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HHV-8, also known as Kaposi’s sarcoma associated herpesvirus, is a gammaherpesvirus found only in humans.1 AIDS-related Kaposi’s sarcoma (KS) was first discovered in 1981, and the association with HHV-8 was identified through DNA sequencing by Chang and colleagues in 1994.2 HHV-8 has subsequently been identified in all types of KS, including classic, endemic, posttransplant and AIDS-related KS, all of which have identical histological features.2 Research has shown a possible role for HHV-8 in the development of two rare lymphoproliferative disorders, multicentric Castleman’s disease (MCD) and primary effusion lymphoma (PEL).2

Epidemiology & Pathogenesis
In Europe and North America, the epidemiology of HHV-8 is very close to that of KS.1 HHV-8 antibodies are typically seen in people who have KS or are at high risk of developing it (such as homosexual men), but are usually not found in low risk individuals (general blood donors).1 HHV-8 infections in the general population are high in Africa, intermediate in Eastern Europe and the Mediterranean, and low in Europe and the United States.1

In the same fashion as the other herpesviruses, HHV-8 establishes latency in the human host after a primary infection.1 The preponderance of the evidence suggests that sexual contact, predominantly among homosexual men, is the principal route of transmission in Europe and North America, where it is rare to non-existent among children.1 Recent prevalence data from Central Africa and the Mediterranean suggest a horizontal, nonsexual method of transmission among children in those regions.1

Clinical Manifestations
A primary HHV-8 infection presents as a fever and rash.1 The fever typically lasts from 2-14 days, and a maculopapular rash persists for 3-8 days.1

When HHV-8 reactivates, it is in the form of Kaposi’s sarcoma.3 KS was first identified in 1872 by Moriz Kaposi, and has since been characterized into 4 well-documented clinical variants3:

  • Classic KS primarily affects older males of Eastern European and Mediterranean lineage, and typically presents as cutaneous lesions on the lower extremities.3
  • Endemic KS occurs in Africa, and may involve the lymph nodes in addition to typical skin lesions.3 This variant is often seen in HIV-negative individuals and in children.3
  • Iatrogenic KS occurs in recipients of solid organ transplants who are being treated with immunosuppressive medications.3 This form of KS occurs more commonly in individuals of Mediterranean descent.3
  • AIDS KS is a very aggressive form that was first identified in the early 1980s in homosexual men who were otherwise healthy.3 In addition to cutaneous and lymphatic involvement, this variant often spreads to the lungs, GI tract, liver and spleen. When AIDS KS was originally identified, the lifetime incidence was approximately 50% in gay men.3 Because of antiviral therapy advances in the late 1990s, the incidence has declined markedly.3

There is a high risk of KS in transplant patients, due to their level of immunosuppression.3 In renal transplant patients, the overall risk is in the range of 1-3%, with a median diagnosis interval of 29-31 months.3 One study of patients who were HHV-8 positive prior to renal transplant found that 23% of them developed KS, while only 0.7% of the seronegative controls did.3 KS development posttransplantation has also been seen in heart and lung patients.3 Kidney transplant patients can develop KS prior to the actual transplant due to reactivation of latent HHV-8 by immunosuppressive therapy.3 In these patients, screening of the host as well as the organ donor are important.3 HHV-8 infection has also been noted as a cause of BMT failure.3 In these patients, the reactivated infection presents as fever with plasmacytosis, resulting in disseminated KS.3

Serology and molecular testing methods such as PCR are recommended.3 Monitoring of all transplant recipients for HHV-8 infections may offer a means to provide more effective antiviral therapy.6

While low dose cidofovir and high dose foscarnet or ganciclovir have been shown to suppress reactivation of HHV-8, they do not inhibit episomal virus DNA polymerase.3 This is suggestive of replication by host DNA polymerase with the latent form of the virus.3 Acyclovir has not been shown to be effective against HHV-8.3 Highly active retroviral therapy (HAART) has been shown to effectively reduce the incidence of

  1. Jenson HB. Human Herpesvirus 8 infection. Current Opinions in Pediatrics. 2003;15:85-91.
  2. Stebbing J, Portsmouth S, Gotch F, Gazzard B. Kaposi’s sarcoma—an update. International Journal of STD & AIDS. 2003;14:225-227.
  3. Ablashi DV, Chatlynne LG, Whitman JE, Cesarman E. Spectrum of Kaposi’s Sarcoma-Associated Herpesvirus, or Human Herpesvirus 8, Diseases. Clinical Microbiology Reviews. 2002;15:439-464.
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