期刊
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA
卷 103, 期 10, 页码 3805-3809出版社
NATL ACAD SCIENCES
DOI: 10.1073/pnas.0511218103
关键词
animal model; pathogenesis; reverse genetics; viral hepatitis
资金
- Medical Research Council [G0801976, G0400802] Funding Source: Medline
- NCI NIH HHS [CA85883, CA57973, R01 CA085883, CA10702, R01 CA057973] Funding Source: Medline
- NCRR NIH HHS [P51 RR013986, RR13986] Funding Source: Medline
- NIAID NIH HHS [N01AI40035, N01AI40034] Funding Source: Medline
- NIDDK NIH HHS [DK70497, F32 DK070497] Funding Source: Medline
- Medical Research Council [G0400802, G9818340B] Funding Source: researchfish
- MRC [G0400802] Funding Source: UKRI
Hepatitis C virus (HCV) is a major cause of chronic liver disease, frequently progressing to cirrhosis and increased risk of hepatocellular carcinoma. Current therapies are inadequate and progress in the field has been hampered by the lack of efficient HCV culture systems. By using a recently described HCV genotype 2a infectious clone that replicates and produces infectious virus in cell culture (HCVcc), we report here that HCVcc strain FL-J6/JFH can establish long-term infections in chimpanzees and in mice containing human liver grafts. Importantly, virus recovered from these animals was highly infectious in cell culture, demonstrating efficient ex vivo culture of HCV. The improved infectivity of animal-derived HCV correlated with virions of a lower average buoyant density than HCVcc, suggesting that physical association with low-density factors influences viral infectivity. These results greatly extend the utility of the HCVcc genetic system to allow the complete in vitro and in vivo dissection of the HCV life cycle.
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