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PRRSV-2 impedes lysosomes from eliminating secondary infected bacteria

Zifang Zheng1,2, Xue Ling1,2, Shuang Qiao1,2

  • 1State Key Laboratory of Animal Disease Control and Prevention, College of Veterinary Medicine, Lanzhou University, Lanzhou Veterinary Research Institute, Chinese Academy of Agricultural Sciences, Lanzhou, China.

Plos Pathogens
|February 27, 2026
PubMed

Insights

Porcine reproductive and respiratory syndrome virus type 2 (PRRSV-2) disrupts macrophage function by down-regulating RhoA, hindering bacterial clearance and promoting secondary infections. This study reveals a novel mechanism of viral immune evasion.

Area of Science:

  • Virology
  • Immunology
  • Cell Biology

Background:

  • Porcine reproductive and respiratory syndrome virus type 2 (PRRSV-2) is an immunosuppressive virus known to cause secondary bacterial infections.
  • PRRSV-2 evades immune responses, persisting within macrophages.

Purpose of the Study:

  • To elucidate the mechanism by which PRRSV-2 facilitates secondary bacterial survival.
  • To investigate the role of RhoA and F-actin cytoskeleton in PRRSV-2-induced immune suppression.

Main Methods:

  • Investigated the impact of PRRSV-2 infection on macrophage F-actin cytoskeleton and lysosomal bacterial clearance.
  • Utilized RhoA silencing and overexpression to assess its role in bacterial clearance.
  • Examined the interaction between PRRSV-2 nsp5, Smurf1, and RhoA ubiquitination and degradation.

Main Results:

  • PRRSV-2 infection disrupts F-actin, impairing lysosomal transport and bacterial clearance by macrophages.
  • RhoA is essential for F-actin polymerization and efficient bacterial clearance; its suppression by PRRSV-2 increases viable bacteria.
  • PRRSV-2 nsp5 interacts with Smurf1 to ubiquitinate RhoA, leading to its degradation and F-actin disruption.

Conclusions:

  • PRRSV-2 reprograms the host cytoskeleton via RhoA degradation to promote secondary bacterial survival.
  • Targeting the nsp5-Smurf1-RhoA pathway offers a potential strategy for controlling PRRSV-2 secondary infections.

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