Exposure to a Low Pathogenic A/H7N2 Virus in Chickens Protects against Highly Pathogenic A/H7N1 Virus but Not against Subsequent Infection with A/H5N1

Abstract

Recent evidences have demonstrated that the presence of low pathogenic avian influenza viruses (LPAIV) may play an important role in host ecology and transmission of avian influenza viruses (AIV). While some authors have clearly demonstrated that LPAIV can mutate to render highly pathogenic avian influenza viruses (HPAIV), others have shown that their presence could provide the host with enough immunological memory to resist re-infections with HPAIV. In order to experimentally study the role of pre-existing host immunity, chickens previously infected with H7N2 LPAIV were subsequently challenged with H7N1 HPAIV. Pre-infection of chickens with H7N2 LAPIV conferred protection against the lethal challenge with H7N1 HPAIV, dramatically reducing the viral shedding, the clinical signs and the pathological outcome. Correlating with the protection afforded, sera from chickens primed with H7N2 LPAIV reacted with the H7-AIV subtype in hemagglutination inhibition assay and specifically with the N2-neuraminidase antigen. Conversely, subsequent exposure to H5N1 HPAIV resulted in a two days-delay on the onset of disease but all chickens died by 7 days post-challenge. Lack of protection correlated with the absence of H5-hemagglutining inhibitory antibodies prior to H5N1 HPAIV challenge. Our data suggest that in naturally occurring outbreaks of HPAIV, birds with pre-existing immunity to LPAIV could survive lethal infections with HA-homologous HPAIV but not subsequent re-infections with HA-heterologous HPAIV. These results could be useful to better understand the dynamics of AIV in chickens and might help in future vaccine formulations.

Protection Patterns in Duck and Chicken after Homo- or Hetero-Subtypic Reinfections with H5 and H7 Low Pathogenicity Avian Influenza Viruses: A Comparative Study

“…Several studies have investigated the adaptive immunity following infection with homologous or heterologous AIV infections [5] , [6] . Most of these studies addressed protection against infection with H5N1 highly pathogenic avian influenza viruses (HPAIV) [7] , [8] . Humoral immune response is known to play an important role in the control of avian influenza virus infections by reducing virus replication and spread [9] .…”

H7N7 Avian Influenza Virus Mutation from Low to High Pathogenicity on a Layer Chicken Farm in the UK

“…It is speculated that at the time of cull, all susceptible birds that had not been exposed to LPAIV in Shed 5, had already died due to HPAIV infection. This is based on the assumption that susceptible birds, without prior LPAIV infection, would rapidly succumb to HPAIV infection and that birds that had been infected with the LPAIV may have been shedding virus at the time of sampling [ 8 , 25 , 26 ]. The peak HI titers in Sheds 5 and 6 (both 4096), which were the highest of all the sheds, suggest that the immune responses of the birds in these sheds were primed by the LPAIV infection, and then boosted when exposed to the HPAIV at a later time.…”

From low to high pathogenicity-Characterization of H7N7 avian influenza viruses in two epidemiologically linked outbreaks

“…Furthermore, the observation that only part of the animals were AIV‐H7 seropositive points to an early stage of LPAI virus circulation and a rapid LP‐to‐HP mutation, leaving a substantial number of animals susceptible to HPAIV H7 infection. An immune response to the antigenetically homologous/identical LPAI virus would have been able to protect animals from HP AIV‐induced clinical symptoms (Fereidouni et al., ; Vergara‐Alert et al., ). It is therefore reasonable to speculate that the emergence of HPAI requires triggering by the LP‐to‐HP pathogenicity conversion event itself, but also depends on the favourable competition and dynamic of spread of the HP variant within an at least partially susceptible host population.…”