Giuseppe
Emeritus
Virus Res. 2009 Jan 12. [Epub ahead of print]
Factors responsible for plaque formation of A/duck/Siberia/272/1998 (H13N6) influenza virus on MDCK cells.
Tsuda Y, Isoda N, Sakoda Y, Kida H. - Laboratory of Microbiology, Department of Disease Control, Graduate School of Veterinary Medicine, Hokkaido University, Nishi-9, Kita-18, Kita-ku, Sapporo, Hokkaido 060-0818, Japan; Research Center for Zoonosis Control, Hokkaido University, Nishi-10, Kita-20, Kita-ku, Sapporo, Hokkaido 001-0020, Japan.
Many influenza A viruses form plaques on Madin-Darby canine kidney (MDCK) cells in the presence of trypsin.
A/duck/Siberia/272/1998 (H13N6) (Sib272), however, does not form plaque on MDCK cells.
After three blind passages of the strain on MDCK cells, plaque-forming variant was obtained and designated as A/duck/Siberia/272PF/1998 (H13N6) (Sib272PF).
Genetic and functional analyses of Sib272 and Sib272PF revealed that amino acid substitutions, F3L of the HA2 subunit and T379K of the PB1, were responsible for plaque formation of Sib272PF by enhancing fusion and polymerase activities, respectively.
PMID: 19146891 [PubMed - as supplied by publisher]
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Factors responsible for plaque formation of A/duck/Siberia/272/1998 (H13N6) influenza virus on MDCK cells.
Tsuda Y, Isoda N, Sakoda Y, Kida H. - Laboratory of Microbiology, Department of Disease Control, Graduate School of Veterinary Medicine, Hokkaido University, Nishi-9, Kita-18, Kita-ku, Sapporo, Hokkaido 060-0818, Japan; Research Center for Zoonosis Control, Hokkaido University, Nishi-10, Kita-20, Kita-ku, Sapporo, Hokkaido 001-0020, Japan.
Many influenza A viruses form plaques on Madin-Darby canine kidney (MDCK) cells in the presence of trypsin.
A/duck/Siberia/272/1998 (H13N6) (Sib272), however, does not form plaque on MDCK cells.
After three blind passages of the strain on MDCK cells, plaque-forming variant was obtained and designated as A/duck/Siberia/272PF/1998 (H13N6) (Sib272PF).
Genetic and functional analyses of Sib272 and Sib272PF revealed that amino acid substitutions, F3L of the HA2 subunit and T379K of the PB1, were responsible for plaque formation of Sib272PF by enhancing fusion and polymerase activities, respectively.
PMID: 19146891 [PubMed - as supplied by publisher]
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