Skip to content


  • Oral presentation
  • Open Access

Accelerated progression to AIDS in macaques coinfected with simian immunodeficiency virus and human herpesvirus 6A

  • 1,
  • 2,
  • 1,
  • 1,
  • 1,
  • 3,
  • 4 and
  • 2
Retrovirology20063 (Suppl 1) :S62

  • Published:


  • Virus Disease
  • Simian Immunodeficiency Virus
  • Relevant Model
  • Primate Immunodeficiency
  • Human Herpesvirus

Although HIV-1 is the necessary and sufficient causative agent of AIDS, genetic and environmental factors markedly influence the pace of disease progression. Clinical and experimental evidence suggests that human herpesvirus 6 (HHV-6), a cytopathic T-lymphotropic agent, may act as an accelerating factor in the progression of HIV disease, although conclusive in vivo evidence has yet to be attained. To evaluate the effect of HHV-6A on the course of AIDS in a relevant model system, we infected pig-tailed macaques (M. nemestrina) either with HHV-6A (strain GS) or with a pathogenic SIV strain (smE660), or with both viruses. Extensive longitudinal virologic, immunologic and clinical follow-up demonstrated that HHV-6A coinfection dramatically accelerated the progression toward full-blown AIDS. Rapid disease development in coinfected animals was associated with an early depletion of both CD4+ and CD8+ T cells. Simultaneous replication of both viruses was documented in coinfected lymph node tissue. These data establish a new animal model for the study of HHV-6 infection and provide the first conclusive in vivo evidence that HHV-6A acts as a cofactor in the progression of primate immunodeficiency virus disease.

Authors’ Affiliations

Department of Biotechnology, San Raffaele Scientific Institute, Milan, Italy
Institute of Human Virology, University of Maryland, Baltimore, Maryland, USA
Laboratory of Cellular and Molecular Biophysics, National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, Maryland, USA
Advanced BioScience Laboratories, Inc., Kensington, Maryland, USA


© Lusso et al; licensee BioMed Central Ltd. 2006

This article is published under license to BioMed Central Ltd.