Last updated: 15-Jan-2007
Herpesvirus Type 8
HHV-8 appears to have a causal role in several diseases, including certain lymphomas and Kaposi sarcoma. The latter connection lends the virus it’s alternate name, Kaposi sarcoma-associated herpesvirus (KSHV). The virus is detected infrequently in people at low risk for Kaposi sarcoma (KS).[1]
HHV-8 has been isolated in a number of body tissues and fluids, prompting investigation of multiple potential routes of transmission. There is a strong link with HIV infection, as noted earlier. In fact, the predominant means of transmitting HHV-8 appears to be male homosexual sex. About 1 out of 5 men who have sex with men and who have HIV, also show HHV-8 in their blood.[2] The virus is also present in the saliva of 75% of HIV-infected patients who have KS.[3] In contrast, there is no evidence that monogamous heterosexual sex is a usual mode of transmission.[4] Beyond men having sex with men, the only other sexual activity that has been clearly shown to be a risk factor is female prostitution. Studies have shown that the behaviours related to injection-drug use (such as needle sharing) may lead to HHV-8 infection, though less efficiently than HBV, HCV or HIV.[5] This suggests the need to be vigilant about transmission through blood transfusions, though there is no evidence of this risk so far; for instance, haemophiliacs do not acquire KS.[6],[7],[8] Finally, the high rate of HHV-8 among African preadolescent children suggests that nonsexual routes of transmission may be in operation, but these are not well understood.[9]
Associated Cancers
HHV-8 is best known for its connection to KS. A relatively rare condition until 25 years ago, it has become a “sentinel diagnosis” for AIDS, along with a characteristic pneumonia. Prior to the emergence of AIDS, an endemic form of KS has been noted for centuries among elderly males in southern Europe and both adults and children in equatorial Africa.
KS has also long been known as a complication among transplant patients undergoing immunosuppressive therapy.[10] It seems that that a compromised immune system is an essential milieu for the development of KS; the fact is that only a small fraction of immunocompetent people infected with HHV-8 end up with a malignancy.[11]
The more recent form of KS is the epidemic version related to HIV infection. It still requires the presence of HHV-8, with HIV supplying the necessary immunosuppressive component.
KS begins with a few skin lesions, but without treatment it can eventually affect multiple organs, including the lung, liver, digestive tract and spleen.[12] The clinical course of KS is highly variable, ranging from minimal disease to explosive growth, with significant morbidity and mortality.
There are certain rare lymphomas that are closely related to both HIV infection and KS in men who have sex with men. These malignancies have been connected to HHV-8. They are distinguished from other non-Hodgkin’s lymphomas (NHLs) by their presentation as effusions in the visceral cavity; they do not exhibit a significant tumour mass. [13] Only a few cases of this type of lymphoma have been reported in HIV-negative individuals.[14]
Preventive Interventions
In the absence of specific vaccines or treatments in the rather complex world of KS and lymphomas related to HHV-8, it becomes all the more important to follow preventive strategies.[15] The main early primary prevention measures are the same as for HIV, namely, “safe sex” education and practices, especially among male homosexuals (see the earlier section).
There are no specific KS secondary prevention methods. The classic treatments used for KS involve different types of cancer management, and thus are not preventive per se.
The best primary prevention results for HHV-8 diseases are emerging as a by-product of the HIV / AIDS battle. The introduction of effective antiretroviral therapies for HIV infection seems to be having an impact on both KS and AIDS-related NHLs, at least in developed countries.[16] After a rapid rise over a 20 year period, the incidence of these diseases has decreased in the US since the mid-1990s. By contrast, non-AIDS-associated NHL rates have continued to climb.[17],[18]
An unexpected result of successful treatment of immunocompromised individuals, where they then live longer, is the possible development of more NHL in the future.[19]
[1] Whitby D, Howard MR, Tenant-Flowers M et al. Detection of Kaposi sarcoma associated herpesvirus in peripheral blood of HIV-infected individuals and progression to Kaposi's sarcoma. The Lancet. 1995; 346(8978): 799-802.
[2] Whitby D, Boshoff C. Kaposi's sarcoma herpesvirus as a new paradigm for virus-induced oncogenesis. Current Opinion in Oncology. 1998; 10(5): 405-12.
[3] Koelle DM, Huang ML, Chandran B et al. Frequent detection of Kaposi's sarcoma-associated herpesvirus (human herpesvirus 8) DNA in saliva of human immunodeficiency virus-infected men: clinical and immunologic correlates. Journal of Infectious Diseases. 1997; 176(1): 94-102.
[4] Smith NA, Sabin CA, Gopal R et al. Serologic evidence of human herpesvirus 8 transmission by homosexual but not heterosexual sex. Journal of Infectious Diseases. 1999; 180(3): 600-6.
[5] Cannon MJ, Dollard SC, Smith DK et al. Blood-borne and sexual transmission of human herpesvirus 8 in women with or at risk for human immunodeficiency virus infection. New England Journal of Medicine. 2001; 344(9): 637-43.
[6] Engels EA, Eastman H, Ablashi DV et al. Risk of transfusion-associated transmission of human herpesvirus 8. Journal of National Cancer Institute. 1999; 91(20): 1773-5.
[7] Boshoff C, Chang Y. Kaposi's sarcoma-associated herpesvirus: a new DNA tumor virus. Annual Review of Medicine. 2001; 52: 453-70.
[8] Whitby D, Howard MR, Tenant-Flowers M et al. Detection of Kaposi sarcoma associated herpesvirus in peripheral blood of HIV-infected individuals and progression to Kaposi's sarcoma. The Lancet. 1995; 346(8978): 799-802.
[9] Gessain A, Mauclere P, van Beveren M et al. Human herpesvirus 8 primary infection occurs during childhood in Cameroon, Central Africa. International Journal of Cancer. 1999; 81(2): 189-92.
[10] Boshoff C, Chang Y. Kaposi's sarcoma-associated herpesvirus: a new DNA tumor virus. Annual Review of Medicine. 2001; 52: 453-70.
[11] Boshoff C. Kaposi's sarcoma. Coupling herpesvirus to angiogenesis. Nature. 1998; 391(6662): 24-5.
[12] Boshoff C, Chang Y. Kaposi's sarcoma-associated herpesvirus: a new DNA tumor virus. Annual Review of Medicine. 2001; 52: 453-70.
[13] Boshoff C, Chang Y. Kaposi's sarcoma-associated herpesvirus: a new DNA tumor virus. Annual Review of Medicine. 2001; 52: 453-70.
[14] Baris D, Zahm SH. Epidemiology of lymphomas. Current Opinion in Oncology. 2000; 12(5): 383-94.
[15] Fisher SG, Fisher RI. The epidemiology of non-Hodgkin's lymphoma. Oncogene. 2004; 23(38): 6524-34.
[16] Baris D, Zahm SH. Epidemiology of lymphomas. Current Opinion in Oncology. 2000; 12(5): 383-94.
[17] Eltom MA, Jemal A, Mbulaiteye SM et al. Trends in Kaposi's sarcoma and non-Hodgkin's lymphoma incidence in the United States from 1973 through 1998. Journal of National Cancer Institute. 2002; 94(16): 1204-10.
[18] Chiu BC, Weisenburger DD. An update of the epidemiology of non-Hodgkin's lymphoma. Clinical Lymphoma. 2003; 4(3): 161-8.
[19] Fisher SG, Fisher RI. The epidemiology of non-Hodgkin's lymphoma. Oncogene. 2004; 23(38): 6524-34.