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The genome and proteins of HIV (human immunodeficiency virus) have been the subject of extensive research since the discovery of the virus in 1983. [1] [2] "In the search for the causative agent, it was initially believed that the virus was a form of the Human T-cell leukemia virus (HTLV), which was known at the time to affect the human immune system and cause certain leukemias.
HIV can infect a variety of immune cells such as CD4 + T cells, macrophages, and microglial cells. HIV-1 entry to macrophages and CD4 + T cells is mediated through interaction of the virion envelope glycoproteins (gp120) with the CD4 molecule on the target cells' membrane and also with chemokine co-receptors. [26] [44]
Gp41 also known as glycoprotein 41 is a subunit of the envelope protein complex of retroviruses, including human immunodeficiency virus (HIV). Gp41 is a transmembrane protein that contains several sites within its ectodomain that are required for infection of host cells.
HIV-1 is the more commonly associated with AIDS in the US and worldwide, HIV-2 is more rare, and typically restricted to areas in western Africa and southern Asia. HIV-2 is so uncommon that “HIV” almost always refers to HIV-1. Alright HIV targets CD4+ cells, meaning cells that have this specific molecule called CD4 on their membrane.
HIV can infect a variety of cells such as CD4+ helper T-cells and macrophages that express the CD4 molecule on their surface. HIV-1 entry to macrophages and T helper cells is mediated not only through interaction of the virion envelope glycoproteins ( gp120 ) with the CD4 molecule on the target cells but also with its chemokine coreceptors.
By down regulating cell surface expression of CD4 and Lck, Nef creates a narrow TCR response which likely optimizes HIV-1 viral production and generates a susceptible population of cells to further infect. Nef retargets kinase-active Lck away from the plasma membrane to early and recycling endosomes (RE) as well as the Trans-Golgi network (TGN).
Exposed on the surface of the viral envelope, the glycoprotein gp120 binds to the CD4 receptor on any target cell that has such a receptor, particularly the helper T-cell. Strains of HIV-1 have been isolated that are able to enter host cells that are CD4 negative. This CD4-independence is associated with spontaneous mutation in the env gene.
APOBEC3G is thus a host defence to retroviral infection which HIV-1 has overcome by the acquisition of Vif. [5] Vif 1 is additionally able to inhibit human A3C, A3D, A3F, and A3H haplotype II, [6] all of which can similarly be packaged and cause hypermutation in Vif-deficient HIV-1. Different surfaces on Vif 1 are used to bind A3C, A3F, and A3G ...