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Identification of a VapA virulence factor functional homolog in Rhodococcus equi isolates housing the pVAPB plasmid

Jennifer M Willingham-Lane1, Garry B Coulson1, Mary K Hondalus1

  • 1Department of Infectious Disease, University of Georgia, Athens, Georgia, United States of America.

Plos One
|October 5, 2018
PubMed

Insights

Rhodococcus equi virulence factors VapK1 and VapK2 are essential for intracellular replication in macrophages. These VapK proteins are functionally equivalent to the major virulence determinant VapA, impacting bacterial survival within host cells.

Area of Science:

  • Microbiology
  • Bacterial Pathogenesis
  • Immunology

Background:

  • Rhodococcus equi is an important pathogen causing abscesses in animals and immunocompromised individuals.
  • The major virulence factor, VapA, on pVAPA plasmids disrupts phagosome development and is crucial for intracellular replication.
  • Different R. equi strains carry distinct plasmids (pVAPA, pVPB) influencing virulence.

Purpose of the Study:

  • To investigate the role of VapK1 and VapK2 in the intracellular replication of R. equi.
  • To determine if VapK proteins can compensate for the absence of VapA.

Main Methods:

  • Construction and analysis of Rhodococcus equi gene deletion mutants.
  • Complementation assays using VapK1 and VapK2 in a ΔvapA strain.
  • Assessment of bacterial replication within equine macrophages.

Main Results:

  • VapK1 or VapK2 is required for optimal intracellular replication of pVAPB-type R. equi.
  • VapK proteins restored replication capacity to a VapA-deficient strain.
  • Deletion of vapK1 and vapK2 in a pVAPB-type plasmid abolished intracellular replication in equine macrophages.

Conclusions:

  • VapK1 and VapK2 are functionally equivalent to VapA in promoting intracellular replication.
  • These findings highlight novel virulence mechanisms in R. equi strains lacking VapA.

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