in 2011 , public health laboratories in 5 states detected 12 cases of human infection with a novel variant of influenza virus , influenza a(h3n2)v virus , by using the cdc rrt - pcr protocol . however , swine contact could not be verified for the other 6 , suggesting that these infections might have been contracted through limited person - to - person transmission ( 1113 ) ( table 1 ) . all 12 patients recovered fully from their illness ( 1012 ) . * influenza a(h3n2)v , influenza virus variant identified in humans ; rrt - pcr , real - time reverse transcription pcr ; nps ,  nasopharyngeal swab ; pb , polymerase basic protein ; ha , hemagglutinin ; np nucleoprotein ; na , neuraminidase ; m , matrix protein ; ns , nonstructural protein ; pa , polymerase acidic protein ; npw ,  nasopharyngeal wash ; ns ,  nasal swab . results obtained by using the centers for disease control and prevention human influenza virus real - time rt - pcr diagnostic panel . this patient was > 18 years of age ; all others were < 18 . genetic sequence analysis of rna isolated from clinical respiratory specimens ( table 1 ) revealed that these influenza a(h3n2)v viruses possessed a combination of gene segments not previously found in humans ( figure 1 ) . of the 8 gene segments , 7 ( hemagglutinin , neuraminidase , polymerase basic proteins 1 and 2 , polymerase acidic protein , nucleoprotein , and nonstructural protein ) were similar to those of triple - reassortant siv a(h3n2 ) currently circulating in north america and to those from human triple - reassortant influenza a(h3n2 ) viruses isolated in 2010 from pennsylvania , minnesota , and wisconsin ( 4 ) , including the proposed vaccine virus of swine origin , a / minnesota/11/2010 ( 14 ) ( figure 2 , panel a ; technical appendix figure ) . however , the m genes of all 2011 influenza a(h3n2)v viruses were inherited from a pandemic ( h1n1 ) 2009 virus ( figure 2 , panel b ) . although sivs of subtypes a(h3n2 ) and a(h1n2 ) with the m gene of influenza a(h1n1)pdm09 virus have been detected in swine since 2009 ( 15 ) , influenza a(h3n2)v virus possessing the m gene of influenza a(h1n1)pdm09 virus had not been detected in humans . derivation of genes segments of novel influenza a(h3n2 ) viruses isolated from humans , united states , 19902011 . phylogenetic analysis of the a ) hemagglutinin and b ) matrix genes of influenza a(h3n2)v viruses . sequences obtained from human a(h3n2)v isolates in the united states during 2011 are shown in boldface ; sequences of proposed vaccine virus are underlined . scale bars indicate number of base substitutions per site . according to genetic analysis results , amino acid diversity among influenza a(h3n2)v hemagglutinins was low ( 03 aa ) compared with that of influenza a / minnesota/11/2010 . in addition , there have been no conserved amino acid changes in the hemagglutinin when comparing 2011 influenza a(h3n2)v from humans with 2011 influenza a(h3n2 ) sivs . in particular , the known receptor binding site of the hemagglutinin protein of influenza a(h3n2)v virus was typical of siv a(h3n2 ) viruses recently isolated in north america . hemagglutinins of the influenza a(h3n2)v viruses differed substantially from the hemagglutinin of the 201112 human seasonal vaccine virus , a / perth/16/2011 ( 5860 aa ) , which resulted from divergent evolutionary paths for the h3 hemagglutinin in swine and human viruses . the effect of these substitutions on virus antigenicity was examined in the hemagglutination - inhibition assay by using a panel of reference ferret antiserum . hemagglutination - inhibition analysis of 6 available influenza a(h3n2)v virus isolates revealed no measureable inhibition by antiserum against the current human seasonal influenza a(h3n2 ) vaccine virus , a / perth/16/2009 ( table 2 ) , indicating that influenza a(h3n2)v virus is antigenically distinct from influenza a(h3n2 ) viruses currently circulating among humans . reassortant virus possessing the hemagglutinin and neuraminidase genes of a / minnesota/11/2010 and the remaining 6 genes of a / pr/8/34 . all influenza a(h3n2)v viruses tested were antigenically similar , demonstrating hemagglutination - inhibition titers with only a 2-fold difference from antiserum against other influenza a(h3n2)v viruses . these viruses were also antigenically closely related to earlier human triple - reassortant virus isolates that contained the m gene from classical sivs ( a / wisconsin/12/2010 , a / pennsylvania/14/2010 , and a / minnesota/11/2010 ) . all influenza a(h3n2)v viruses tested were also antigenically closely related to the proposed vaccine reassortant x-203 ( 13 ) between triple - reassortant a / minnesota/11/2010 ( h3n2 ) and a / pr/8/34 ( h1n1 ) ( table 2 ) . the level of cross - protective immunity against influenza a(h3n2)v in humans previously vaccinated and/or exposed to previously circulated seasonal influenza a(h3n2 ) viruses is unknown . the antigenic characterization described here demonstrates that vaccination with the current trivalent influenza vaccine might not provide immune protection against influenza a(h3n2)v virus . a vaccine containing a contemporary influenza a(h3n2)v or an antigenically similar virus ( such as a / minnesota/11/2010 ) functional neuraminidase inhibition assays indicated that 6 influenza a(h3n2)v virus isolates were sensitive to the neuraminidase inhibitors oseltamivir and zanamivir . no genetic markers known to decrease sensitivity to neuraminidase inhibitors were found in the neuraminidase genes of all 12 influenza a(h3n2)v viruses . similar to pandemic ( h1n1 ) 2009 viruses , influenza a(h3n2)v viruses have genetic markers ( v27a , s31n ) in the m2 protein that confer resistance to the antiviral medications amantadine and rimantadine . the detection of multiple cases of human infection with influenza a(h3n2)v virus within a 5-month period in 5 us states , coupled with possible human - to - human transmission , underscores the need for continued influenza surveillance at the swine  human interface . coordinated surveillance of human and animal influenza viruses enables rapid detection of human infections with novel influenza viruses and timely identification of new virus variants in swine . as was evident during the 2009 influenza pandemic , this information is vital for development of resources that might be needed to effectively respond to the emergence and spread of a novel influenza virus in humans .
during july  december 2011 , a variant virus , influenza a(h3n2)v , caused 12 human cases of influenza . 
 the virus contained genes originating from swine , avian , and human viruses , including the m gene from influenza a(h1n1)pdm09 virus . 
 influenza a(h3n2)v viruses were antigenically distinct from seasonal influenza viruses and similar to proposed vaccine virus a / minnesota/11/2010 .