Monkeys exposed to alcohol have higher SHIV viral load

Macaques infected with the simian immunodeficiency virus and exposed to alcohol in their drinking water had significantly higher SHIV viral load after 18 to 24 weeks of alcohol exposure, according to findings from a small study published in the August 1^st edition of the Journal of Acquired Immune Deficiency Syndromes.

Several test tube studies have shown that HIV replication can be increased in the presence of alcohol, but evidence from human studies is less clearcut, and a large prospective study in injecting drug users found no effect of alcohol consumption on disease progression.

In the light of such contradictory evidence, researchers at San Juan University, Puerto Rico, USA, designed a study in which adult rhesus macaques were acclimatised to alcohol consumption over a seven week period before being infected with a mixture of SHIV (a form of HIV adapted for experimental purposes to cause AIDS in macaques) and a simian immunodeficiency virus known to replicate well in the brain. The mixture of viruses was designed to cause disease progression in a relatively short time.

The researchers then measured SHIV viral load and CD4 cell counts over the following 24 weeks in three macaques exposed to alcohol and three macaques also infected but not exposed to alcohol.

One week after infection the monkeys that received alcohol had lost significantly more CD4 cells (P=0.03), the key marker of the immune system’s health. However, the difference in CD4 cell counts narrowed over time and by week 16 this difference was no longer significant.

In contrast, monkeys that received alcohol did not show early differences in viral load from the control group, but as time went on levels of viral replication became significantly greater. By week 24 viral load was 89-fold higher (almost 1.9log₁₀ copies/ml) in the three macaques that received alcohol. SIV levels in the cerebrospinal fluid also began to diverge after eight weeks – although it became undetectable in the control group, viral replication in the CSF continued to be detectable throughout the follow-up period in the alcohol group.

The alcohol exposure was designed to mimic the effects of chronic binge drinking each day, but it should be noted that after week 1 of the study macaques were deprived of alcohol-free drinking water overnight and could only drink an alcohol-containing sweet drink for the first three hours of the following day, effectively compelling the animals to consume some alcohol each day.

This exposure is the equivalent of the United States' definition of binge drinking – five alcoholic drinks within the space of two hours. In the United Kingdom binge drinking is defined as eight units of alcohol (two thirds of a bottle of wine or four pints of beer) consumed in one 24 hour period. This level of alcohol consumption would not be considered unusual in the British Isles, eastern Europe, Australia or southern Africa, especially among men. The UK’s Institute of Alcohol Studies reported in 2004 that 40% of drinking occasions reported by British men in a 15 country survey of drinking patterns could be described as binge drinking, compared with 9% in France.

The authors say that they believe alcohol has a direct effect on HIV replication as well as an indirect effect on the immune system, but it is not possible to say at this stage whether the alcohol-consuming monkeys will develop disease more quickly, and longer term follow-up is needed. However, the authors do speculate that the alcohol group may be at higher risk for HIV-related encephalitis and other brain disorders as a result of higher level of HIV replication in the CSF of these animals.

At this stage the authors are careful not to overstate the implications of their findings, and make no reference to implications for humans infected with HIV.