Abstract
Tuberculosis (TB) is the leading cause of death among HIV-1-infected individuals and Mycobacterium tuberculosis (Mtb) co-infection is an early precipitate to AIDS. We aimed to determine whether Mtb strains differentially modulate cellular susceptibility to HIV-1 infection (cis- and trans-infection), via surface receptor interaction by their cell envelope lipids. Total lipids from pathogenic (lineage 4 Mtb H37Rv, CDC1551 and lineage 2 Mtb HN878, EU127) and non-pathogenic (Mycobacterium bovis BCG and Mycobacterium smegmatis) Mycobacterium 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 cis- and trans-infection of TZM-bl cells using single-cycle infectious virus particles. Mtb glycolipids did not affect HIV-1 direct infection however, trans-infection of both R5 and X4 tropic HIV-1 strains were impaired in the presence of glycolipids from M. bovis, Mtb H37Rv and Mtb 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 trans-infection. These findings indicate that variant strains of Mtb have differential effect on HIV-1 trans-infection with the potential to influence HIV-1 disease course in co-infected individuals.
Highlights
We investigated the influence of Mycobacterium tuberculosis (Mtb) lipids on HIV-1 trans-infection via binding the dendritic cells (DCs)-SIGN receptor using the same in vitro system of pseudo-typed virus particles that allows a single-round of infection
We investigated the role of Mycobacterium lipid extracts presented via liposomes monocyte derived dendritic cells (mDCs) and further used to mediate HIV-1 trans-infection to TZM-bl in the presence of on influencing HIV-1 cis- and trans-infection
Observed efficiency of virus generated liposomes containing extract antigenwe from variant variant pathogenic
Summary
Human immunodeficiency virus type 1 (HIV-1) and Mycobacterium tuberculosis (Mtb) co-infection results in a loss of numerous immunological functions and leads to death when not treated. In the case of HIV-1, numerous cells of the immune system, including dendritic cells, can bind and capture HIV-1 via an array of C-type lectins expressed on the cell surface. Binding promotes the capture, processing and subsequent presentation of HIV-1 antigen to other cells of the immune system but can result in the capture and transfer of HIV-1 virions to susceptible cells, a mechanism termed trans-infection [6,7,8,9]. Different receptors have been described to be involved with trans-infection, such as the mannose receptor MR [6,10,11] and the C-type lectin receptor DC-SIGN [12,13,14,15], alongside Siglec via interactions with ganglioside GM3 localised on the virus membrane [16,17,18,19,20]
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