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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. [ABSTRACT FROM AUTHOR]

Feline upper respiratory tract disease (URTD) is a common but complicated disease that occurs in domestic cats, worldwide. 396 cats in Guangxi Province, China were screened for URTD-associated pathogens from March 2022 to August 2023. Mycoplasma felis was found to be the most prevalent infectious agent with a positivity rate of 24.75 %, followed by feline calicivirus (FCV), Chlamydia felis , feline herpesvirus 1 (FHV-1) and feline influenza A virus (FeIAV) with rates of 15.91, 11.62, 5.56 and 1.52 %, respectively. In particular, C. felis and M. felis were found in 13 of 55 co-infected cats. Of the 46 C. felis -positive samples, one strain, named as GXNN36, was successfully isolated using chicken embryos and it was characterized both in vivo and in vitro. For the cat studies, both high- and low-dose challenged groups showed severe conjunctivitis, accompanied by transient fever and respiratory symptoms. C. felis replicated well in turbinate, trachea and lung tissues with high copy numbers and the infection subsequently spread to the livers, spleens, pancreas, kidneys, hearts and intestines. These findings will help our understanding of the role of C. felis in feline URTD and provide a valuable model to evaluate the efficacy of vaccines and therapeutic remedies in the future. • Chlamydia felis plays an important role in feline URTD, co-infecting with Mycoplasma felis. • The isolation and identification of Chlamydia felis was systemically described. • The pathogenesis was evaluated in cat study, which provided a valuable model to develop the vaccine and medicine. [ABSTRACT FROM AUTHOR]

H1N1 reassortants between the swine Eurasian avian-like (EA) and H1N1 2009 pandemic (H1N1 pdm/09) viruses have been circulating stably in pig populations for more than ten years, and they may have contributed to increased human infections. Whether these H1N1 viruses acquire adaptive mutations to increase their pathogenicity towards a new host is unknown. To address this problem, mouse-adapted (MA) variants of swine-origin EA H1N1 influenza virus isolated from dogs (A/canine/Guangxi/LZ57/2015[LZ57-MA]) were generated by serial lung-to-lung passages in BALB/c mice. These exhibited greater virulence and replication capability than the wild-type virus (LZ57-WT). Of the six adaptive mutations, two were mapped to the ribonucleoprotein (RNP) complex (PB2-E578D and PA-T97I), two to hemagglutinin (HA-N198D and HA-A227E) and two to the non-structural protein 1 (NS1) and nuclear export protein (NS1-A53D and NEP-R42K, respectively). Reverse genetic substitution of the viral genes and mutation experiments demonstrated that the mutations in PA-T97I could enhance the polymerase activity, but a significant downregulation of activity was seen with PB2-E578D, which was consistent with a decrease in virulence. However, HA and NS, which are genes that act synergistically, were found to be determinants of virulence in mice. The reassortant viruses bearing HA mutations (N198D and A227E) were acquired during adaptation enhanced early-stage viral replication in mammalian cells. The single-point mutations in the NS genes had limited effects on virulence. Furthermore, a combination of HA (N198D and A227E) with NS(A53D) in the rLZ57-WT backbone resulted in efficient replication and a significant increase in virulence. The results suggest that these substitutions could compensate for the polymerase function and contribute to enhanced virulence, which highlights a major role for mutations in the HA and NS genes. • The mouse-adapted H1N1 variant virus (LZ57) was generated, which exhibited six adaptive mutations located in the PB2, PA, HA, NS1 and NEP. • Using reverse genetics, the combination of HA and NS gene contributed largely to enhanced virulence in mice when compared to the other genes. • Combining HA-N198D and A227E and NS-A53D in rLZ57-WT backbone resulted in efficient replication and significantly increased virulence. [ABSTRACT FROM AUTHOR]