Interplay of autophagy and apoptosis during PRRSV infection of Marc145 cell

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Shuaifeng Li1, Ao Zhou1, Jiaxing Wang1

  • 1Key Lab of Agricultural Animal Genetics, Breeding and Reproduction of Ministry of Education, Huazhong Agricultural University, Wuhan 430070, China.

Infection, Genetics and Evolution : Journal of Molecular Epidemiology and Evolutionary Genetics in Infectious Diseases
|January 18, 2016
PubMed

Insights

Autophagy and apoptosis are triggered by Porcine Reproductive and Respiratory Syndrome Virus (PRRSV) infection. Autophagy deficiency hinders PRRSV replication, while apoptosis inhibition enhances it, revealing their complex interplay.

Area of Science:

  • Virology
  • Cellular Biology
  • Immunology

Background:

  • Autophagy and apoptosis are critical cellular processes involved in viral infections.
  • The specific roles of autophagy and apoptosis in Porcine Reproductive and Respiratory Syndrome Virus (PRRSV) replication remain incompletely understood.

Purpose of the Study:

  • To investigate the intricate relationship between autophagy and apoptosis during PRRSV infection.
  • To elucidate how these two programmed cell death pathways influence viral replication dynamics.

Main Methods:

  • PRRSV infection was used to induce autophagy and apoptosis in host cells.
  • Autophagy-deficient cells were utilized to assess the impact of autophagy on viral replication.
  • Apoptosis inhibition was employed to determine its effect on PRRSV replication in both normal and autophagy-deficient cells.

Main Results:

  • PRRSV infection successfully induced both autophagy and apoptosis.
  • Autophagy deficiency led to attenuated PRRSV replication.
  • Inhibition of apoptosis potentiated viral replication.
  • Crucially, apoptosis inhibition restored PRRSV replication in autophagy-deficient cells.

Conclusions:

  • Autophagy plays a suppressive role in PRRSV replication.
  • Apoptosis appears to promote PRRSV replication.
  • There is a significant functional interplay between autophagy and apoptosis in modulating PRRSV replication, with implications for viral pathogenesis.
Keywords:
ApoptosisAutophagyMarc145 cellPRRSV

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