HIV virion

HIV virion

Virology A virion with a 100 nm in diameter lipid envelope surrounding a dense cylindrical nucleoid containing core proteins, reverse transcriptase and a genome with sequence similarity to non-cell-transforming lentiviridae–eg, visna and caprine encephalitis viruses; envelope proteins gp41, gp120; nucelocapsid proteins p24, p17, p9, p7
References in periodicals archive ?
HIV protease plays an important role in the cleavage of long polyprotein at Gag and Gag-Pol sites into the proper protein-sized pieces to create the mature protein components of an infectious HIV virion [14].
These data may suggest a possible role for antigenic stimulation directly by the HIV virion or other antigens in the pathogenesis of plasma-cell neoplasms in HIV-associated cases, and may indicate a causative role for HIV or an HIV-associated infection in MM.
The role of coinfection by HIV in the transformed cells of this case is unclear Some authors have reported increased HIV virion expression in cells infected by EBV.
HIV has previously been detected in the urine of HIV+ patients; however, it was shown that HIV virions are associated with cell pellets and not in centrifuged urine [50, 51].
In HIV, mathematical models have provided a framework for understanding the viral dynamics and have been used in the optimal allocation of the various interventions against the HIV virions [2-4].
Ogunlaran and Oukouomi Noutchie [11] analyzed a three-dimensional model, which included the [CD4.sup.+] T-cells, the infected [CD4.sup.+] T-cells, and the HIV virions. This study was more interested in establishing how to maximize the number of the infected cells after introduction of ARTs.
The Nef favors the intrinsic infectivity of HIV virions necessary for the full deployment of virus infectivity.
This protein is also considered an HIV protein inactivator because it was proved to inactivate free HIV virions. Furthermore, the 2DLT protein bound specifically with gp120 and gp41 on the surface of HIV-1 virions and destabilized the gp41 prehairpin fusion intermediate induced by CD4 domains, thereby significantly reducing sCD4-mediated enhancing effects on HIV-1 infection and providing a new solution for CD4-induced infection.
However, opposite data were also reported: overexpression of peroxide-scavenging enzyme, GPx1, enhances production of HIV virions, whereas treatment of such cells with buthionine sulfoximine (BSO) that inhibits glutathione biosynthesis inhibits such increase [158].
The second theory of entry postulates that HIV virions in the blood physically penetrate the BBB at the tight junctions of the basement membrane and cross freely into the CNS to infect local microglial cells that also differentiate into macrophage and, further, HIV infection and replication (Ghafouri et al., 2006; Strazza, Pirrone, Wigdahl, & Nonnemacher, 2011).
(2) HIV virions and virion-infected cells cross epithelial barriers of the genital tract within a matter of hours, remain in the submucosa for three to six days where they may infect WBCs, then rapidly disseminate via draining lymphatics and establish CD4 T-cell viral reservoirs.
But HIV virions do not allow for that possibility because the gp160 spikes are too far apart.