OPEN ACCESS
This Article
OPEN ACCESS ARTICLE
Right arrow OA Full Text
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrowReprints and Permissions
Right arrow Copyright Information
Right arrow Books from ASM Press
Right arrow MicrobeWorld
Google Scholar
Right arrow Articles by Grantham, M. L.
Right arrow Articles by Pekosz, A.
PubMed
Right arrow PubMed Citation
Right arrow Articles by Grantham, M. L.
Right arrow Articles by Pekosz, A.

 Previous Article  |  Next Article 

Journal of Virology, September 2009, p. 8655-8661, Vol. 83, No. 17
0022-538X/09/$08.00+0     doi:10.1128/JVI.01129-09
Copyright © 2009, American Society for Microbiology. All Rights Reserved.

Palmitoylation of the Influenza A Virus M2 Protein Is Not Required for Virus Replication In Vitro but Contributes to Virus Virulence{triangledown}

Michael L. Grantham,1 Wai-Hong Wu,1 Erin N. Lalime,1 Maria E. Lorenzo,1,3 Sabra L. Klein,1,2 and Andrew Pekosz1*

W. Harry Feinstone Department of Molecular Microbiology and Immunology,1 Department of Biochemistry and Molecular Biology, Johns Hopkins University, Bloomberg School of Public Health, 615 North Wolfe Street, Suite 5132, Baltimore, Maryland 21205,2 Department of Molecular and Comparative Pathobiology, Johns Hopkins University School of Medicine, Baltimore, Maryland 212043

Received 3 June 2009/ Accepted 16 June 2009

The influenza A virus M2 protein has important roles during virus entry and in the assembly of infectious virus particles. The cytoplasmic tail of the protein can be palmitoylated at a cysteine residue, but this residue is not conserved in a number of human influenza A virus isolates. Recombinant viruses encoding M2 proteins with a serine substituted for the cysteine at position 50 were generated in the A/WSN/33 (H1N1) and A/Udorn/72 (H3N2) genetic backgrounds. The recombinant viruses were not attenuated for replication in MDCK cells, Calu-3 cells, or in primary differentiated murine trachea epithelial cell cultures, indicating there was no significant contribution of M2 palmitoylation to virus replication in vitro. The A/WSN/33 M2C50S virus displayed a slightly reduced virulence after infection of mice, suggesting that there may be novel functions for M2 palmitoylation during in vivo infection.

* Corresponding author. Mailing address: W. Harry Feinstone Department of Molecular Microbiology and Immunology, Johns Hopkins University, Bloomberg School of Public Health, 615 North Wolfe St., Suite 5132, Baltimore, MD 21205. Phone: (410) 502-9306. Fax: (410) 955-0105. E-mail: apekosz{at}jhsph.edu

{triangledown} Published ahead of print on 24 June 2009.

Journal of Virology, September 2009, p. 8655-8661, Vol. 83, No. 17
0022-538X/09/$08.00+0     doi:10.1128/JVI.01129-09
Copyright © 2009, American Society for Microbiology. All Rights Reserved.





Copyright © 2009 by the American Society for Microbiology.   For an alternate route to Journals.ASM.org, visit: http://intl-journals.asm.org | More Info»