Researchers identify new cause of inflammation in HIV patients
According to the study, after infection, HIV becomes a part of an infected person's DNA forever, and in most cases, infected cells are silent and do not replicate the virus.
New York: In a major study, researchers have identified the important factors which could be contributing to the chronic inflammation in people living with HIV.
While current antiretroviral treatments for HIV are highly effective, data has shown that people living with HIV appear to experience accelerated aging and have shorter lifespans — by up to five to 10 years — compared to people without HIV.
These outcomes have been associated with chronic inflammation, which could lead to the earlier onset of age-associated diseases, such as atherosclerosis, cancers, or neurocognitive decline.
The research team examined what factors could be contributing to this inflammation, and identified the inability to control HIV RNA production from existing HIV DNA as a potential key driver of inflammation.
Published in The Journal of Infectious Diseases, the results underscore the need to develop new treatments targeting the persistent inflammation in people living with HIV in order to improve outcomes.
According to the study, after infection, HIV becomes a part of an infected person’s DNA forever, and in most cases, infected cells are silent and do not replicate the virus.
Occasionally, however, RNA is produced from this HIV DNA, which is a first step towards virus replication.
Antiretroviral treatments help prevent HIV and AIDS-related complications, but they do not prevent the chronic inflammation that is common among people with HIV and is associated with mortality.
“Our study set out to identify a possible association between HIV latently infected cells with chronic inflammation in people with HIV who have suppressed viral loads,” said study author Nina Lin from the Boston University in the US.
For this study, researchers had a cohort of 57 individuals with HIV who were treated with antiretroviral therapy.
They compared inflammation in the blood and various virus measurements among younger (age less than 35 years) and older (age greater than 50 years) people living with HIV.
They also compared the ability of the inflammation present in the blood to activate HIV production from the silent cells with the HIV genome.
Their results suggest that an inability to control HIV RNA production even with antiretroviral drugs correlates with inflammation.
“Our findings suggest that novel treatments are needed to target the inflammation persistent in people living with HIV,” said the study authors
‘Current antiretroviral drugs prevent new infection, but they do not prevent HIV RNA production, which our results point as a potential key factor driving inflammation in people living with HIV,” they noted.
