Immune-escape mutations and stop-codons in HBsAg develop in a large proportion of patients with chronic HBV infection exposed to anti-HBV drugs in Europe.

doi:10.1186/s12879-018-3161-2

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Article

Immune-escape mutations and stop-codons in HBsAg develop in a large proportion of patients with chronic HBV infection exposed to anti-HBV drugs in Europe.

BMC infectious diseases - 1 Jun 2018

Colagrossi Luna, Hermans Lucas E, Salpini Romina, Di Carlo Domenico, Pas Suzan D, Alvarez Marta, Ben-Ari Ziv, Boland Greet, Bruzzone Bianca, Coppola Nicola, Seguin-Devaux Carole, Dyda Tomasz, Garcia Federico, Kaiser Rolf, Köse Sukran, Krarup Henrik, Lazarevic Ivana, Lunar Maja M, Maylin Sarah, Micheli Valeria, Mor Orna, Paraschiv Simona, Paraskevis Dimitros, Poljak Mario, Puchhammer-Stöckl Elisabeth, Simon François, Stanojevic Maja, Stene-Johansen Kathrine, Tihic Nijaz, Trimoulet Pascale, Verheyen Jens, Vince Adriana, Lepej Snjezana Zidovec, Weis Nina, Yalcinkaya Tülay, Boucher Charles A B, Wensing Annemarie M J, Perno Carlo F, Svicher Valentina

Abstract excerpt

BACKGROUND: HBsAg immune-escape mutations can favor HBV-transmission also in vaccinated individuals, promote immunosuppression-driven HBV-reactivation, and increase fitness of drug-resistant strains. Stop-codons can enhance HBV oncogenic-properties. Furthermore, as a consequence of the overlapping structure of HBV genome, some immune-escape mutations or stop-codons in HBsAg can derive from drug-resistance...

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PMID: 29859062
DOI: 10.1186/s12879-018-3161-2
PMCID: PMC5984771

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