Dynamics of HIV-1 coinfection in different susceptible target cell populations during cell-free infection.

HIV-1 mutations rapidly accumulate through genetic recombination events, which require the infection of a single cell by two virions (coinfection). Accumulation of mutations in the viral population may lead to immune escape and high-level drug resistance. The existence of cell subpopulations characterized by different susceptibility to HIV-1 infection has been proposed as an important parameter driving coinfection (Dang et al.

Number of infection events per cell during HIV-1 cell-free infection.

HIV-1 accumulates changes in its genome through both recombination and mutation during the course of infection. For recombination to occur, a single cell must be infected by two HIV strains. These coinfection events were experimentally demonstrated to occur more frequently than would be expected for independent infection events and do not follow a random distribution.

Identification of protein interfaces within the multi-aminoacyl-tRNA synthetase complex: the case of lysyl-tRNA synthetase and the scaffold protein p38.

Human cytoplasmic lysyl-tRNA synthetase (LysRS) is associated within a multi-aminoacyl-tRNA synthetase complex (MSC). Within this complex, the p38 component is the scaffold protein that binds the catalytic domain of LysRS via its N-terminal region. In addition to its translational function when associated to the MSC, LysRS is also recruited in nontranslational roles after dissociation from the MSC.

Kinetics of the establishment of HIV-1 viral interference and comprehensive analysis of the contribution of viral genes.

Viral interference defines the reduced susceptibility of an infected cell to reinfection. For HIV-1, both receptor-dependent and independent pathways were described. The relative importance of different receptor-independent pathways has not been addressed.