Increased proportion of apoptotic cells in cat kidney tissues infected with feline morbillivirus

Kripitch Sutummaporn1,2,3, Kazuhiko Suzuki4, Noboru Machida5

  • 1Laboratory of Veterinary Microbiology, Cooperative Department of Veterinary Medicine, Faculty of Agriculture, Tokyo University of Agriculture and Technology, Tokyo, 183-8509, Japan.

Archives of Virology
|August 27, 2020
PubMed

Insights

Feline morbillivirus (FeMV) infection in cats significantly increases kidney cell apoptosis. FeMV P protein is present in many apoptotic cells, suggesting FeMV induces cell death as a pathological mechanism.

Area of Science:

  • Veterinary Virology
  • Cellular Pathology
  • Infectious Diseases

Background:

  • Feline morbillivirus (FeMV) is an emerging viral pathogen affecting domestic cats.
  • Understanding FeMV's pathogenic mechanisms is crucial for feline health and disease management.
  • Kidney tissues are a target for FeMV, but the cellular impact remains unclear.

Purpose of the Study:

  • To investigate the pathogenic mechanisms of FeMV in infected feline kidney cells.
  • To determine if FeMV infection induces apoptosis in kidney tissues.
  • To correlate FeMV presence with apoptotic cell markers.

Main Methods:

  • Terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) assay to detect apoptosis.
  • Immunofluorescence assay (IFA) using an anti-FeMV P protein antibody.
  • Analysis of 38 cat kidney tissues, including 12 FeMV-positive samples.

Main Results:

  • FeMV-positive kidney tissues showed significantly higher numbers of apoptotic cells compared to FeMV-negative tissues.
  • A substantial percentage (mean 37.4%) of TUNEL-positive cells in infected tissues contained the FeMV P protein.
  • This indicates a direct link between FeMV infection and cellular apoptosis.

Conclusions:

  • Apoptosis induction is a significant pathological mechanism in FeMV-infected cat kidneys.
  • FeMV P protein is associated with apoptotic cells, supporting its role in inducing cell death.
  • These findings advance our understanding of FeMV pathogenesis and its impact on feline renal health.

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