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Biswas, S.* ; Rust, L.N.* ; Wettengel, J.M. ; Yusova, S.* ; Fischer, M.* ; Carson, J.N.* ; Johnson, J.* ; Wei, L.* ; Thode, T.* ; Kaadige, M.R.* ; Sharma, S.* ; Agbaria, M.* ; Bimber, B.N.* ; Tu, T.* ; Protzer, U. ; Ploss, A.* ; Smedley, J.V.* ; Golomb, G.* ; Sacha, J.B.* ; Burwitz, B.J.*

Long-term hepatitis B virus infection of rhesus macaques requires suppression of host immunity.

Nat. Commun. 13:2995 (2022)
Verlagsversion Forschungsdaten DOI PMC
Open Access Gold
Creative Commons Lizenzvertrag
Hepatitis B virus has infected a third of the world's population, and 296 million people are living with chronic infection. Chronic infection leads to progressive liver disease, including hepatocellular carcinoma and liver failure, and there remains no reliable curative therapy. These gaps in our understanding are due, in large part, to a paucity of animal models of HBV infection. Here, we show that rhesus macaques regularly clear acute HBV infection, similar to adult humans, but can develop long-term infection if immunosuppressed. Similar to patients, we longitudinally detected HBV DNA, HBV surface antigen, and HBV e antigen in the serum of experimentally infected animals. In addition, we discovered hallmarks of HBV infection in the liver, including RNA transcription, HBV core and HBV surface antigen translation, and covalently closed circular DNA biogenesis. This pre-clinical animal model will serve to accelerate emerging HBV curative therapies into the clinic.
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Publikationstyp Artikel: Journalartikel
Dokumenttyp Wissenschaftlicher Artikel
Korrespondenzautor
ISSN (print) / ISBN 2041-1723
e-ISSN 2041-1723
Zeitschrift Nature Communications
Quellenangaben Band: 13, Heft: 1, Seiten: , Artikelnummer: 2995 Supplement: ,
Verlag Nature Publishing Group
Verlagsort London
Nichtpatentliteratur Publikationen
Begutachtungsstatus Peer reviewed
Institut(e) Institute of Virology (VIRO)
Förderungen
ODCDC CDC HHS
NIAID NIH HHS