Seasonal Trivalent Inactivated Influenza Vaccine Does Not Protect against Newly Emerging Variants of Influenza A (H3N2v) Virus in Ferrets

Houser, Katherine V.; Katz, Jacqueline M.; Tumpey, Terrence M.

doi:10.1128/jvi.02625-12

Cited by 34 publications

(32 citation statements)

References 12 publications

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“…However, even with an identical antigenic match between the challenge and vaccine virus, TIV does not provide sterilizing immunity against homologous virus challenge in ferrets, as observed here (Fig. 2B) and previously (7). The inability of seasonal TIV immunization to block transmission of A(H3N2)v virus to naive-contact animals prompted us to prepare a monovalent vaccine to a seasonal influenza H3N2 virus, Beijing/92, that showed some, albeit low, antigenic similarity to A(H3N2)v virus using postinfection ferret antisera (4,6).…”

Section: Discussionsupporting

confidence: 65%

“…The H3 HA of human and swine influenza viruses followed divergent evolutionary pathways resulting in antigenically distinct influenza H3N2 viruses (4)(5)(6). Experimentally, the seasonal 2011-2012 trivalent inactivated influenza virus vaccine (TIV) failed to generate a cross-reactive antibody response to A(H3N2)v virus in ferrets and offered no protection from A(H3N2)v virus challenge (7). However, A(H3N2)v viruses retained a low degree of serologic cross-reactivity with human H3N2 viruses that circulated in the early 1990s (4,6).…”

mentioning

confidence: 99%

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Impact of Prior Seasonal H3N2 Influenza Vaccination or Infection on Protection and Transmission of Emerging Variants of Influenza A(H3N2)v Virus in Ferrets

Houser

Pearce

Katz

et al. 2013

J Virol

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Section: Discussionsupporting

confidence: 65%

mentioning

confidence: 99%

Impact of Prior Seasonal H3N2 Influenza Vaccination or Infection on Protection and Transmission of Emerging Variants of Influenza A(H3N2)v Virus in Ferrets

Houser

Pearce

Katz

et al. 2013

J Virol

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“…Serological studies with human serum samples demonstrate that while a significant proportion of adolescents and young adults have cross-reactive antibodies against A(H3N2)v viruses, young children lack such preexisting immunity (35,36). Investigations in the ferret model suggest that vaccination with seasonal trivalent inactivated influenza vaccines does not provide protection against transmission of A(H3N2)v virus (37,38). These findings highlight the antigenic difference between circulating H3N2 and the swine-origin viruses and the need to evaluate and approve A(H3N2)v vaccines.…”

Section: Discussionmentioning

confidence: 91%

Amino Acids in Hemagglutinin Antigenic Site B Determine Antigenic and Receptor Binding Differences between A(H3N2)v and Ancestral Seasonal H3N2 Influenza Viruses

Wang

Ilyushina

Lugovtsev

et al. 2017

J Virol

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Influenza A H3N2 variant [A(H3N2)v] viruses, which have caused human infections in the UnitedStates in recent years, originated from human seasonal H3N2 viruses that were introduced into North American swine in the mid-1990s, but they are antigenically distinct from both the ancestral and current circulating H3N2 strains. A reference A(H3N2)v virus, A/Minnesota/11/2010 (MN/10), and a seasonal H3N2 strain, A/Beijing/32/1992 (BJ/92), were chosen to determine the molecular basis for the antigenic difference between A(H3N2)v and the ancestral viruses. Viruses containing wild-type and mutant MN/10 or BJ/92 hemagglutinins (HAs) were constructed and probed for reactivity with ferret antisera against MN/10 and BJ/92 in hemagglutination inhibition assays. Among the amino acids that differ between the MN/10 and BJ/92 HAs, those in antigenic site A had little impact on the antigenic phenotype. Within antigenic site B, mutations at residues 156, 158, 189, and 193 of MN/10 HA to those in BJ/92 switched the MN/10 antigenic phenotype to that of BJ/ 92. Mutations at residues 156, 157, 158, 189, and 193 of BJ/92 HA to amino acids present in MN/10 were necessary for BJ/92 to become antigenically similar to MN/ 10. The HA amino acid substitutions responsible for switching the antigenic phenotype also impacted HA binding to sialyl receptors that are usually present in the human respiratory tract. Our study demonstrates that antigenic site B residues play a critical role in determining both the unique antigenic phenotype and receptor specificity of A(H3N2)v viruses, a finding that may facilitate future surveillance and risk assessment of novel influenza viruses. IMPORTANCE Influenza A H3N2 variant [A(H3N2)v] viruses have caused hundreds of human infections in multiple states in the UnitedStates since 2009. Most cases have been children who had contact with swine in agricultural fairs. These viruses originated from human seasonal H3N2 viruses that were introduced into the U.S. swine population in the mid-1990s, but they are different from both these ancestral viruses and current circulating human seasonal H3N2 strains in terms of their antigenic characteristics as measured by hemagglutination inhibition (HI) assay. In this study, we identified amino acids in antigenic site B of the surface glycoprotein hemagglutinin (HA) that explain the antigenic difference between A(H3N2)v and the ancestral H3N2 strains. These amino acid mutations also alter binding to minor human-type glycans, suggesting that host adaptation may contribute to the selection of antigenically distinct H3N2 variants which pose a threat to public health.

