Serotype a is now the most common seen in the North American Arctic; highest rates occur in indigenous children.

Very little is known of hepatitis B virus (HBV) in Canadian Arctic indigenous populations, where HBV was considered endemic prior to the introduction of HBV vaccine. This study expands upon an HBV seroepidemiological survey conducted between 1983 and 1985 throughout the Canadian Arctic, to characterize HBV in this population. Archived hepatitis B surface antigen (HBsAg)-positive sera (n = 401) were processed for HBV DNA, followed by sequencing and phylogenetic analysis of the HBsAg- and HBcAg-coding regions. Sixty-nine per cent of samples (277/401) were DNA positive, with most having low viral load (median 3.4 log 10 IU/mL). The predominant HBV genotype observed was genotype B (HBV/B, 75%), followed by HBV/D (24%) and HBV/A (1%). All HBV/B strains clustered within subgenotype B6, a newly recognized HBV genotype among western circumpolar Inuit and Alaska Native people. HBV/D strains included both D3 (88%) and D4 (12%) subgenotypes, while all HBV/A strains were subgenotype A2. An association of HBV genotype B with Inuit living in the eastern Arctic and an association of genotype D with First Nation (Dene) living in the western Arctic was observed. This study establishes the high prevalence of HBV/B6 and HBV/D genotypes in Arctic populations and reveals their marked distribution within the Canadian Arctic based on geographical and demographic attributes.

The results of the present study showed that serological evidence of HEV infection was present in 3% of the observed Canadian Inuit population; the presence of IgM anti-HEV suggested recent infection and HEV did not appear to coinfect with other common hepatotropic viruses. The source of HEV infection in the population remains unclear. These findings are interesting but preliminary. Additional data are required to determine whether HEV infections are responsible for otherwise unexplained acute hepatitis in the Canadian Inuit population and visitors returning from northern North American communities.

Hepatitis C virus (HCV) establishes persistent infection in the majority of infected individuals. The currently accepted hypothesis of immune evasion by antigenic variation in hypervariable region 1 (HVR1) of glycoprotein E2 does not however, explain the lack of subsequent immune recognition. Here, we show that the N-terminal region of E2 is antigenically and structurally similar to human immunoglobulin (Ig) variable domains. E2 is recognized by anti-human IgG antibodies and also possesses common amino acid (aa) sequence features of the conserved v-gene framework regions of human Ig light chains in particular but also heavy chains and T cell receptors. Using a position specific scoring system, the degree of similarity of HVR1 to Ig types correlated with immune escape and persistence in humans and experimentally infected chimpanzees. We propose a unique role for threshold levels of Ig molecular mimicry in HCV biology that not only advances our concept of viral immune escape and persistent infection but also provides insight into host-dependent disease patterns.

Diseases induced by animal retroviruses are not considered to be good models for the human acquired immunodeficiency syndrome (AIDS) at present. The lack of an animal model for the human immunodeficiency virus (HIV) infection presents a main problem in the complete understanding of the pathogenesis of HIV-mediated diseases. Because of the homologies between simian immunodeficiency virus (SIV) and HIV-2, we inoculated rhesus monkeys with HIV-2 and HIV-2 adapted in vitro to monkey cells. One of the ten animals inoculated developed clinical symptoms that might be related to the infection with HIV-2.