Novel mutation in Hepatitis B virus preventing HBeAg production and resembling primate strains

Abstract

Chronic carriers of hepatitis B infection often harbour virus strains with mutations in the precore region. These mutations are temporally associated with the development of HBeAg loss and seroconversion to anti-HBe. The most common precore mutation is a stop codon at position 1896, but other mutations leading to abolished HBeAg secretion have been described. Here, a novel precore mutation introducing a lysine in the precore position 28, a sequence shared by non-human primates but not by other human isolates, is described. However, the insertion causes a frame-shift preventing the expression of HBeAg by introducing a stop codon 5 aa downstream of the mutation. Analysis of the predicted RNA secondary structure indicates that the insertion could occur without fatally affecting the stability of the stem-loop encapsidation signal.

Prevalence, whole genome characterization and phylogenetic analysis of hepatitis B virus in captive orangutan and gibbon

“…This substitution had occurred in all gibbon and orangutan HBV sequences described here, and was commonly found in non‐human primate sequences. It has been proposed that the difference of RNA secondary structure between infected humans and non‐human primates may be responsible for this discrepancy [25, 26].…”