HIV takes advantage of certain human cells in the reproductive and intestinal tracts to infect CD4 immune cells and spread through the body. This finding could help researchers develop new HIV prevention methods.
Publishing their findings in PLOS Pathogens, researchers used an experimental model of the mucosa and surrounding tissues to study how HIV evades the body’s defenses against infection.
A protective layer of cells known as the mucosa coats the reproductive and intestinal tracts in humans. Breaches in the mucosa—as a result of physical trauma or certain sexually transmitted infections—can permit HIV to pass through and access the immune cells it targets for infection.
The researchers found that highly prevalent connective-tissue cells in the mucosa called fibroblasts add a considerable boost to HIV’s ability to infect immune cells. HIV piggybacks on fibroblasts, which transport the virus to immune cells without themselves becoming infected. The investigators also found that fibroblasts make immune cells more prone to infection, although exactly how is unclear at this point. The scientists hope their further research will shed light on this mystery and identify a new target for HIV prevention methods.
Looking at mucosal fibroblasts from the common sites of initial HIV infection, including the cervix, uterus, foreskin, male urethra and intestines, the scientists found that fibroblasts from all these tissues facilitated HIV infection.
The researchers also studied epithelial cells, which line the mucosa and provide a barrier against pathogens while admitting desirable substances. These cells secreted considerable amounts of antiviral proteins that warded against HIV infection.
Considering the collective findings about fibroblasts and epithelial cells, the researchers believe that HIV infection may be facilitated by breaches in the outer layer of epithelial cells. This exposes the fibroblast cells to HIV, which uses those cells as a means of transport to CD4 cells.
To read a press release about the study, click here.
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