Hepatitis B virus (HBV) is a human pathogen of global concern, while a high diversity of viruses related to HBV have been discovered in other animals during the last decade. Recently, the novel mammalian hepadnavirus, tentatively named domestic cat hepadnavirus (DCH), was detected in an immunocompromised cat. Herein, a collection of 209 cat sera and 15 hepato-diseased cats were screened for DCH using PCR, resulting in 12.4% and 20% positivity in the tested sera and necropsied cats, respectively. Among the DCH-positive sera, a significantly high level of co-detection with retroviral infection was found, with the highest proportion being co-detection with feline immunodeficiency virus (FIV). Full-length genome characterization of DCH revealed the genetic diversity between the nine Thai DCH sequences obtained, and that they phylogenetically formed three distinct monophyletic clades. A putative DCH recombinant strain was found, suggesting a possible role of recombination in DCH evolution. Additionally, quantitative PCR was used to determine the viral copy number in various organs of the DCH-moribund cats, while the pathological findings were compared to the viral localization in hepatocytes, adjacent to areas of hepatic fibrosis, by immunohistochemical (IHC) and western blot analysis. In addition to the liver, positive-DCH immunoreactivity was found in various other organs, including kidneys, lung, heart, intestine, brain, and lymph nodes, providing evidence of systemic infection. Ultrastructure of infected cells revealed electron-dense particles in the nucleus and cytoplasm of hepatocytes, bronchial epithelial cells, and fibroblasts. We propose the intracellular development mechanism of this virus. Although the definitive roles of pathogenicity of DCH remains undetermined, a contributory role of the virus associated with systemic diseases is possible.

Feline bocavirus-1 (FBoV-1) was identified in cats from different households with hemorrhagic enteritis during outbreaks of an unusual clinical presentation of feline panleukopenia virus (FPLV) in Thailand. Use of polymerase chain reaction revealed the presence of the FBoV-1 DNA in several tissues, suggesting hematogenous viremia, with the viral nucleic acid, detected by in situ hybridization (ISH), was localized in intestinal cells and vascular endothelium of intestinal mucosa and serosa, and in necrosis areas primarily in various lymph nodes while FPLV-immunohistochemical analysis revealed viral localization only in cryptal cells, neurons, and limited to leukocytes in the mesenteric lymph node. Full-length coding genome analysis of the Thai FBoV-1 strains isolated from moribund cats revealed three distinct strains with a high between-strain genetic diversity, while genetic recombination in one of the three FBoV-1 strains within the NS1 gene. This is the first report identifying natural genetic recombination of the FBoV-1 and describing the pathology and viral tropism of FBoV-1 infection in cats. Although the role of FBoV-1 associated with systemic infection of these cats remained undetermined, a contributory role of enteric infection of FBoV-1 is possible. Synergistic effects of dual infection with FPLV and FBoV-1 are hypothesized, suggesting more likely severe clinical presentations.

Background Cutaneous mastocytosis (CM) is a rare disease of dogs characterized by rash, pruritus and proliferation of mast cells in the skin. Oral H1 antihistamines are recommended as the treatment to control pruritus. Hypothesis/Objective To describe the effective treatment of pruritus associated with CM with lokivetmab in one dog. Animal A 4‐year‐old, spayed female cross‐bred dog presented with severely pruritic, erythematous to pigmented macules and papules involving the ventral abdomen, interdigital skin, perivulval area and both pinnae; the pruritus had been unresponsive to treatment with antihistamines, prednisone and ciclosporin. Methods and materials Complete blood count and serum biochemistry, abdominal ultrasound, blood smear and skin cytological evaluation, PCR, histopathological and immunohistochemical examination of skin biopsies. Results Skin cytological evaluation revealed high numbers of uniform, heavily granulated mast cells; histopathological findings showed focal dermal proliferations of well‐differentiated, uniform mast cells consistent with a low‐grade mast cell tumour (MCT). Clinical staging revealed that the disease was confined to the skin. Mutations of c‐kit exon 8 and 11 were not detected. Treatment was initiated with anti‐canine‐interleukin (IL)‐31 monoclonal antibody lokivetmab; antihistamines were continued. The dog's pruritus resolved within seven days and was maintained in remission over 15 months with once monthly lokivetmab injections; the skin lesions improved but did not resolve. Conclusion and clinical importance Lokivetmab treatment was effective in resolving and maintaining pruritus remission in this dog with widespread cutaneous mast cell disease. Whether CM in dogs represent a separate entity that should be distinguished from a low‐grade MCT requires further investigation.

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Background Whether domestic cat hepadnavirus (DCH) infection is associated with clinical disease remains to be determined. Objectives To determine the relationship between DCH detection, hematology, serum bichemistry and liver histology in DCH‐positive cats. Animals One thousand twenty‐two cats in Thailand without concurrent diseases and not undergoing treatments adversely affecting the liver. Methods Retrospective cross‐sectional study. Samples derived from cats with concurrent virus detection were excluded. DCH detection was determined in blood and fresh‐frozen liver by quantitative polymerase chain reaction (qPCR) and further investigated in liver sections showing histological parenchymal disorders (HPD) and normal liver (HNL) using in situ hybridization (ISH). Proliferative/apoptotic activities were determined using immunohistochemistry and ISH panels. Biochemical variables and risk factors for DCH infection were investigated. Results Six hundred sixty‐one (557 blood and 119 liver samples) cats were included. DCH was detected in 18.50% (103/557), 13.85% (9/65), and 3.70% (2/54) of the blood, HPD, and HNL groups, respectively. Cats with DCH revealed abnormally high activity of aspartate aminotransferase (AST) (P = .001) and alanine aminotransferase (ALT) (P < .001). Among DCH‐positive HPD case 2/9 an 7/9 were acute and chronic hepatitis, of which 4/7 had hepatitis. Log viral copy number (LVCN) was positively correlated with ALT (P < .001), triglyceride (P < .001), and gamma‐glutamyl transpeptidase (GGT) (P = .022). The LVCN also had a positive association with degree of hepatitis (P < .05). There was hepatocyte proliferation activity in DHC positive cats. Conclusion and Clinical Importance Domestic cat hepadnavirus infection was associated with high serum activity of liver enzymes and chronic lymphoplasmacytic hepatitis (LPH).