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Junin Virus Activates p38 MAPK and HSP27 Upon Entry.

Collin J Fitzpatrick1, Rajini R Mudhasani1, Louis A Altamura1

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Frontiers in Cellular and Infection Microbiology
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Junín virus (JUNV) infection alters host cell proteins, particularly those involved in viral entry and replication. Inhibiting p38 MAPK or HSP27 reduces JUNV replication, revealing key molecular pathways.

Keywords:
HSP27Junin virusantiviralcellular pathwaysp38 MAPK

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Area of Science:

  • Virology
  • Molecular Biology
  • Immunology

Background:

  • Junín virus (JUNV) causes Argentine hemorrhagic fever, a severe disease with poorly understood molecular pathogenesis.
  • Understanding host-pathogen interactions is crucial for developing effective treatments and vaccines.

Purpose of the Study:

  • To investigate global host proteome alterations following JUNV infection using a human cell culture model.
  • To identify key host proteins and pathways involved in JUNV replication and pathogenesis.

Main Methods:

  • Utilized Reverse Phase Protein Microarrays (RPPA) to analyze proteomic changes in human small airway epithelial cells infected with JUNV strains (Candid#1 and XJ13).
  • Examined protein alterations at early timepoints (1, 3, 8, and 24 hours post-infection).
  • Validated key protein alterations using western blot analysis and assessed the impact of inhibiting p38 MAPK and HSP27 on viral replication.

Main Results:

  • RPPA identified 14 significantly altered proteins out of 113 examined.
  • Commonly phosphorylated proteins, including p38 MAPK, HSP27, and NFκB, were identified, correlating with viral entry and early replication.
  • Inhibition of p38 MAPK or HSP27 significantly reduced JUNV replication.
  • HSP27 phosphorylation at S82 was found to be dependent on p38 MAPK activity.

Conclusions:

  • JUNV infection induces significant changes in the host proteome, involving key signaling pathways.
  • p38 MAPK and HSP27 play critical roles in JUNV replication, suggesting potential therapeutic targets.
  • This study provides insights into the molecular mechanisms of arenavirus pathogenesis.