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Hepadnaviruses have been identified in several animal species. The hepadnavirus prototype, human hepatitis B virus (HBV), is a major public health problem associated with chronic liver diseases and hepatocellular carcinoma. Recently, a novel hepadnavirus, similar to HBV, was identified in domestic cats. Since several pathogens can be shared between cats and dogs, we hypothesized that dogs could also harbor hepadnaviruses and we tested a collection of canine sera with multiple molecular strategies. Overall, hepadnavirus DNA was identified in 6.3% (40/635) of canine serum samples, although the viral load in positive sera was low (geometric mean of 2.70 × 10 2 genome copies per mL, range min 1.36 × 10 2 —max 4.03 × 10 4 genome copies per mL). On genome sequencing, the canine hepadnaviruses revealed high nucleotide identity (about 98%) and similar organization to the domestic cat hepadnavirus. Altered hepatic markers were found in hepadnavirus-positive dogs, although the role of hepadnavirus in canine health remains to be elucidated.

We conducted a survey for domestic cat hepadnavirus, an analog of human hepatitis B virus, in the endangered felid species Iberian lynx. Results revealed specific antibodies in 32.3% of serum samples and DNA in 0.5% of available liver samples. Phylogenetically, the virus segregated apart from other Europe strains of the virus.

Canine parvovirus and feline panleukopenia virus (FPV) are variants of Carnivore protoparvovirus 1. We identified and characterized FPV in dogs from Italy and Egypt using genomic sequencing and phylogenetic analyses. Cost-effective sequencing strategies should be used to monitor interspecies spread, evolution dynamics, and potential host jumping of FPV.

Hepadnaviruses infect several animal species. The prototype species, human hepatitis B virus (HBV), increases the risk of liver diseases and may cause cirrhosis and hepatocellular carcinoma. Recently a novel hepadnavirus, similar to HBV, has been identified through transcriptomics studies in a domestic cat with large cell lymphoma in Australia. Herewith, a collection of 390 feline serum samples was screened for hepadnavirus. Overall, the virus was identified in 10.8% of the sera with a significantly higher prevalence (17.8%) in the sera of animals with a clinical suspect of infectious disease. Upon genome sequencing, the virus was closely related (97.0% nt identity) to the prototype Australian feline virus Sydney 2016. The mean and median values of hepadnavirus in the feline sera were 1.3 × 10 6 and 2.1 × 10 4 genome copies per mL (range 3.3 × 10 0 –2.5 × 10 7 genome copies per mL). For a subset of hepadnavirus-positive samples, information on the hemato-chemical parameters was available and in 10/20 animals a profile suggestive of liver damage was present. Also, in 7/10 animals with suspected hepatic disease, virus load was >10 4 genome copies per mL, i.e. above the threshold considered at risk of active hepatitis and liver damage for HBV.

The virus species Protoparvovirus carnivoran 1 encompasses pathogens that infect both domestic and wild carnivores, including feline panleukopenia virus. We identified and characterized feline panleukopenia virus strains in a Marsican brown bear (Ursus arctos marsicanus) and a crested porcupine (Hystrix cristata) in Italy, extending the known host range of this virus.

Two feral cats (from the same colony) were presented to the veterinary clinic for weakness, weight loss, and anorexia. The cats were part of a study on feline hepatotropic viruses (collection A, 43 animals). On metaviromic investigation, parvoviral reads were identified in the sera of the two cats. The feline parvovirus genome was 5.3 kb long with an organization similar to other members of the Erythroparvovirus genus. In the ORF1 (nonstructural proteins) and ORF2 (VP1/VP2 precursor) the feline virus displayed 43.1% and 49.1% nucleotide identity to human parvovirus B19, and 48.9% and 56.6% to chipmunk parvovirus. Sequence identity to canine/feline protoparvovirus (Protoparvovirus carnivoran 1) was as low as 36.5% % and 29.2% in the ORF1 and ORF2, respectively. Using a quantitative PCR assay, the virus was also identified in an additional ten cats (prevalence 27.6%, 12/43) from collection A and in 15/1150 (1.3%) of archival sera (collection B), revealing a higher infection rate in cats with altered hepatic markers, suggestive of hepatic distress. The findings of our study extend the list of known parvoviruses in the feline host.

