Background: Cytokines and host factors triggering innate immunity against hepatitis B virus (HBV) are not well understood.Results: IL-1 and TNFα induced cytidine deaminase AID, an anti-HBV host factor, and reduced HBV infection into hepatocytes.Conclusion: IL-1/TNFα reduced host susceptibility to HBV infection through AID up-regulation.Significance: Proinflammatory cytokines modulate HBV infection through a novel innate immune pathway involving AID.

To investigate whether a principal neutralization epitope exists in hypervariable region 1 (HVR1) within the putative envelope of hepatitis C virus (HCV), we generated a hyperimmune rabbit serum against a synthetic peptide corresponding to HVR1 of HCV isolate H77. The reactivity of the serum in the enzyme-linked immunosorbent assay was correlated with the 13 amino acids (position 398-410) in HVR1. The serum prevented infection with H77 virus in cell cultures but did not prevent infection with H90 virus, a genetically divergent isolate from the same patient. The study demonstrated that neutralization of HCV was mediated, in part, by isolate-specific antibody recognizing HVR1.

Background. Hepatitis A infection is caused by hepatitis A virus (HAV) contracted through fecal‐oral transmission. Life‐long immunity is conferred after infection. Improved sanitary conditions have generally resulted in a significant decline in the incidence of hepatitis A. However, a low incidence of infection results in increased HAV susceptibility. The present study investigates the prevalence of anti‐HAV antibody and clarifies the current HAV status and HAV susceptibility in Japan at 2003. Methods. A total of 2,430 serum specimens collected during 2003 from Japanese individuals ranging in age from 0–92 years, were tested for anti‐HAV antibody using an inhibition enzyme linked immunosorbent assay. All specimens were obtained from the WHO and the National Serum Reference Bank/National Institute of Infectious Diseases, Tokyo, Japan. Results. The overall seroprevalence was 12.2%. Anti‐HAV antibodies were rarely detected in individuals between 0–44 years of age. Starting from the age of 45–49 years, seropositivity gradually increased through age 65 years and above. Seroprevalence was not affected by gender, and geographic distribution did not affect age‐specific seroprevalence until the age of 60 years. Conclusions. HAV susceptibility in Japan is increasing annually. Particularly, the prevalence of anti‐HAV antibody in individuals older than 50 years in 2003 was 50.3%, which is significantly lower than that of corresponding studies in 1994 (74.3%), 1984 (96.9%) and 1973 (96.9%). The growing susceptible population of advanced age results in more frequent HAV infection among them. The surveillance of anti‐HAV antibody prevalence is useful for implementing preventive measures and for controlling the spread of HAV.

The resurgence of HAV in 2010 can be attributed to importation of two newly emerged HAV genotypes.

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Hepatitis A virus (HAV) causes acute hepatitis and sometimes leads to fulminant hepatitis. Amantadine is a tricyclic symmetric amine that inhibits the replication of many DNA and RNA viruses. Amantadine was reported to suppress HAV replication, and the efficacy of amantadine was exhibited in its inhibition of the internal ribosomal entry site (IRES) activities of HAV. Interferon (IFN) also has an antiviral effect through the induction of IFN stimulated genes (ISG) and the degradation of viral RNA. To explore the mechanism of the suppression of HAV replication, we examined the effects of the combination of amantadine and IFN-alpha on HAV IRES-mediated translation, HAV replicon replication in human hepatoma cell lines, and HAV KRM003 genotype IIIB strain replication in African green monkey kidney cell GL37. IFN-alpha seems to have no additive effect on HAV IRES-mediated translation inhibition by amantadine. However, suppressions of HAV replicon and HAV replication were stronger with the combination than with amantadine alone. In conclusion, amantadine, in combination of IFN-alpha, might have a beneficial effect in some patients with acute hepatitis A.

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