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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.
The HIV capsid consists of roughly 2000 copies of the p24 protein. The p24 structure is shown in two representations: cartoon (top) and isosurface (bottom) The p24 capsid protein is the most abundant HIV protein with each virus containing approximately 1,500 to 3,000 p24 molecules. [1]
A 3D representation that includes the retroviral psi packaging element. This is a solution RNA structure model of the HIV-1 dimerization initiation site in the kissing-loop dimer. [7] In HIV, the psi element is around 80–150 nucleotides in length, and located at the 5' end of the genome just upstream of the gag initiation codon. [8]
Two types of HIV have been characterized: HIV-1 and HIV-2. HIV-1 is the virus that was initially discovered and termed both lymphadenopathy associated virus (LAV) and human T-lymphotropic virus 3 (HTLV-III). HIV-1 is more virulent and more infective than HIV-2, [20] and is the cause of the majority of HIV infections globally. The lower ...
Other therapies target the Rev protein itself, since it is an essential component of HIV-1 infection. M10 is a mutated form of Rev and has a single amino acid substitution (Aspartic acid to Leucine). If delivered to cells, Rev M10 will compete with the wild-type Rev protein for the RRE binding site, and therefore decrease Rev's normal cellular ...
The Vpu gene is found exclusively in HIV-1 and some HIV-1-related simian immunodeficiency virus isolates, such as SIV cpz, SIV gsn, and SIV mon, but not in HIV-2 or the majority of SIV isolates. [3] Structural similarities between Vpu and another small viral protein, M2, encoded by influenza A virus were first noted soon after the discovery of Vpu.
After the virus enters the body there is a period of rapid viral replication, leading to an abundance of virus in the peripheral blood. During primary infection, the level of HIV may reach several million virus particles per milliliter of blood. [2] This response is accompanied by a marked drop in the numbers of circulating CD4 + T cells.
HIV-1 is the most common and most pathogenic strain of the virus. As of 2022, approximately 1.3 million such infections occur annually. [4] [5] Scientists divide HIV-1 into a major group (group M) and two or more minor groups, namely groups N, O and possibly a group P.