Pathogenesis of HIV-1 Infection

HIV-1 is a retrovirus and belongs to the family of Lentiviruses. The life cycle of HIV-1 is divided into early and late phases. In the early phase; an HIV-1 virion binds to CD4 receptors and chernokine co-receptors on the human host cell surface, viral and host cell membranes fuse and the viral core is entered into host cell, Viral particle is uncoated, The viral genome is reverse transcribed and the viral preinteg ration complex (PIC) forms. The PIC is transported through the nuclear pore into the nucleoplasm, and the viral reverse transcript is integrated into a host cell DNA. In the late phase, viral RNAs are transcribed from the integrated viral genome and processed to generate viral mRNAs and full-length viral genomic RNAs. The viral RNAs are exported through the nuclear pore into the cytosol. Viral mRNAs are translated and the resulting viral proteins are post-translationally processed, core particles containing viral ganomic RNA and envelope proteins assemble at the host cell membrane. Immature viral particles are released by budding. The released particles mature to become infectious. There are three main ways HIV-1 incites cell death in CD4*TH lymphocytes, namely through the budding process, infected cell-to-cell fusion and through tricking the immune system. The stimulation of CDT lymphocytes and the formation of antigen-specific cytotoxic CD8+T lymphocytes depend on the presentation of a peptide together with MHC-I. Cytotoxic CD8+T lymphocytes are able to recognize and eliminate HIV-1 infected cells Nef induce downregulation of CD4 and MHC-I molecules from the HIV-1-infected cells, which represent an escape mechanism for the virus to evade an attack mediated by cytotoxic CD8+T lymphocytes and to avoid recognition by CD(4)(+)TH1 lymphocytes, The spectrum of vaccine strategies against HIV includes HIV-derived peptides or proteins, the use of viral or bacterial vectors, naked DNA, the use of live attenuated HIV strains.