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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.
P24 is a structural protein that plays a crucial role in the formation and stability of the viral capsid, which protects the viral RNA. p24 capsid protein's roles in the HIV replicative process are summarized as follows: [citation needed] Fusion: HIV replication cycle begins when HIV fuses with the surface of the host cell.
A negative result rules out HIV exposure, while a positive one must be followed by an HIV-1/2 antibody differentiation immunoassay to detect which antibodies are present. This gives rise to four possible scenarios: 1. HIV-1 (+) & HIV-2 (−): HIV-1 antibodies detected; 2. HIV-1 (−) & HIV-2 (+): HIV-2 antibodies detected; 3.
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.
The p24 capsid protein (CA) is a 24 kDa protein fused to the C-terminus of MA in the unprocessed HIV Gag polyprotein. After viral maturation, CA forms the viral capsid. CA has two generally recognized domains, the C-terminal domain (CTD) and the N-terminal domain (NTD). The CA CTD and NTD have distinct roles during HIV budding and capsid structure.
Nucleic-acid-based tests amplify and detect one or more of several target sequences located in specific HIV genes, such as HIV-I GAG, HIV-II GAG, HIV-env, or the HIV-pol. [33] [34] Since these tests are relatively expensive, the blood is screened by first pooling some 8–24 samples and testing these together; if the pool tests positive, each ...
HIV-1 protease labelled according to its resemblance to an English Bulldog or a fat cat. [7] The blue and cyan-green ribbons depict the peptide backbone of a wild-type ( ) and a mutant ( ) structure, respectively. Mature HIV protease exists as a 22 kDa homodimer, with each subunit made up of 99 amino acids. [1]
These studies found that >95% of CD4 T cells die because of abortive HIV infection. [9] These dying cells are resting and thus are nonpermissive for productive HIV infection. Full viral replication was limited to the ~5% of activated CD4 T cells present in these tissues; these cells die by apoptosis. [10]