ArticleJournal of virology2005
Attenuating mutations of the matrix gene of influenza A/WSN/33 virus.
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.
- Experimental infection of chickens, Pekin ducks, Eurasian wigeons and Barnacle geese with two recent highly pathogenic avian influenza H5N1 clade 2.3.4.4b viruses.Emerging microbes & infections · 2024Article
- Fitness Determinants of Influenza A Viruses.Viruses · 2023Review
- Article
- Broad Spectrum Anti-Influenza Agents by Inhibiting Self-Association of Matrix Protein 1.Scientific reports · 2016Article
- The compensatory G88R change is essential in restoring the normal functions of influenza A/WSN/33 virus matrix protein 1 with a disrupted nuclear localization signal.Journal of virology · 2013Article
- Influenza A virus inhibits alveolar fluid clearance in BALB/c mice.American journal of respiratory and critical care medicine · 2008Article
- Genetic contributions to influenza virus attenuation in the rat brain.Journal of neurovirology · 2008Article
- Matrix protein 1: A comparative in silico study on different strains of influenza A H5N1 Virus.Bioinformation · 2006Article
- Mutations in influenza virus M1 CCHH, the putative zinc finger motif, cause attenuation in mice and protect mice against lethal influenza virus infection.Journal of virology · 2006Article
- Functional constraints of influenza A virus epitopes limit escape from cytotoxic T lymphocytes.Journal of virology · 2005Article
Corrections and comments
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Authors and funding
2 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The matrix protein (M1) of influenza virus plays an essential role in viral replication. Our previous studies have shown that basic amino acids 101RKLKR105 of M1 are involved in RNP binding and nuclear localization. For the present work, the functions of 101RKLKR105 were studied by introducing mutations into the M gene of influenza virus A/WSN/33 by reverse genetic methods. Individual substitution, R101S or R105S, had a minimal effect on viral replication. In contrast, the double mutation R101S-R105S was synergistic and resulted in temperature sensitivity reflected by reduced viral replication at a restrictive temperature. To investigate the in vivo effect on infection, BALB/c mice were infected with either A/WSN/33 wild-type (Wt) or mutant viruses and assessed for signs of illness, viral replication in the lungs, and survival rates. The results from mouse studies indicated that the R101S-R105S double mutant virus was strongly attenuated, while single mutant viruses R101S and R105S were minimally attenuated compared to A/WSN33 Wt under the same conditions. In challenge studies, mice immunized by infection with R101S-R105S were fully protected from lethal challenge with A/WSN/33. The replication and attenuating properties of R101S-R105S suggest its potential in development of live influenza virus vaccines.
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