Abstract
The host immune response, in addition to viral factors, is the critical determinant of the pathological consequences of hepatitis C virus infection. Current therapies for genotype 1 are unsuccessful in a substantial number of patients. Histamine dihydrochloride by virtue of its histamine H2 agonistic activity, has the potential to prevent damage induced by oxidative stress in tissues and can protect T and natural killer lymphocytes from oxygen radical-induced functional inhibition and apoptosis, thereby, potentiating interferon-α-induced activation of these cells. Coadministration of histamine dihydrochloride and interferon therapy for chronic hepatitis C virus infection was tested in several clinical trials. However, conflicting data and the relatively small numbers of patients enrolled, suggest that this combination should be the focus of further investigation.
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