Chronic alcohol consumption generates a vulnerable immune environment during early SIV infection in rhesus macaques

Alcohol consumption is a common problem in HIV-infected individuals, and the effects of alcohol may alter the efficiency of the immune response, potentially aggravating the disease as well as affecting end organs, such as the brain. However, the elements of the virus-host interaction that are modulated by ethanol are poorly dissected.

Ethanol intake was conditioned in rhesus macaques prior to SIV infection, in order to mimic this common human behavior, and allow the evaluation of aspects of the virus-immune system interactions during acute time-points, when important facets of the infection are set up and when virus reproducibly enters the brain.

Although ethanol had a limited effect on the acute plasma viral load, it resulted in reduced circulating memory CD4(+) T cells and increased levels of monocytes expressing the viral coreceptor CCR5. In organs, ethanol consumption impacted immune cells in the liver as well as lymphoid and other nonlymphoid tissues, where CD4(+) T cells were predominantly affected.

Overall, the consumption of alcohol causes immune cell alterations that can contribute to the generation of a disease susceptible environment upon SIV infection.