To the Editor: Two recent articles by Moulignier et al.1 and MacGowen et al.2 present clinical and laboratory evidence of a probable increased incidence of ALS in patients infected by human immunodeficiency viruses (HIV)-1 and HIV-2. Several possible mechanisms were suggested including direct neuronal damage, disease due to cytokine production and autoimmunity. The fact that symptoms and signs of ALS improved with antiretroviral therapy implied that the effect was specifically on HIV-induced disease. However, Kaposi’s sarcoma (KS), which now appears almost certainly to be due to human herpesvirus-8 (HHV-8), also often disappears with antiretroviral therapy. It is of more than passing interest that up to 35% of homosexual men with the acquired immunodeficiency syndrome demonstrate antibodies to HHV-8,3 whereas they are present in less than 4% of US blood donors.3 We have recently had an opportunity to study HHV-8 antibody levels in five non-HIV+ patients with ALS. Two of the five patients were women, one was black, and all five had associated medical disorders including monoclonal gammopathy, lymphoma of the lung, scleroderma, osteoarthritis, and hyperlipidemia. Their ages ranged from 70 to 81 years. Three ultimately died from aspiration pneumonia. Antibody titers as measured by indirect immunofluorescence using the BCP-1 cell line4 were positive in all patients and ranged from 1:20 to 1:60. HHV-8 in blood by PCR was identified in only one patient. The presence of HHV-8 antibody in all of our patients in this small study would suggest that this may also be the case in patients with …
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Cone et al. (2002) studied this question.
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