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Tuberculosis (TB) is the leading cause of death among HIV-1-infected individuals and <i>Mycobacterium tuberculosis</i> (<i>Mtb</i>) co-infection is an early precipitate to AIDS. We aimed to determine whether <i>Mtb</i> strains differentially modulate cellular susceptibility to HIV-1 infection (<i>cis</i>- and <i>trans</i>-infection), via surface receptor interaction by their cell envelope lipids. Total lipids from pathogenic (lineage 4 <i>Mtb</i> H37Rv, CDC1551 and lineage 2 <i>Mtb</i> HN878, EU127) and non-pathogenic (<i>Mycobacterium bovis</i> BCG and <i>Mycobacterium smegmatis</i>) <i>Mycobacterium</i> strains were integrated into liposomes mimicking the lipid distribution and antigen accessibility of the mycobacterial cell wall. The resulting liposomes were tested for modulating in vitro HIV-1 <i>cis</i>- and <i>trans</i>-infection of TZM-bl cells using single-cycle infectious virus particles. <i>Mtb</i> glycolipids did not affect HIV-1 direct infection however, <i>trans</i>-infection of both R5 and X4 tropic HIV-1 strains were impaired in the presence of glycolipids from <i>M. bovis</i>, <i>Mtb</i> H37Rv and <i>Mtb</i> EU127 strains when using Raji-DC-SIGN cells or immature and mature dendritic cells (DCs) to capture virus. SL1, PDIM and TDM lipids were identified to be involved in DC-SIGN recognition and impairment of HIV-1 <i>trans</i>-infection. These findings indicate that variant strains of <i>Mtb</i> have differential effect on HIV-1 <i>trans</i>-infection with the potential to influence HIV-1 disease course in co-infected individuals.