Structure, Molecular Virology, Natural History, And Experimental Models

Hepatitis A virus (HAV), a small, naked, single-stranded, positive RNA virus that belongs to the Picornaviridae, causes acute hepatitis in humans and nonhuman primates. HAV infection typically does not induce cytopathic effect in cell culture, and disease results from an immunopathogenic process that clears the virus without leaving chronic sequelae. HAV is transmitted through the oral-fecal route, but it is unknown how it reaches the liver. The pathogenic process of HAV is poorly understood. However, recent advances in the understanding of the effects of the interaction of HAV with its cellular receptor 1 (HAVCR1), which blocks the activation of T cell receptors and shuts off regulatory T cell (Treg) functions, help explain how HAV modulates the immune response to evade detection during its long incubation period and is cleared with limited liver damage. The shut-off of Treg functions may also explain the protective effect of HAV infection in the development of atopy and autoimmunity.