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 Previous Article

Journal of Virology, January 2008, p. 1059-1063, Vol. 82, No. 2
0022-538X/08/$08.00+0     doi:10.1128/JVI.01499-07
Copyright © 2008, American Society for Microbiology. All Rights Reserved.

Extending the Cytoplasmic Tail of the Influenza A Virus M2 Protein Leads to Reduced Virus Replication In Vivo but Not In Vitro{triangledown}

Wai-Hong Wu1 and Andrew Pekosz1,2*

Departments of Molecular Microbiology,1 Pathology & Immunology, Washington University in St. Louis School of Medicine, 660 S. Euclid Ave., Campus Box 8230, St. Louis, Missouri 631102

Received 9 July 2007/ Accepted 26 October 2007

A carboxy-terminal epitope tag introduced into the coding region of the A/WSN/33 M2 protein resulted in a recombinant virus (rWSN M2myc) which replicated to titers similar to those of the parental virus (rWSN) in MDCK cells. The rWSN M2myc virus was attenuated in its ability to induce mortality and weight loss after the intranasal inoculation of BALB/c mice, indicating that the M2 cytoplasmic tail plays a role in virus virulence. Mice infected with rWSN M2myc were completely protected from subsequent challenge with rWSN, suggesting that epitope tagging of the M2 protein may be a useful way of attenuating influenza A virus strains.

* Corresponding author. Present address: W. Harry Feinstone Department of Molecular Microbiology and Immunology, Johns Hopkins University, Bloomberg School of Public Health, 615 North Wolfe Street, Suite E5132, Baltimore, MD 21205. Phone: (410) 955-3223. Fax: (410) 955-0105. E-mail: apekosz{at}jhsph.edu

{triangledown} Published ahead of print on 7 November 2007.

Journal of Virology, January 2008, p. 1059-1063, Vol. 82, No. 2
0022-538X/08/$08.00+0     doi:10.1128/JVI.01499-07
Copyright © 2008, American Society for Microbiology. All Rights Reserved.





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