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The history of the identification of human herpesvirus 8 (HHV-8; also known as Kaposi sarcoma herpesvirus [KSHV] or Kaposi sarcoma [KS] virus) was unique among the Herpesviridae insofar as the virus was initially “discovered” purely on a molecular biologic basis using a powerful detection technique.1 Working with tissue from HIV- infected individuals with KS, Chang and colleagues used a technique referred to as “representational difference analysis” to identify disease-specific DNA sequences in KS tissue. On DNA sequence analysis, the deduced amino acid sequences were found to have strong homology to proteins from the gamma herpesvirus subfamily, the subfamily of the Herpesviridae that includes Epstein-Barr virus (EBV). This observation was striking in view of the known ability of EBV to persist in lymphocytes, immortalize cells, and produce human malignancies (Burkitt lymphoma and nasopharyngeal carcinoma). Hence, the novel gamma herpesvirus, HHV-8, appeared to be a new herpesvirus associated with human malignancy, Kaposi sarcoma. Eventually HHV-8 was cultivated in tissue culture, proving that these DNA sequences corresponded to a morphologically identifiable viral particle.2




The epidemiology of primary human herpesvirus 8 (HHV-8) infection appears to vary considerably worldwide. The routes of acquisition of infection and mechanisms responsible for person-to-person transmission remain uncertain. After the virus was initially discovered, the unique role it seemed to play in inducing malignant disease in HIV-infected patients suggested that the primary route of transmission of HHV-8 was through sexual contact, particularly among gay men. However, more recent evidence suggests that other routes of infection exist, including transmission by saliva.4 A cross-sectional study of the seroprevalence of HHV-8 in children and adolescents in the United States indicated a prevalence of approximately 1%.5 There appears to be considerable regional variation in prevalence in the United States. In a population of children in south Texas, the seroprevalence was 26%, strongly suggesting that nonsexual modes of transmission predominate.6 In sub-Saharan Africa, prevalence in children is even higher, approaching 60% in some studies (reviewed in 7). There are reports of maternal-to-child transmission that suggest the possible of vertical infection (reviewed in 8), but the mechanisms of transmission and clinical manifestations in newborns are unclear. HHV-8 can also be transmitted by blood transfusion.9 As serologic and nucleic acid-based diagnostics tests become more widely available, a better assessment of the worldwide seroepidemiology of HHV-8 infection will become feasible.




Structurally, human herpesvirus 8 (HHV-8) consists of a prototypical enveloped particle, morphologically similar to other herpesviruses. The virus presumably establishes latent infection following primary infection, although the site(s) of latency are unknown. Evolutionarily, HHV-8 appears to have undergone considerable recombination with host genes, and the viral genome contains a variety of transduced cellular oncogenes and chemokine homologs that are probably important in the pathogenesis of KS.3 It is estimated that 10% of the genes encoded by HHV-8 promote KS development due to mitogenic, antiapoptotic, chemoattractive, angiogenic, or transforming activities.

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