The historic Rockborn strain of the canine distemper virus was widely used as a vaccine, but its use was discontinued due to safety concerns. Yet, Rockborn-like canine distemper virus strains are still used in some vaccine formulations. Genetic analysis of this strain was previously limited to the H gene, leaving its full evolutionary and pathogenic potential unclear. This study aimed to determine the complete genome sequence of the Rockborn strain to reconstruct its origin, understand its evolution, and provide a reference for improving diagnostics and future research on virulence markers. An amplicon-based sequencing protocol using MinION nanopore technology was employed to determine the complete genome of the Rockborn-46th laboratory strain. The genome was assembled, annotated, and analyzed in comparison with 223 genomes. The complete genome of the Rockborn strain was 15,690 nucleotides in length. Phylogenetic analysis revealed that Rockborn forms a unique lineage with field isolates from a masked civet in China and a dog in the United States. Crucially, a significant recombination event was identified, showing that the Rockborn strain acted as a parental strain, contributing its F and H genes to create mosaic viruses. The full-genome characterization of the Rockborn strain confirms that Rockborn-like viruses persist and actively contribute to the evolution of canine distemper virus through recombination. This finding highlights the inadequacy of single-gene analysis for diagnostics and surveillance, and underscores the necessity of whole-genome sequencing to accurately track the virus epidemiology and evolution.

Objective: To analyze the composition of the oral microbiome in periodontal pocket lesions and on the tongue dorsum of patients with Helicobacter pylori-associated gastric disease. Materials and Methods: Patients diagnosed with gastric disease and H. pylori (HP+) were evaluated in comparison to a control group of H. pylori-negative patients without gastric disease (HP−). Periodontal and oral health clinical parameters (PPD, BoP, PSE, plaque score and modified DMFT) were assessed for each patient. Microbiological samples were collected from the deepest periodontal pockets and tongue dorsum, followed by DNA extraction, 16S rRNA PCR amplification, and Next-Generation-Sequencing (NGS) analyses. Results: Sixty-seven patients (27F; 40M, aged 35–85 years) were enrolled. Of these, 52 were HP+ and 15 were HP−. HP+ patients exhibited a significantly higher presence of decayed teeth (p < 0.05) and slightly fewer missing teeth (p > 0.05). The plaque score was significantly higher in HP+ patients (p < 0.05), while PPD and BoP showed no significant differences (p > 0.05). NGS analysis revealed no presence of H. pylori in any samples of both periodontal and tongue sites. HP+ patients showed a distinct microbial composition, including higher prevalence of Capnocytophaga, Fusobacterium, and Peptostreptococcus genera in both locations (pockets and tongue dorsum). Conclusions: The study demonstrated that HP+ patients exhibit distinct oral microbial profiles compared to HP− patients, especially in areas with deeper periodontal pockets. H. pylori was not detected in the oral microbiomes of either group.

Group A rotaviruses (RVAs) are a major cause of acute dehydrating diarrhea in infants and young animals worldwide. In rabbits, RVAs are associated with enteric disease, likely in combination with other pathogens. We report the identification and characterization of a lapine RVA strain in an Italian rabbit breeding farm. Increased mortality rates associated with enteric symptoms were reported in the facility in post-weaning rabbits around 40 days of age. By quantitative RT-PCR, an RVA strain was identified in the intestinal contents of deceased rabbits. A PCR-based enrichment protocol coupled with Nanopore sequencing allowed the reconstruction of the nearly complete genome of a rabbit RVA strain, Rabbit-wt/ITA/36-9/2022/G3P[14], with a genotype constellation (G3-P[14]-I2-R2-C2-M3-A9-N2-T6-E5-H3) conserved among lapine RVAs. Each of the 11 gene segments displayed high nucleotide identity and phylogenetic clustering with lapine rotavirus strains, as well as two Belgian human G3P[14] strains, which had been shown to have a zoonotic (lapine) origin. However, the NSP2 gene of strain 36-9 clustered closer with a group of rare human G3P[9] strains, suggesting a common path during their evolution. Gathering sequence data on animal RVAs is pivotal to reconstructing the history of homologous and heterologous RVAs in various mammals, including humans.

Feline coronavirus (FCoV) is an alphacoronavirus (αCoV) that causes moderate or chronic asymptomatic infection in cats. However, in a single infected cat, FCoV can modify its cellular tropism by acquiring the ability to infect macrophages, resulting in the development of feline infectious peritonitis (FIP). In this context, to restrain the impact of FCoV infection, scientific research has focused attention on the development of antiviral therapies involving novel mechanisms of action. Recent studies have demonstrated that aryl hydrocarbon receptor (AhR) signaling regulates the host response to different human and animal CoVs. Hence, the mechanism of action of AhR was evaluated upon FCoV infection in Crandell Feline Kidney (CRFK) and in canine fibrosarcoma (A72) cells. Following infection with feline enteric CoV (FECV), strain “München”, a significant activation of AhR and of its target CYP1A1, was observed. The selective AhR antagonist CH223191 provoked a reduction in FCoV replication and in the levels of viral nucleocapsid protein (NP). Furthermore, the effect of the AhR inhibitor on the acidity of lysosomes in infected cells was observed. Our findings indicate that FCoV acts on viral replication that upregulates AhR. CH223191 repressed virus yield through the inhibition of AhR. In this respect, for counteracting FCoV, AhR represents a new target useful for identifying antiviral drugs. Moreover, in the presence of CH223191, the alkalinization of lysosomes in FCoV-infected CRFK cells was detected, outlining their involvement in antiviral activity.