HBV replication status, as measured by the HBV DNA polymerase (DNA-p) activity, has been shown to affect the HCV RNA titer. This represents reciprocal viral suppression of HCV by HBV, but the mechanism that governs this interaction remains speculative. HCV RNA in serum was detected less frequently in patients with highly replicating HBV (DNA-p >100 cpm). Higher titers of HCV RNA were measured in those with low-replicating HBV (DNA-p <100 cpm). HCV RNA titers in co-infected patients with DNA-p <100 cpm were still lower than those in patients with anti-HCV but without HBsAg (8). In an in vitro co-transfection experiment, wild-type HBV DNA was shown to suppress the secretion of HCV RNA. However, co-transfection of HCV RNA with the HBV DNA silent mutant, (i.e., HBV DNA with eight-nucleotide deletion in the region encoding the X gene) resulted in the release of higher levels of HCV RNA (14).
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