ArticleJournal of virology2026
Natural immune escape mutations in the envelope proteins of hepatitis B virus (HBV) regulate the assembly and infectivity of human hepatitis delta virus (HDV).
Article in Journal of virology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
The study examined how 35 natural immune escape mutations (IEMs) of hepatitis B virus (HBV) located in the major antigenic loop (MAL) of the envelope proteins regulate the assembly and infectivity of the natural sub-viral agent of HBV, hepatitis delta virus (HDV). All IEMs were permissive for the assembly and secretion of HDV virions. Only seven IEMs resulted in considerably decreased levels of secreted HDV virions in the context of one to three tested HBV genotypes, B, C, or D. The effects of IEMs on HDV infectivity were much more pronounced than on the assembly. Thirteen IEMs considerably inhibited the infectivity of HDV virions. All of them greatly reduced both the levels of HDV RNA genomes accumulated in the infected cells and the percentage of HDV-infected cells. Only one mutant R(169)P generated completely non-infectious HDV virions. Our analysis of the IEMs-mediated effects on the HDV life cycle therefore identified a number of critically important amino acid residues in the MAL, and aided the mechanistic understanding of the MAL functioning during the processes of HDV assembly and infectivity. The inhibition of either HDV assembly and/or infectivity is expected to suppress the viral spread and super-infection
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