Waterborne Outbreak of Microsporidiosis

host cellular immune response among HTLV-I carriers. In data published elsewhere, we documented subclinical immunosuppression on the basis of the association of HTLV-I infection with reduced response to the tuberculin-purified protein derivative (PPD) recall antigen [3, 4]. In vitro studies suggest that the nonresponsiveness to PPD in these HTLV-I carriers may be related to a lack of IFN-g production [5]. Other investigators reported evidence of altered cellular immune function in asymptomatic HTLV-I carriers [6, 7]. Unpublished data from the Miyazaki Cohort Study indicate a possible negative interaction between HTLV-I and HCV with respect to abnormal levels of alanine aminotransferase (ALT), with the prevalence of elevated ALT levels being lower in coinfected subjects than in subjects with HCV infection alone. Other researchers in Japan reported a similar effect of coinfection on ALT levels [8]. We postulate that coinfection with HTLV-I could reduce the acute immune-mediated damage to HCV-infected hepatocytes and the release of ALT while at the same time enhancing the persistence of HCV infection and the subsequent risk of liver disease development. However, HCV infection itself could cause liver cancer without the induction of chronic hepatitis, as has been observed in transgenic mice [9]. In addition, we found that HCV coinfection increased the association of HTLV-I with diminished PPD response, although HCV seropositivity itself was not related to the lack of PPD reactivity [10]. As suggested by Dr. Casseb [1], it also is possible that increased cytokine levels play a role in HCV-associated disease progression in HTLV-I carriers. Woitas et al. [11] noted an increased induction of IL-2 and IFN-g among patients with HCV and human immunodeficiency virus infections but not among patients with HCV alone. The effect of HTLV-I infection on host immunity in general and on HCV-specific immune response is likely a complicated one. It seems clear that HTLV-I induces dysregulation of cellular immune function. However, to characterize this effect as either immunosuppressive or immune stimulatory, with respect to the natural history of HCV coinfection, may be overly simplistic.