Apoptosis and porcine reproductive and respiratory syndrome virus

Vet Immunol Immunopathol. 2004 Dec 8;102(3):131-42. doi: 10.1016/j.vetimm.2004.09.004.

Abstract

Despite numerous studies examining the possible induction of apoptosis in porcine reproductive and respiratory syndrome virus (PRRSV)-infected cells, it remains unclear if PRRSV infection results in direct apoptotic induction. There is clear evidence that apoptotic cells are present in tissues from PRRSV-infected pigs. However, many of these studies have failed to show that the apoptotic cells are infected with PRRSV. This has led some investigators to propose that "bystander" cells, not infected cells, become apoptotic during PRRSV infection by a yet undetermined mechanism. Studies examining the induction of the apoptotic gene expression response to PRRSV infection are needed to determine if PRRSV replication triggers an apoptotic response. We have utilized microarray and semi-quantitative reverse-transcription polymerase chain reaction (sqRT-PCR) to evaluate apoptotic gene expression in PRRSV-infected MARC-145 cells. Twenty-six apoptosis-related genes were examined during the first 24 h of infection and found to be unaltered, indicating that apoptotic induction was not occurring in PRRSV-infected cells. Additionally, using detection of free nucleosomal complexes, we examined cells for both apoptotic and necrotic death resulting from PRRSV infection at varying multiplicities of infection. This study indicates that PRRSV-infected MARC-145 cells undergo necrosis at a much higher level than apoptosis, and increases with virus levels used to infect the cells.

Publication types

  • Review

MeSH terms

  • Animals
  • Apoptosis* / genetics
  • Cell Line
  • Gene Expression Profiling / veterinary
  • Gene Expression Regulation
  • Necrosis / veterinary
  • Necrosis / virology
  • Porcine Reproductive and Respiratory Syndrome / pathology*
  • Porcine Reproductive and Respiratory Syndrome / virology
  • Porcine respiratory and reproductive syndrome virus / pathogenicity*
  • Swine / virology
  • Transcription, Genetic