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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.
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 ...
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.
This viral DNA is sensed by gamma-interferon-inducible protein 16 , [11] which produces an innate immune response against the virus by activating caspase 1 in IFI16 inflammasomes and inducing pyroptosis, a highly inflammatory form of programmed cell death. [12] [13] These findings cast CD4 T-cell death during HIV infection in a different light.
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]
SARS-CoV-2 and HIV-1 have similarities—notably both are RNA viruses—but there are important differences. As a retrovirus, HIV-1 can insert a copy of its RNA genome into the host's DNA, making total eradication more difficult. [156] The virus is also highly mutable making it a challenge for the adaptive immune system to develop
Upon entry into the host cell cytoplasm, the HIV-1 capsid is recognized and bound by cyclophilin A (CypA); this affinity interaction stabilizes the capsid and prevents exposure of the HIV-1 cDNA to pattern recognition receptors in the cytoplasm. This shielding allows the HIV-1 cDNA to translocate to the nucleus where it may begin replication. [7]
Diagram of an HIV virion structure Scanning electron micrograph of HIV-1, colored green, budding from a cultured lymphocyte HIV is the cause of the spectrum of disease known as HIV/AIDS. HIV is a retrovirus that primarily infects components of the human immune system such as CD4 + T cells, macrophages and dendritic cells .