ArticleJournal of virology2005
Growth of hepatitis A virus in a mouse liver cell line.
Article in Journal of virology, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed.
- Host species-specific mutations in the thumb domain of the 3Dpol polymerase are required for efficient replication of human hepatitis A virus in mice.PLoS pathogens · 2026Article
- Preservation of Anti-cytomegalovirus Activity in Human Milk Following High-Pressure Processing Compared to Holder Pasteurization.Frontiers in nutrition · 2022Article
- Review
- Murine Models of Hepatitis A Virus Infection.Cold Spring Harbor perspectives in medicine · 2019Review
- HAVCR1 (CD365) and Its Mouse Ortholog Are Functional Hepatitis A Virus (HAV) Cellular Receptors That Mediate HAV Infection.Journal of virology · 2018Article
- MAVS-dependent host species range and pathogenicity of human hepatitis A virus.Science (New York, N.Y.) · 2016Article
- Molecular biology and inhibitors of hepatitis A virus.Medicinal research reviews · 2014Review
- Cell type-specific functions of period genes revealed by novel adipocyte and hepatocyte circadian clock models.PLoS genetics · 2014Article
- A simple and rapid Hepatitis A Virus (HAV) titration assay based on antibiotic resistance of infected cells: evaluation of the HAV neutralization potency of human immune globulin preparations.Virology journal · 2008Article
- Stable growth of wild-type hepatitis A virus in cell culture.Journal of virology · 2006Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Hepatitis A virus (HAV) has been adapted to grow efficiently in primate and some nonprimate cell lines but not in cells of murine origin. To understand the inability of the virus to grow in mouse cells, we studied the replication of HAV in immortalized and nontransformed MMH-D3 mouse liver cells, which require growth factors and collagen to maintain their phenotype. HAV grew in MMH-D3 cells transfected with virion RNA but not in those infected with viral particles, indicating a cell entry block for HAV. However, MMH-D3 cells cultured under suboptimal conditions in the absence of growth factors acquired susceptibility to HAV infection. Serial passages of the virus in MMH-D3 cells under suboptimal growth conditions resulted in the selection of HAV variants that grew efficiently in MMH-D3 cells cultured under both optimal and suboptimal conditions. Nucleotide sequence analysis of the MMH-D3 cell-adapted HAV revealed that N1237D and D2132G substitutions were present in the capsid regions of six viral clones. These two mutations are most likely located on the surface of the virion and may play a role in the entry of HAV into the mouse liver cells. Our results demonstrate that mouse hepatocyte-like cells code for all factors required for the efficient growth of HAV in cell culture.
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