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

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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.

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Correspondence to Paolo Lusso.

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Open Access This article is published under license to BioMed Central Ltd. This is an Open Access article is distributed under the terms of the Creative Commons Attribution 2.0 International License (, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

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About this article


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