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Cell surface influenza haemagglutinin can mediate infection by other animal viruses.
Author(s) -
Fuller S.D.,
Bonsdorff C.H.,
Simons K.
Publication year - 1985
Publication title -
the embo journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 7.484
H-Index - 392
eISSN - 1460-2075
pISSN - 0261-4189
DOI - 10.1002/j.1460-2075.1985.tb03959.x
Subject(s) - virology , biology , virus , vesicular stomatitis virus , semliki forest virus , permissive , microbiology and biotechnology , gene , genetics , rna
We have used filter‐grown Madin‐Darby canine kidney (MDCK) cells to explore the mechanism by which influenza virus facilitates secondary virus infection. Vesicular stomatitis virus (VSV) and Semliki Forest virus (SFV) infect only through the basolateral surface of these polarized epithelial cells and not through the apical surface. Prior infection with influenza virus rendered the cell susceptible to infection by VSV or SFV through either surface. The presence of both a permissive and a restrictive surface for virus entry in the same cell allowed us to determine how the influenza infection enhanced the subsequent infection of a second virus. Biochemical and morphological evidence showed that influenza haemagglutinin on the apical surface serves as a receptor for the superinfecting virus by binding to its sialic acid‐bearing envelope proteins. Influenza virus also facilitates secondary virus infection in non‐epithelial cells; baby hamster kidney cells (BHK‐21), which are normally resistant to infection by the coronavirus (mouse hepatitis virus MHV‐A59), could be infected via the haemagglutinin‐sialic acid interaction. Facilitation of secondary virus infection requires only the sialic acid‐binding properties of the haemagglutinin since the uncleaved haemagglutinin could also mediate virus entry.