Sally Furniss
Well-known member
Journal of Virology, February 2002, p. 1781-1786, Vol. 76, No. 4
0022-538X/01/$04.00+0 DOI: 10.1128/JVI.76.4.1781-1786.2002
Copyright ? 2002, American Society for Microbiology. All Rights Reserved.
Cooperation between the Hemagglutinin of Avian Viruses and the Matrix Protein of Human Influenza A Viruses
Christoph Scholtissek,1,{dagger} J?rgen Stech,2 Scott Krauss,1 and Robert G. Webster1,3*
http://jvi.asm.org/cgi/content/abstract/76/4/1781
Departments of Virology,1 Pathology, St. Jude Children's Research Hospital, Memphis, Tennessee 38105-2794 ,3 Institute of Virology, Philipps University Marburg, D-35032 Marburg, Germany2
Received 12 July 2001/ Accepted 1 November 2001
To analyze the compatibility of avian influenza A virus hemagglutinins (HAs) and human influenza A virus matrix (M) proteins M1 and M2, we doubly infected Madin-Darby canine kidney cells with amantadine (1-aminoadamantane hydrochloride)-resistant human viruses and amantadine-sensitive avian strains. By using antisera against the human virus HAs and amantadine, we selected reassortants containing the human virus M gene and the avian virus HA gene. In our system, high virus yields and large, well-defined plaques indicated that the avian HAs and the human M gene products could cooperate effectively; low virus yields and small, turbid plaques indicated that cooperation was poor. The M gene products are among the primary components that determine the species specificities of influenza A viruses. Therefore, our system also indicated whether the avian HA genes effectively reassorted into the genome and replaced the HA gene of the prevailing human influenza A viruses. Most of the avian HAs that we tested efficiently cooperated with the M gene products of the early human A/PR/8/34 (H1N1) virus; however, the avian HAs did not effectively cooperate with the most recently isolated human virus that we tested, A/Nanchang/933/95 (H3N2). Cooperation between the avian HAs and the M proteins of the human A/Singapore/57 (H2N2) virus was moderate. These results suggest that the currently prevailing human influenza A viruses might have lost their ability to undergo antigenic shift and therefore are unable to form new pandemic viruses that contain an avian HA, a finding that is of great interest for pandemic planning.
0022-538X/01/$04.00+0 DOI: 10.1128/JVI.76.4.1781-1786.2002
Copyright ? 2002, American Society for Microbiology. All Rights Reserved.
Cooperation between the Hemagglutinin of Avian Viruses and the Matrix Protein of Human Influenza A Viruses
Christoph Scholtissek,1,{dagger} J?rgen Stech,2 Scott Krauss,1 and Robert G. Webster1,3*
http://jvi.asm.org/cgi/content/abstract/76/4/1781
Departments of Virology,1 Pathology, St. Jude Children's Research Hospital, Memphis, Tennessee 38105-2794 ,3 Institute of Virology, Philipps University Marburg, D-35032 Marburg, Germany2
Received 12 July 2001/ Accepted 1 November 2001
To analyze the compatibility of avian influenza A virus hemagglutinins (HAs) and human influenza A virus matrix (M) proteins M1 and M2, we doubly infected Madin-Darby canine kidney cells with amantadine (1-aminoadamantane hydrochloride)-resistant human viruses and amantadine-sensitive avian strains. By using antisera against the human virus HAs and amantadine, we selected reassortants containing the human virus M gene and the avian virus HA gene. In our system, high virus yields and large, well-defined plaques indicated that the avian HAs and the human M gene products could cooperate effectively; low virus yields and small, turbid plaques indicated that cooperation was poor. The M gene products are among the primary components that determine the species specificities of influenza A viruses. Therefore, our system also indicated whether the avian HA genes effectively reassorted into the genome and replaced the HA gene of the prevailing human influenza A viruses. Most of the avian HAs that we tested efficiently cooperated with the M gene products of the early human A/PR/8/34 (H1N1) virus; however, the avian HAs did not effectively cooperate with the most recently isolated human virus that we tested, A/Nanchang/933/95 (H3N2). Cooperation between the avian HAs and the M proteins of the human A/Singapore/57 (H2N2) virus was moderate. These results suggest that the currently prevailing human influenza A viruses might have lost their ability to undergo antigenic shift and therefore are unable to form new pandemic viruses that contain an avian HA, a finding that is of great interest for pandemic planning.