Feline calicivirus (FCV) is a highly infectious pathogen that causes upper respiratory tract disease (URTD), but the enteric FCVs raise concerns regarding their role of an enteric pathogen. In this study, between 2019 and 2020, 101 clinical samples from domestic cats with symptoms of URTD, with or without enteritis, were collected for FCV‐specific detection. The FCV‐positive rate reached to 42.4% (28/66) in cats with respiratory symptoms. The rates were 11.1% (3/27) and 12.5% (1/8) when faeces and serum samples were measured using reverse transcription polymerase chain reaction (RT‐PCR), respectively. Ten FCV strains were successfully isolated from respiratory and enteric sources in domestic cats from Guangxi. Phylogenetic analysis based on the genome sequences of 11 isolates (including GX01‐13 isolated in 2013) indicated that the newly characterized FCV strains had two recombinant events in comparison with other FCVs and were of respiratory and enteric origins. These strains displayed high genetic diversity, and they were divided into two genogroups (I and II). Of these, the GXNN02‐19 isolate was grouped with previously published Chinese isolates that were identified as genogroup II, which contained three specific amino acid residues (377K, 539V and 557S) in the VP1 protein. In addition, the three enteric viruses appeared genetically heterogeneous to each other. All isolates were found to be more sensitive when exposed to low pH conditions, but they were resistant to treatment with trypsin and bile salts. Furthermore, there were no significant differences between the respiratory and enteric FCVs. Our results showed that the genetically distinct FCV strains with genogroups I and II from respiratory and enteric origins were co‐circulating in this geographical area. Also, it was revealed that the potential recombinant events between the enteric and respiratory FCVs suggested an important role of enteric FCV during the evolution.

Feline calicivirus (FCV) is a highly contagious pathogen associated with oral and upper respiratory tract diseases (URTD), and it is also possibly considered as an enteric pathogen. Some studies found FCV-like viruses in the enteric tract of dogs, but there was a lack of understanding regarding the epidemiology and biological properties of FCVs in dogs. In this study, 252 fecal/feces samples were collected from dogs, with or without diarrhea, from 2020 to 2021. There were 6 FCV-positive samples (2.41%, 6/252), from which only two FCVs were successfully isolated and the complete genome sequences obtained. Phylogenetic analysis showed that the two canine-origin FCV isolates belonged to genogroup I and formed a monophyletic cluster with previous FCV strains, sharing a common ancestor. However, there was genetic diversity when the nt identity of the VP1 proteins between the two canine-origin FCV isolates (77.4% nt identity) was compared. In particular, the genomic sequence of the canine/GXHC01-21 isolate showed evidence of recombination at the 3ʹ end of the ORF1 gene with sequence identity very similar to the FCV strain, GX2019, previously isolated from cats in Guangxi in 2019. A comparison of their replication properties indicated that the two isolates could not replicate efficiently in MDCK cells. This was also seen in the enteric FCV isolate, GXNN04-20. However, both displayed similar plaque phenotypes to the respiratory FCV isolate, GX01-13. In addition, it was found that sera from vaccinated cats had low cross-reactivity in a neutralizing antibody test against the two canine-origin FCV isolates. Moreover, high neutralizing antibody titers (≥1 : 128) against canine-origin FCV viruses were observed in the two canine serum samples. This confirmed that interspecies transmission had occurred between cats and dogs. Our results provided an in-depth understanding of the genetic evolution and characteristics of FCVs circulating in dogs.

Swine-origin H1N1 influenza virus caused an outbreak in human in 2009 (H1N1/pdm09). We isolated several novel reassortant influenza A viruses bearing the H1N1/pdm09 segments (PB2, PB1, PA and NP) from dogs, which showed high similarity with H1N1 swine influenza virus in the previous study. To understand the molecular basis of swine-origin H1N1 reassortant canine influenza virus adaptation to new host species, the mouse-adapted variants of H1N1 canine virus were obtained by serial lung-to-lung passages in BALB/c mice. After thirteen passages, the virus significantly enhanced replication in MDCK cells and became lethal to mice. Six adaptive mutations mapped to two in the ribonucleoprotein (RNP) complex (PB2-E578D, PA-T97I), two in hemagglutinin (HA-N198D and A227E), two in the non-structural protein 1 and nuclear export protein (NS1-A53D and NEP-R42K), indicating that they may contribute to the increased virulence and replication. The results provided valuable insights into how the swine-origin influenza virus adapt to a new host that deserves more attentions.