tetano
Editor, Senior Moderator
Vet Res
. 2024 Jan 3;55(1):5.
doi: 10.1186/s13567-023-01257-8. The role of PB1-F2 in adaptation of high pathogenicity avian influenza virus H7N7 in chickens
Luise Hohensee[SUP] 1 2 [/SUP], David Scheibner[SUP] 3 [/SUP], Alexander Schäfer[SUP] 1 [/SUP], Holly Shelton[SUP] 4 [/SUP], Thomas C Mettenleiter[SUP] 5 [/SUP], Angele Breithaupt[SUP] 6 [/SUP], Anca Dorhoi[SUP] 1 [/SUP], Elsayed M Abdelwhab[SUP] 3 [/SUP], Ulrike Blohm[SUP] 7 [/SUP]
Affiliations
Avian influenza viruses (AIV) of the H7N7 subtype are enzootic in the wild bird reservoir in Europe, cause infections in poultry, and have sporadically infected humans. The non-structural protein PB1-F2 is encoded in a second open frame in the polymerase segment PB1 and its sequence varies with the host of origin. While mammalian isolates predominantly carry truncated forms, avian isolates typically express full-length PB1-F2. PB1-F2 is a virulence factor of influenza viruses in mammals. It modulates the host immune response, causing immunopathology and increases pro-inflammatory responses. The role of full-length PB1-F2 in IAV pathogenesis as well as its impact on virus adaptation and virulence in poultry remains enigmatic. Here, we characterised recombinant high pathogenicity AIV (HPAIV) H7N7 expressing or lacking PB1-F2 in vitro and in vivo in chickens. In vitro, full-length PB1-F2 modulated viability of infected chicken fibroblasts by limiting apoptosis. In chickens, PB1-F2 promoted gastrointestinal tropism, as demonstrated by enhanced viral replication in the gut and increased cloacal shedding. PB1-F2's effects on cellular immunity however were marginal. Overall, chickens infected with full-length PB1-F2 virus survived for shorter periods, indicating that PB1-F2 is also a virulence factor in bird-adapted viruses.
Keywords: H7N7; PB1-F2; apoptosis; cellular immunity; chicken; polymerase; replication; survival; tissue tropism; virulence.
. 2024 Jan 3;55(1):5.
doi: 10.1186/s13567-023-01257-8. The role of PB1-F2 in adaptation of high pathogenicity avian influenza virus H7N7 in chickens
Luise Hohensee[SUP] 1 2 [/SUP], David Scheibner[SUP] 3 [/SUP], Alexander Schäfer[SUP] 1 [/SUP], Holly Shelton[SUP] 4 [/SUP], Thomas C Mettenleiter[SUP] 5 [/SUP], Angele Breithaupt[SUP] 6 [/SUP], Anca Dorhoi[SUP] 1 [/SUP], Elsayed M Abdelwhab[SUP] 3 [/SUP], Ulrike Blohm[SUP] 7 [/SUP]
Affiliations
- PMID: 38173025
- PMCID: PMC10765749
- DOI: 10.1186/s13567-023-01257-8
Avian influenza viruses (AIV) of the H7N7 subtype are enzootic in the wild bird reservoir in Europe, cause infections in poultry, and have sporadically infected humans. The non-structural protein PB1-F2 is encoded in a second open frame in the polymerase segment PB1 and its sequence varies with the host of origin. While mammalian isolates predominantly carry truncated forms, avian isolates typically express full-length PB1-F2. PB1-F2 is a virulence factor of influenza viruses in mammals. It modulates the host immune response, causing immunopathology and increases pro-inflammatory responses. The role of full-length PB1-F2 in IAV pathogenesis as well as its impact on virus adaptation and virulence in poultry remains enigmatic. Here, we characterised recombinant high pathogenicity AIV (HPAIV) H7N7 expressing or lacking PB1-F2 in vitro and in vivo in chickens. In vitro, full-length PB1-F2 modulated viability of infected chicken fibroblasts by limiting apoptosis. In chickens, PB1-F2 promoted gastrointestinal tropism, as demonstrated by enhanced viral replication in the gut and increased cloacal shedding. PB1-F2's effects on cellular immunity however were marginal. Overall, chickens infected with full-length PB1-F2 virus survived for shorter periods, indicating that PB1-F2 is also a virulence factor in bird-adapted viruses.
Keywords: H7N7; PB1-F2; apoptosis; cellular immunity; chicken; polymerase; replication; survival; tissue tropism; virulence.