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Microtubule depolymerization limits porcine betacoronavirus PHEV replication.

Qianyu Zhou1, Yungang Lan1, Yifei Tang1

  • 1Key Laboratory of Zoonosis Research, Ministry of Education, College of Veterinary Medicine, Jilin University, Changchun, China.

Veterinary Microbiology
|May 9, 2022
PubMed
Summary
This summary is machine-generated.

Porcine hemagglutinating encephalomyelitis virus (PHEV) infection disrupts microtubules (MTs) in pigs. MT depolymerization inhibits viral RNA replication, suggesting a novel therapeutic target for PHEV.

Keywords:
Acetylated modificationDepolymerizationHDAC6MicrotubulePorcine hemagglutinating encephalomyelitis virus

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Area of Science:

  • Virology
  • Cell Biology
  • Microbiology

Background:

  • Porcine hemagglutinating encephalomyelitis virus (PHEV), a neurotropic betacoronavirus, causes significant disease in neonatal pigs.
  • While actin's role in PHEV invasion is known, the impact on the microtubule (MT) cytoskeleton remains unclear.

Purpose of the Study:

  • To investigate the effects of PHEV infection on the host cell's microtubule cytoskeleton.
  • To determine the role of microtubule dynamics in PHEV replication.

Main Methods:

  • Observation of MTs and microtubule organizing centers in PHEV-infected cells.
  • Treatment with nocodazole (MT depolymerization) and paclitaxel (MT polymerization) to assess viral RNA replication.
  • Analysis of histone deacetylase 6 (HDAC6) expression and activity during infection.

Main Results:

  • PHEV infection induced MT depolymerization and loss of microtubule organizing centers.
  • MT depolymerization significantly inhibited PHEV RNA replication, while MT over-polymerization had no substantial effect.
  • HDAC6 expression increased during infection, but altering its activity did not enhance PHEV proliferation.

Conclusions:

  • PHEV infection subverts the host MT cytoskeleton to facilitate viral entry and replication.
  • MT depolymerization negatively impacts PHEV replication, independent of HDAC6 activity, presenting a potential therapeutic avenue.