Autophagy postpones apoptotic cell death in PRRSV infection through Bad-Beclin1 interaction

Ao Zhou1, Shuaifeng Li1, Faheem Ahmed Khan1

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

Virulence
|December 17, 2015
PubMed

Insights

Autophagy helps Porcine Reproductive and Respiratory Syndrome Virus (PRRSV) replicate by delaying apoptosis. This occurs through a Bad-Beclin1 complex, highlighting a key interaction in PRRSV infection.

Area of Science:

  • Virology
  • Cellular Biology
  • Immunology

Background:

  • Autophagy and apoptosis are crucial in Porcine Reproductive and Respiratory Syndrome Virus (PRRSV) infection.
  • The interplay between autophagy and apoptosis during PRRSV replication remains poorly understood.

Purpose of the Study:

  • To investigate the interaction between autophagy and apoptosis in MARC-145 cells during PRRSV infection.
  • To elucidate the molecular mechanisms by which these processes influence viral replication.

Main Methods:

  • PRRSV infection of MARC-145 cells.
  • Inhibition of autophagy using 3-methyladenine (3-MA).
  • Analysis of apoptosis and autophagy markers (Bad, Beclin1).
  • Co-immunoprecipitation and co-localization assays.
  • Gene silencing (knockdown) of Beclin1 and Bad.
  • Western blot analysis for phosphorylated Bad (Ser112).

Main Results:

  • PRRSV infection activated both autophagy and apoptosis in MARC-145 cells.
  • Autophagy inhibition (3-MA) increased PRRSV-induced apoptosis.
  • Bad and Beclin1 expression increased, forming a complex and co-localizing in infected cells.
  • Beclin1 knockdown reduced viral replication and autophagy.
  • Bad silencing enhanced autophagy and viral replication.
  • PRRSV infection phosphorylated Bad (Ser112), promoting cell survival.

Conclusions:

  • Autophagy promotes PRRSV replication by inhibiting apoptosis via a Bad-Beclin1 complex.
  • Targeting the Bad-Beclin1 interaction could be a strategy to control PRRSV infection.

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