After SIV infection, plasma viral loads, as well as viral loads in tissues (brain, liver, spleen) in alcohol-consuming animals did not differ than controls, who were fed just the orange solution without alcohol. However, alcohol consumption did significantly increase the viral load in the CSF. Furthermore, when looking at inflammatory cytokines and lymphocyte subsets, the authors found that alcohol decreased IFN-alpha, CD4 T cells, and NK cells in the brain, suggesting that alcohol may dampen the immune response to the virus in the brain. As SIVmac251 is known to infect the CNS, this data suggests that chronic alcohol may increase the susceptibility of the CNS to HIV infection and further complications, such as HIV encephalitis. However, as actual brain tissue did not show increased viral load, a definitive link between alcohol and CNS HIV infection/complications needs to researched.
The authors followed monocytes and macrophages (another population of immune cells susceptible to HIV infection; CD14+CD16low and CD14+CD16+, respectively) as well and found them to be decreased at 7 dpi in the alcohol-consuming population. In addition, looking more specifically, in the blood these monocytes and macrophages had increased expression of CCR5 (a coreceptor frequently used by HIV/SIV), CD44v6 (an adhesion molecule correlated to brain-inflammatory HIV/SIV), and CCR2 (a chemokine receptor linked to monocyte infiltration and cognitive decline). Correspondingly, they found that tissue macrophages had increased CCR5 and CD44v6 expression in the liver and brain, respectively. This reaffirms the author's suspicion that alcoholism can induce vulnerability to HIV/SIV infection in certain microenvironments within the body.
By simulating HIV infection in macaques that consume alcohol chronically in similar quantities as seen in human consumption, Marcondes et al have found results that support the notion that alcoholism can increase susceptibility to HIV infection. Mainly they found that inflammatory cytokines and lymphocyte subsets were altered, especially in brain, where they were decreased. This could perhaps mean more CNS involvement during HIV infection in chronic alcohol abusers. They found CD4 T cells (central and effector memory) were decreased in SIV+EtOH animals, suggesting that perhaps HIV killing of these cells were more efficient when alcohol was present. They also found that CCR5, one of the HIV coreceptors, was upregulated in monocytes and macrophages, suggesting that alcohol perhaps made these cells more vulnerable to HIV/SIV infection. However, the results presented in this paper need to be taken with a grain of salt. Although they found altered lymphocyte populations, overall viral load in the blood and in the tissues were no different in the alcohol consuming condition; in addition, results were mixed for other tissues such as the spleen, liver, LN, etc. It is also important to differentiate the alterations in lymphocyte populations with their role in HIV infection. A decrease in lymphocyte population may not necessarily suggest more vulnerability but rather more killing. An increase in inflammatory cytokines/lymphocytes in peripheral blood may mean a better immune response to HIV infection, but in the brain it may have negative consequences (e.g. encephalitis, leading to cognitive decline). Overall, while this study has shown somewhat mixed results for different tissues, these authors have been able to show that alcohol does have negative effects on the immune response during SIV/HIV infection, although the extent to which alcohol effects viremia and conversion to AIDS (in general HIV progression), and HIV encephalitis, needs to be studied further. Nevertheless, we can add vulnerability to HIV to the long list of reason to avoid alcohol abuse; this is very pertinent to those young persons undergoing secondary education who, by most parameters, qualify for chronic alcoholism. wink.
Marcondes, M. C. G., Watry, D., Zandonatti, M., Flynn, C., Taffe, M. A. and Fox, H. (2008), Chronic Alcohol Consumption Generates a Vulnerable Immune Environment During Early SIV Infection in Rhesus Macaques. Alcoholism: Clinical and Experimental Research, 32: 1583–1592.
, , , , () . : –
Grant, B. F. (1994), Alcohol consumption, alcohol abuse and alcohol dependence. The United States as an example. Addiction, 89: 1357–1365.
Molina, P. E., McNurlan, M., Rathmacher, J., Lang, C. H., Zambell, K. L., Purcell, J., Bohm, R. P., Zhang, P., Bagby, G. J. and Nelson, S. (2006), Chronic Alcohol Accentuates Nutritional, Metabolic, and Immune Alterations During Asymptomatic Simian Immunodeficiency Virus Infection. Alcoholism: Clinical and Experimental Research, 30: 2065–2078.
, , , (). . :–.