13.12.2020
Emerging Infectious Diseases. 2020;26(12):2966-2969.
Highly pathogenic avian influenza viruses (HPAIVs) have devastating impacts on the poultry industries. With infections in poultry, H5 and H7 low-pathogenicity avian influenza viruses (LPAIVs) have spontaneously mutated into HPAIVs by different mechanisms, one of which is acquisition of basic amino acids at the hemagglutinin (HA) cleavage site.
In March 2020, an outbreak of LPAIV H7N3 occurred in turkey farms, affecting 11 premises in North Carolina and 1 in South Carolina, USA. The initial decision to depopulate LPAIV-affected flocks was based on a risk assessment that included the location of affected premises, the poultry density in the area, and the presence of a basic amino acid substitution at the cleavage site among the initial LPAIV detections (PEKPKTR/GLF; substitution sequence is highlighted). During the ongoing response for this event, the Clemson Veterinary Diagnostic Center in Columbia, South Carolina, a member of the National Animal Health Laboratory Network, detected an influenza A(H7) outbreak in a second turkey location in South Carolina, with increased death and respiratory signs; oropharyngeal and cloacal swab samples were forwarded to the National Veterinary Services Laboratories in Ames, Iowa, USA. On April 8, the National Veterinary Services Laboratories confirmed 1 of 6 pooled samples as HPAIV H7N3. Subsequent testing from all infected barns on the premises determined that HPAIV was present in only 1 of the 5 barns, but LPAIV was identified in the other 4 barns. All the premises affected by LPAIV and HPAIV H7N3 were located in 3 adjacent counties and 1 across state lines, indicating that geographic proximity was relevant to the outbreaks. Immediate depopulation was performed on the LPAIV- and HPAIV-affected premises, affecting 361,000 birds.
Complete genome sequencing and phylogenetic analyses were conducted to trace the origin and evolution of the H7N3 viruses. A total of 29 H7N3 viruses from 13 premises were sequenced. The intravenous pathogenicity index of selected LPAIV strains was 0 and of selected HPAIV strains, 2.46. Based on the HA cleavage site motif and supported by the intravenous pathogenicity index, 2 H7N3 viruses from 1 house in South Carolina were considered to be HPAIV. For the 2 HPAIVs, 34 (5.7%) and 1,076 (38.8%) reads had no insertion, whereas the rest of the reads were found to have an identical 27 nucleotides insertion from host cellular 28S rRNA in the cleavage site. The presence of LPAIV and HPAIV in 1 barn at the same time suggests that the mutation was caught early. The 27-nt insertion coding for 9 amino acids at the HA cleavage site (PENPKTDRKSRHRRIR/GLF; insertion sequence is highlighted) is identical to that found in a 2017 HPAIV H7N9 from a poultry outbreak that occurred in Tennessee. The potential role of a palindromic sequence was suggested to be a cause of RNA recombination with host 28S rRNA, and similar structure is often observed among the H7 subtype.
