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.
Highlights
Avian influenza viruses (AIV) can be classified into low (LPAIV) and high (HPAIV) pathogenic avian influenza viruses depending on the severity of the disease that they cause, which ranges from asymptomatic infection to acute systemic disease and even death [1]
In order to assess the role of pre-existing immunity in subsequent highly pathogenic avian influenza viruses (HPAIV) infections, specific pathogen free (SPF)-chickens were experimentally inoculated with H7N2 low pathogenic avian influenza viruses (LPAIV) and 15 days later challenged with H7N1 HPAIV
No clinical signs or lesions were observed after H7N2 LPAIV inoculation (G1), whereas inoculation of naıve animals with H7N1 HPAIV (G2) induced severe clinical signs and mortality from day 2 after inoculation (Figure 1A)
Summary
Avian influenza viruses (AIV) can be classified into low (LPAIV) and high (HPAIV) pathogenic avian influenza viruses depending on the severity of the disease that they cause, which ranges from asymptomatic infection to acute systemic disease and even death [1]. HPAIV have been involved in several outbreaks in poultry and wild birds around the world. HPAIV could appear as a consequence of reassortments between different LPAIV subtypes that co-infect wild birds, their natural reservoirs [6,7]. It seems important that surveillance programs should focus on the control of LPAIV, mainly those caused by viruses of the H5 or H7 subtypes, to prevent future emergences of HPAIV [8]. The virulence can be linked to the presence of multiple basic amino acids in the hemagglutinin (HA) cleavage site, the acquisition of a multibasic cleavage site alone can be insufficient to increase viral pathogenicity [9]
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