Researchers find byproducts of bacteria in gum disease activate HIV in dormant T-cells

January 7, 2015

Researchers at Case Western Reserve University in Cleveland have found a critical reason to treat periodontal disease as soon as possible.

Researchers at Case Western Reserve University in Cleveland have found a critical reason to treat periodontal disease as soon as possible.

In a recent study, they discovered the byproducts of bacteria in gum disease, called metabolic small chain fatty acid (SCFA), can work together to activate HIV in dormant T-cells, causing the virus to replicate.

The findings help explain why people with HIV infections and periodontal disease have higher levels of the virus in their saliva than patients with healthy gums. The researchers, Fengchun Ye, assistant professor in the Department of Biological Sciences, and Jonathan Karn, Reinberger professor of microbiology and director of the Case Center for AIDS Research, think byproducts from other bacteria infections in other diseases might change gene expression using similar mechanisms.

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For dental patients with HIV, these findings also show the importance of treating bacterial infections in gum disease early. In the interaction between gum disease and HIV, five SCFA byproducts from two common oral bacteria-Porphyromonas gingivalis (Pg) and Fusobacterium nucleatum (Fn)-activate resting immune T-cells carrying the inactive HIV-1 virus. Ye and Karn describe the process like jumper cables attached to a live battery to recharge a dead one.

The researchers explained humans have a reservoir of resting T-cells that activate and respond to inflammation to ward off an infection in the body. In a healthy person, the reservoir remains untapped. However, in people with HIV, these T-cells can also have the sleeper HIV-1 virus, which remains dormant until activated.

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HIV antiviral therapy prevents active HIV cells from replicating and doesn't affect the quiet viruses in sleeping T-cells. As long as the patient is free of gum disease, the virus sleeps and remains dormant.

The study, "Short chain fatty acids potently induce latent HIV-1 in T-cells by activating P-TEFb and multiple histone modifications," was published in the journal Virology.

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