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Proteasomal degradation of core protein variants from chronic hepatitis B patients
Author(s) -
Braun Sabine,
Zajakina Anna,
Aleksejeva Jekaterina,
Sharipo Anatoly,
Bruvere Ruta,
Ose Velta,
Pumpens Paul,
Garoff Henrik,
Meisel Helga,
Kozlovska Tatyana
Publication year - 2007
Publication title -
journal of medical virology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.782
H-Index - 121
eISSN - 1096-9071
pISSN - 0146-6615
DOI - 10.1002/jmv.20939
Subject(s) - virology , core protein , chronic hepatitis , medicine , biology , virus
The accumulation of complex hepatitis B virus (HBV) variants with internal in‐frame deletions in the C gene in immunosuppressed renal transplant recipients is associated with a severe course of the infection leading to end‐stage liver disease (ESLD). A set of six HBV C genes with internal in‐frame deletions corresponding to the pattern of HBV population in immunosuppressed patients has been expressed in two different eukaryotic cell lines. Synthesis and proteasomal degradation of HBV core (HBc) protein variants were compared with those of the wild‐type HBc. In all cases, the steady‐state level of internally deleted HBc proteins, predominantly with longer deletions, were considerably lower and turnover was significantly higher in comparison with those of the wild‐type HBc, since all deletion variants were degraded rapidly via the proteasome pathway. Involvement and consequences of the proteasomal degradation machinery in the HBc protein turnover during HBV infection with complex HBV variants in the immunosuppressed patients are discussed. J. Med. Virol. 79:1312–1321, 2007. © Wiley‐Liss, Inc.