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Viral interleukin-6 encoded by rhesus macaque rhadinovirus is associated with lymphoproliferative disorder (LPD)

B U Orzechowska1, M Manoharan, J Sprague

  • 1Vaccine and Gene Therapy Institute, Oregon Health & Science University, West Campus, Beaverton, OR 97006, USA.

Journal of Medical Primatology
|October 30, 2009
PubMed
Abstract

Insights

Rhesus macaques co-infected with simian immunodeficiency virus (SIV) and rhesus macaque rhadinovirus (RRV) can develop abnormal cell growths. Viral interleukin-6 (vIL-6) from RRV may play a critical role in these lymphoproliferative disorders.

Area of Science:

  • Virology
  • Oncology
  • Immunology

Background:

  • Co-infection with simian immunodeficiency virus (SIV) and rhesus macaque rhadinovirus (RRV) in rhesus macaques (RM) leads to abnormal cellular proliferations, including extra-nodal lymphoma and retroperitoneal fibromatosis (RF).
  • RRV encodes a viral interleukin-6 (vIL-6), analogous to the cytokine encoded by Kaposi's sarcoma-associated herpesvirus.
  • The role of RRV vIL-6 in the development of these proliferative lesions was investigated.

Purpose of the Study:

  • To determine the presence of RRV in lymphoproliferative lesions in co-infected rhesus macaques.
  • To investigate the expression of RRV-encoded vIL-6 within these lesions.
  • To understand the potential role of vIL-6 in the pathogenesis of these disorders.

Main Methods:

  • Analysis of formalin-fixed tissues from SIV and RRV co-infected RM.
  • In situ hybridization was used to detect RRV genomes within the lesions.
  • Immunofluorescence analysis was employed to assess RRV vIL-6 expression and cellular markers (vimentin, CD117, SMA) and immune cell infiltrates (T cells, B cells, monocytes/macrophages).

Main Results:

  • RRV genomes were detected in both lymphoma and retroperitoneal fibromatosis lesions.
  • Immunofluorescence confirmed the presence of vIL-6 in these proliferative lesions.
  • RF lesions exhibited markers characteristic of Kaposi's sarcoma, including vimentin, CD117, SMA, and infiltrates of T cells, B cells, and monocytes/macrophages.

Conclusions:

  • The presence of RRV and its vIL-6 in abnormal cellular proliferations suggests a significant role for this viral cytokine.
  • Data indicate that RRV vIL-6 may be crucial for the development and progression of lymphoproliferative disorders in SIV/RRV-coinfected RM.
  • These findings highlight the potential oncogenic mechanisms mediated by viral cytokines in the context of retroviral co-infections.

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