In addition, the data provide the first evidence that, like the antibody response, T-cell priming by previous exposure to HCV does not prevent infection by homologous virus. These observations suggest that HBV may be susceptible to similar regulatory processes during natural infection. I, in addition to the conventional immune-mediated destruction of infected cells. We do not know, however, if these cytokines are the final mediators in this system or if other downstream factors are involved. Nitric oxide is a highly unstable product of l-arginine metabolism that exerts a wide variety of biological functions, including antiviral activities, in a paracrine and autocrine fashion.
Nitric oxide is produced by distinct categories of nitric oxide synthase isoforms.
The constitutive forms are present in many different cell types, including endothelial and neuronal cells, that synthesize small amounts of nitric oxide. Interestingly, iNOS knockout mice replicated HBV in the liver at higher levels than did their littermate controls that expressed iNOS, suggesting that nitric oxide present in the normal liver may repress HBV replication. Malaria affects the liver, and it is widespread in areas where HBV is endemic. We recently showed that intrahepatic HBV replication is inhibited in mice infected by Plasmodium species that cause murine malaria. When injected into susceptible mice, malaria sporozoites infect and multiply in hepatocytes, where they develop into merozoites and are released into the circulation.