The human Wa strain of rotaviruses, initially unable to grow in liver cells, was adapted by multiple passages to grow in HepG2 cells. The genome segment 4 of both the parental and passaged strains was cloned and sequenced. Five amino acid differences (residues 38, 120, 421, 525, and 618) were found in the HepG2-passaged variant compared to the parental Wa strain. Our results support the hypothesis that viral variants that have improved capabilities for infecting liver cells can be generated during infection.
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rdfs:comment |
The human Wa strain of rotaviruses, initially unable to grow in liver cells, was adapted by multiple passages to grow in HepG2 cells. The genome segment 4 of both the parental and passaged strains was cloned and sequenced. Five amino acid differences (residues 38, 120, 421, 525, and 618) were found in the HepG2-passaged variant compared to the parental Wa strain. Our results support the hypothesis that viral variants that have improved capabilities for infecting liver cells can be generated during infection.
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skos:exactMatch | |
uniprot:name |
Arch. Virol.
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uniprot:author |
Estes M.K.,
Kitamoto N.,
Mattion N.M.
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uniprot:date |
1993
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uniprot:pages |
179-185
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uniprot:title |
Alterations in the sequence of the gene 4 from a human rotavirus after multiple passages in HepG2 liver cells.
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uniprot:volume |
130
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dc-term:identifier |
doi:10.1007/BF01319006
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