficient CTL response, is required to prevent HIV-1 from cell-to-cell transmission. In previous investigations, we have shown that B1 peptide derived by Fourier transformation of HIV-1 primary structures and sharing no sequence homology with the parent proteins was able to generate antiserum which recognizes envelope and Tat proteins. Here we have investigated cellular immune response towards a novel non-homologous peptide, referred to as cA1 peptide.Methodology/Principal FindingsThe 20 amino acid sequence of cA1 peptide was predicted using the notion of peptide hydropathic properties; the peptide is encoded by the complementary anti-sense DNA strand to the sense strand of previously described non-homologous A1 peptide. In this report we demonstrate that the cA1 peptide can be a target for major histocompatibility complex (MHC) class I-restricted cytotoxic T lymphocytes in HIV-1-infected or envelope-immunized individuals. The cA1 peptide is recognized in association with different MHC class I allotypes and could prime in vitro CTLs, derived from gp160-immunized individuals capable to recognize virus variants.Conclusions/SignificanceFor the first time a theoretically designed immunogen involved in broad-based cell-immune memory activation is described. Our findings may thus contribute to the advance in vaccine research by describing a novel strategy to develop a synthetic AIDS vaccine.
Highlights
A major objective of current HIV-1 vaccination strategies is the induction of HIV-1-specific CD8+ major histocompatibility complex (MHC) class I-restricted CTL responses, suggested to play a pivotal role in viral clearance and protection against HIV-1 disease progression [1]
It is noteworthy that T cells derived from healthy HIV-1seronegative individuals did not initiate proliferation in the presence of cA1 peptide, suggesting that the cA1 peptide recognition might have been processed after the viral infection
T cells that mediate cellular immunity can detect the presence of intracellular pathogens, because infected cells display on their surface peptide fragments derived from the pathogen’s proteins, so that T cells recognise the peptide–MHC molecule complex and kill the infected cells
Summary
A major objective of current HIV-1 vaccination strategies is the induction of HIV-1-specific CD8+ MHC class I-restricted CTL responses, suggested to play a pivotal role in viral clearance and protection against HIV-1 disease progression [1]. Despite the antigenic complexity of most viruses, the CTL response to viral infection in many instances is dominated by the reactivities directed against a limited number of immunodominant peptidic epitopes. The identities of these epitopes are controlled by the particular Major Histocompatibility Complex (MHC) class I alleles of the host [7,8]. In this report we demonstrate that the cA1 peptide can be a target for major histocompatibility complex (MHC) class I-restricted cytotoxic T lymphocytes in HIV-1-infected or envelope-immunized individuals. Our findings may contribute to the advance in vaccine research by describing a novel strategy to develop a synthetic AIDS vaccine
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