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“…However, current human seasonal trivalent influenza vaccine (TIV) did not boost antibody levels (HI antibody titers) in individuals with pre-existing antibody to H3N2v virus (32). In addition, seasonal TIV did not protect again H3N2v infection or disease in ferrets (33). Thus, if H3N2v were to establish itself in the human population by gaining the ability to be transmitted between people, a new specific vaccine would be needed (32).…”

Section: Discussionmentioning

confidence: 99%

Efficacy in Pigs of Inactivated and Live Attenuated Influenza Virus Vaccines against Infection and Transmission of an Emerging H3N2 Similar to the 2011-2012 H3N2v

Loving

Lager

Vincent

et al. 2013

J Virol

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cVaccines provide a primary means to limit disease but may not be effective at blocking infection and pathogen transmission. The objective of the present study was to evaluate the efficacy of commercial inactivated swine influenza A virus (IAV) vaccines and experimental live attenuated influenza virus (LAIV) vaccines against infection with H3N2 virus and subsequent indirect transmission to naive pigs. The H3N2 virus evaluated was similar to the H3N2v detected in humans during 2011-2012, which was associated with swine contact at agricultural fairs. One commercial vaccine provided partial protection measured by reduced nasal shedding; however, indirect contacts became infected, indicating that the reduction in nasal shedding did not prevent aerosol transmission. One LAIV vaccine provided complete protection, and none of the indirect-contact pigs became infected. Clinical disease was not observed in any group, including nonvaccinated animals, a consistent observation in pigs infected with contemporary reassortant H3N2 swine viruses. Serum hemagglutination inhibition antibody titers against the challenge virus were not predictive of efficacy; titers following vaccination with a LAIV that provided sterilizing immunity were below the level considered protective, yet titers in a commercial vaccine group that was not protected were above that level. While vaccination with currently approved commercial inactivated products did not fully prevent transmission, certain vaccines may provide a benefit by limitating shedding, transmission, and zoonotic spillover of antigenically similar H3N2 viruses at agriculture fairs when administered appropriately and used in conjunction with additional control measures.

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Seasonal Trivalent Inactivated Influenza Vaccine Does Not Protect against Newly Emerging Variants of Influenza A (H3N2v) Virus in Ferrets

Cited by 34 publications

References 12 publications

Impact of Prior Seasonal H3N2 Influenza Vaccination or Infection on Protection and Transmission of Emerging Variants of Influenza A(H3N2)v Virus in Ferrets

Impact of Prior Seasonal H3N2 Influenza Vaccination or Infection on Protection and Transmission of Emerging Variants of Influenza A(H3N2)v Virus in Ferrets

Amino Acids in Hemagglutinin Antigenic Site B Determine Antigenic and Receptor Binding Differences between A(H3N2)v and Ancestral Seasonal H3N2 Influenza Viruses

Efficacy in Pigs of Inactivated and Live Attenuated Influenza Virus Vaccines against Infection and Transmission of an Emerging H3N2 Similar to the 2011-2012 H3N2v

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