Abstract
The association between mucosal microbiota and HIV-1 infection has garnered great attention in the field of HIV-1 research. Previously, we reported a receptor-independent HIV-1 entry into epithelial cells mediated by a Gram-negative invasive bacterium, Porphyromonas gingivalis. Here, we present evidence showing that P. gingivalis outer membrane vesicles (OMVs) promote mucosal transmission of HIV-1. We demonstrated, using the Dynabeads technology, a specific interaction between HIV-1 and P. gingivalis OMVs which led to an OMV-dependent viral entry into oral epithelial cells. HIV-1 was detected in human oral keratinocytes (HOKs) after a 20 minute exposure to the HIV-vesicle complexes. After entry, most of the complexes appeared to dissociate, HIV-1 was reverse-transcribed, and viral DNA was integrated into the genome of HOKs. Meanwhile, some of the complexes exited the original host and re-entered neighboring HOKs and permissive cells of HIV-1. Moreover, P. gingivalis vesicles enhanced HIV-1 infection of MT4 cells at low infecting doses that are not able to establish an efficient infection alone. These findings suggest that invasive bacteria and their OMVs with ability to interact with HIV-1 may serve as a vehicle to translocate HIV through the mucosa, establish mucosal transmission of HIV-1, and enhance HIV-1 infectivity.
Highlights
The human immunodeficiency virus (HIV)/AIDS pandemic continues to be a major global health problem, as millions of people worldwide are currently living with HIV/AIDS1
We previously reported that HIV-1 binds to the surface of P. gingivalis through the interaction between the binding domains (HGP17 and HGP44) of gingipains and HIV-1 gp12010
We speculated that P. gingivalis may serve as a vehicle for carrying HIV-1 into cells that are non-permissive to HIV, such as oral epithelial cells
Summary
The human immunodeficiency virus (HIV)/AIDS pandemic continues to be a major global health problem, as millions of people worldwide are currently living with HIV/AIDS1. Mucosal dendritic cells may facilitate HIV entry through the epithelium by capturing cell-free- or cell-associated HIV-1 using their extending dendrites within the epithelial layers. Mirmonsef and Spear showed that lower levels of Lactobacillus in the genital tract are associated with an increased risk of acquiring HIV-1 and female-to-male transmission[6] Another example is that Porphyromonas gingivalis, an invasive bacterium usually found in the oral cavity may play a role in HIV-1 transmission. We further examined the ability of P. gingivalis vesicles to promote HIV-1 entry into and spreading among human oral keratinocytes (HOKs) as well as HIV-1 permissive cells. These findings provide insights into the potential mechanisms of mucosal HIV-1 transmission
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