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. 2013 Dec;87(24):13480-9.
doi: 10.1128/JVI.02434-13. Epub 2013 Oct 2.

Impact of prior seasonal H3N2 influenza vaccination or infection on protection and transmission of emerging variants of influenza A(H3N2)v virus in ferrets

Katherine V Houser  1 , Melissa B Pearce, Jacqueline M Katz, Terrence M Tumpey
Affiliations

Impact of prior seasonal H3N2 influenza vaccination or infection on protection and transmission of emerging variants of influenza A(H3N2)v virus in ferrets

Katherine V Houser et al. J Virol. 2013 Dec.

Abstract

Influenza H3N2 A viruses continue to circulate in swine and occasionally infect humans, resulting in outbreaks of variant influenza H3N2 [A(H3N2)v] virus. It has been previously demonstrated in ferrets that A(H3N2)v viruses transmit as efficiently as seasonal influenza viruses, raising concern over the pandemic potential of these viruses. However, A(H3N2)v viruses have not acquired the ability to transmit efficiently among humans, which may be due in part to existing cross-reactive immunity to A(H3N2)v viruses. Although current seasonal H3N2 and A(H3N2)v viruses are antigenically distinct from one another, historical H3N2 viruses have some antigenic similarity to A(H3N2)v viruses and previous exposure to these viruses may provide a measure of immune protection sufficient to dampen A(H3N2)v virus transmission. Here, we evaluated whether prior seasonal H3N2 influenza virus vaccination or infection affects virus replication and transmission of A(H3N2)v virus in the ferret animal model. We found that the seasonal trivalent inactivated influenza virus vaccine (TIV) or a monovalent vaccine prepared from an antigenically related 1992 seasonal influenza H3N2 (A/Beijing/32/1992) virus failed to substantially reduce A(H3N2)v (A/Indiana/08/2011) virus shedding and subsequent transmission to naive hosts. Conversely, ferrets primed by seasonal H3N2 virus infection displayed reduced A(H3N2)v virus shedding following challenge, which blunted transmission to naive ferrets. A higher level of specific IgG and IgA antibody titers detected among infected versus vaccinated ferrets was associated with the degree of protection offered by seasonal H3N2 virus infection. The data demonstrate in ferrets that the efficiency of A(H3N2)v transmission is disrupted by preexisting immunity induced by seasonal H3N2 virus infection.

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Figures

Fig 1
Fig 1
Transmissibility of seasonal H3N2 and A(H3N2)v influenza viruses among naive ferrets in the respiratory droplet model. Ferrets were inoculated i.n. with 106 PFU of virus with 3 transmission pairs per experiment. Contact animals were placed in adjacent cages with perforated side walls 24 h postinoculation. (A) Transmission of seasonal H3N2 virus, Perth/09. (B) Transmission of A(H3N2)v virus, IN/11. Each bar represents the virus titer detected in nasal washes of an inoculated ferret (left half of figure) and its corresponding contact animal (right half). Limit of virus detection, 1 log10 PFU/ml.
Fig 2
Fig 2
Transmission of seasonal H3N2 and A(H3N2)v viruses following vaccination with the seasonal TIV. Five weeks after the final vaccine boost, TIV-immune ferrets were challenged with heterologous IN/11 virus (A) or homologous seasonal Perth/09 virus (B). Each bar represents the viral titer detected in nasal washes of inoculated ferrets (n = 6) and their corresponding contact animals (n = 6). Limit of virus detection, 1 log10 PFU/ml.
Fig 3
Fig 3
Impact of vaccination of a historical seasonal H3N2 virus on A(H3N2)v virus transmission. Five weeks after the final vaccine boost, monovalent-vaccinated ferrets were placed into transmission cages and challenged with IN/11 virus. Groups of ferrets were vaccinated with inactivated vaccines prepared from Perth/09 (A), Beijing/92 (B), or IN/11 (C) virus. Transmission from inoculated (vaccinated) ferrets (n = 3) to naive contacts (n = 3) was determined. Limit of virus detection, 1 log10 PFU/ml.
Fig 4
Fig 4
Effect of prior seasonal H3N2 virus infection on cross-protection and transmission of A(H3N2)v virus. Six weeks after primary seasonal H3N2 virus infection, naive and Perth/09-immune ferrets were challenged with homologous Perth/09 (A) or heterologous IN/11 (B) virus. Protection against challenge is represented by virus titers in nasal wash samples of naive ferrets (white bars) and Perth/09-immune ferrets (gray bars). Error bars correspond to standard deviations. ***, P ≤ 0.005 by Mann-Whitney nonparametric t test. Perth/09-immune (C) or Beijing/92-immune (D) ferrets were placed into transmission cages and challenged with heterologous IN/11 virus. Transmission from inoculated ferrets to naive contacts was determined. Limit of virus detection, 1 log10 PFU/ml.
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