Trichodysplasia spinulosa-associated polyomavirus (TSV) and Merkel cell polyomavirus: correlation between humoral and

Arun Kumar1, Anu Kantele, Tommi Järvinen

  • 1Departments of Virology, Haartman Institute, University of Helsinki, Helsinki, Finland. arun.kumar@helsinki.fi

Plos One
|October 3, 2012
PubMed

Insights

This study investigated T-cell immunity against Merkel cell polyomavirus (MCV) and Trichodysplasia spinulosa-associated polyomavirus (TSV). While TSV showed strong T-cell and antibody correlations, MCV responses were weaker, with no cross-reactivity observed.

Area of Science:

  • Immunology
  • Virology
  • Oncology

Background:

  • Merkel Cell Polyomavirus (MCV) is linked to Merkel cell carcinoma (MCC).
  • Trichodysplasia spinulosa-associated polyomavirus (TSV) is detected in TS skin lesions, suggesting a causal role.
  • Previous research shows strong MCV-specific T-cell responses, but TSV T-cell immunity is uncharacterized.

Purpose of the Study:

  • To characterize T-helper (Th)-cell immunity against TSV.
  • To compare TSV-specific Th-cell immunity with MCV-specific Th-cell immunity.
  • To investigate potential cross-reactivity between MCV and TSV Th-cell responses.

Main Methods:

  • Studied TSV-specific proliferation, IFN-γ, IL-10, and IL-13 responses.
  • Assessed MCV-specific IFN-γ and IL-10 responses.
  • Utilized recombinant TSV and MCV VP1 virus-like particles (VLPs) as antigens in 51 healthy volunteers and one MCC patient.

Main Results:

  • A significant correlation between virus-specific Th-cell and antibody responses was found for TSV, but weaker for MCV.
  • No evident Th-cell cross-reactivity was observed between TSV and MCV, despite amino acid sequence homology.
  • Some individuals seronegative for both viruses displayed Th-cell responses to both, indicating an unknown priming agent.

Conclusions:

  • TSV-specific Th-cell immunity correlates with antibody responses, unlike MCV.
  • MCV VP1-specific Th-cells, potentially via IFN-γ, may inhibit MCV replication and contribute to preventing oncogenesis.
  • The priming agent for observed Th-cell responses in seronegative individuals remains unidentified.

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