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Alcohol and Alcoholism Vol. 37, No. 2, pp. 157-163, 2002
© 2002 Medical Council on Alcohol

ALCOHOL CONSUMPTION DURING MURINE ACQUIRED IMMUNODEFICIENCY SYNDROME ACCENTUATES HEART PATHOLOGY DUE TO COXSACKIEVIRUS

R. Tomás Sepúlveda1,2, Shuguang Jiang1, David G. Besselsen3 and Ronald R. Watson1,*

1 College of Public Health,
2 Microbiology and Immunology, College of Medicine and
3 University Animal Care, University of Arizona, Tucson, Arizona, USA

Received 23 July 2001; first review notified 4 September 2001; accepted 1 October 2001

Alcohol, especially after prolonged and excessive consumption, results in marked alteration of host immunity and increased susceptibility to infection. To determine whether ethanol consumption exacerbates coxsackievirus B3 cardiomyopathy during murine acquired immunodeficiency syndrome (AIDS), female C57BL/6 mice were infected with LP-BM5 retrovirus and administered 40% ethanol both in water and in solid agar-based form. Cardiac histopathology was semi-quantitatively assessed for lesion severity and induced production of splenocyte: interleukin (IL)-2, IL-4, IL-6, tumour necrosis factor-{alpha} and interferon-{gamma} were determined. Ethanol consumption during murine retrovirus infection increased coxsackievirus-induced myocarditis in 85% of the animals and also exacerbated the lesion severity. Mice infected with retrovirus and co-infected with coxsackievirus showed significant heart lesions. Retrovirus infection suppressed Th1 responses, causing cytokine dysregulation and immunosuppression, which facilitated coxsackievirus-induced myocarditis. Our data suggest that ethanol consumption heightens the cytokine imbalance to favour a Th2 response by enhancing Th2 and/or by suppressing Th1 function. In conclusion, murine AIDS facilitated severe cardiotoxicity during coxsackievirus infection, while non-retrovirus-infected mice were resistant. These effects were accentuated by ethanol consumption.


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