HIV-1 proviruses may drive chronic systemic inflammation

HIV-1 proviruses may be responsible for driving chronic systemic inflammation in people living with HIV, according to a study by researchers at Boston University's Chobanian & Avedisian School of Medicine. The study, published in the Journal of Virology, suggests that persistent hidden HIV proviruses contribute to inflammation even when antiviral treatments control the expression and spread of the virus.

HIV attacks the body's immune system and remains a global health challenge due to persistent viral reservoirs. Around 40 million people are living with HIV, with 1 million new infections each year. Some HIV proviruses hide in cells and avoid both medicines and the immune system, creating a permanent viral reservoir that prevents complete cures.

People with HIV are at higher risk of developing inflammatory diseases in various tissues, including the brain, heart, intestine, and immune tissues, even while on antiviral treatments that control HIV.

In this study, the researchers used CRISPR technology to create cells with defective HIV viruses, preventing them from normally expressing HIV. They then compared these cells with cells containing normal HIV and measured markers of inflammation. The cells with modified, defective HIV showed increased inflammation markers. This suggests that persistent defective HIV-1 proviruses may play a role in chronic inflammation and immune dysfunction, even in people with suppressed viral expression due to antiretroviral therapy.

The researchers believe their findings could have implications for understanding the persistent inflammation observed in people with HIV, particularly as this population lives longer. Additionally, the study may provide insights into general mechanisms contributing to inflammation associated with autoimmunity or aging. These findings could also inform strategies for HIV cure efforts and targeting the persistent HIV reservoir.