Influenza A virus with defective M2 ion channel activity as a live vaccine.

Abstract

We propose a rational approach to the design of live virus vaccines against influenza infection by alteration of the influenza A virus M2 protein, which is responsible for ion channel activity. Previously we demonstrated that a mutant A/WSN/33 (H1N1) influenza virus with defective M2 ion channel activity did not show appreciable growth defects in cell culture, although its growth was attenuated in mice (T. Watanabe, S. Watanabe, H. Ito, H. Kida, and Y. Kawaoka, 2001, J. Virol. 75, 5656-5662). Here, we show that this M2 ion channel defective mutant virus, the M2del29-31, protected mice against challenge with lethal doses of influenza virus, indicating the potential of incorporating this M2 alteration in a live influenza vaccine as one of the attenuating mutations.

• Authors: Tokiko Watanabe, Shinji Watanabe, Hiroshi Kida, Yoshihiro Kawaoka
• Journal: Virology (Virology) Vol. 299 Issue 2 Pg. 266-70 (Aug 01 2002) ISSN: 0042-6822 [Print] United States
• PMID: 12202229 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)

Chemical References

• Antibodies, Viral
• Influenza Vaccines
• M-protein, influenza virus
• M2 protein, Influenza A virus
• Vaccines, Attenuated
• Viral Matrix Proteins

Topics

• Animals
• Antibodies, Viral (blood)
• Cell Line
• Dogs
• Female
• Immunization
• Influenza A virus (immunology)
• Influenza Vaccines (immunology)
• Mice
• Mice, Inbred BALB C
• Vaccines, Attenuated (immunology)
• Viral Matrix Proteins (physiology)