Background:  Long-term alcohol abuse is known to suppress the immune system, resulting in increased viral and bacterial infections of the host. Studies have indicated that 60% of patients infected with HIV-1 abuse alcohol. However, the exact relationship between long-term alcohol abuse and viral neuroinvasion is currently unknown. 

Methods:  We allowed 7 macaques to voluntarily drink ethanol daily for a total of 9 months, and a group of macaques was maintained on a diet lacking ethanol. Macaques were then inoculated with pathogenic simian/human immunodeficiency virus (SHIV) for 2 weeks followed by full necropsies. The macaque brains were examined by immunohistochemistry for disruption of the blood-brain barrier (BBB), astrocytosis, and microglial activation. The presence of viral sequences and viral loads in central nervous system regions and visceral tissues were measured by polymerase chain reaction methods. 

Results:  Our results indicate that viral loads in the central nervous system were similar in the control and in the alcohol-treated group. Previously, we showed that, following inoculation with a pathogenic SHIV, there is a transient disruption of the BBB and astrocytosis. Our results indicate that while BBB disruption occurred in both groups of macaques, it was more extensive in those macaques that were permitted to consume alcohol. Astrocytosis and the level of microglial activation were similar in those macaques that were permitted to consume ethanol and the control group of macaques. 

Conclusions:  Taken together, these results indicate that long-term ethanol consumption leads to more extensive BBB disruption during the primary phase of infection.