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Human herpesvirus 8 and Kaposi's sarcoma in the Amsterdam cohort studies. Disease association, transmission and natural history - Addendum Timing of Human Immunodeficiency Virus type 1 and Human Herpesvirus 8 Infections and length of the Kaposi's sarcoma-

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Human herpesvirus 8 and Kaposi's sarcoma in the Amsterdam cohort studies.

Disease association, transmission and natural history

Renwick, N.M.

Publication date

2001

Link to publication

Citation for published version (APA):

Renwick, N. M. (2001). Human herpesvirus 8 and Kaposi's sarcoma in the Amsterdam cohort

studies. Disease association, transmission and natural history.

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(2)

ddendum m

Timingg of Human Immunodeficiency Virus type 1

andd Human Herpesvirus 8 Infections and length of the

Kaposi'ss sarcoma-free period in coinfected persons

NeilNeil Renwiek, Gerritjan Weverling, Thomas Schulp and Jaap Goudsmit

(3)

T oo the Editor

Inn 1998, we reported that human immunodeficiency virus typee 1 (HIVT)-infected homosexual men have the highest riskk of developing Kaposi's sarcoma (KS) if they acquire humann herpesvirus 8 (HHV-8) after HIV infection (1). This observationn has been confirmed recently by jacobson e t al. (2),, who also found that the duration of HIV-1 infection be-foree HHV-8 acquisition influences the risk for KS. There-fore,, we (1) and Jacobson et al. (2) suggested that immuno-deficiencyy at the time of primary HHV 8 infection may shortenn the KS-free period.

Inn a subsequent correspondence, Rezza (3) suggested that thiss is not necessarily the case, since most cases of trans-plantt associated KS in an HHV-8-endemic country oc-curredd in patients who had acquired HHV 8 before trans-plantationn (4). Rezza infers from these data that factors like HIV-11 Tat and/or inflammatory cytokines, rather than immunosuppression,, might be responsible for the in-creasedd incidence of KS in HIV-1 and HHV-8 coinfected persons. .

[acobsonn and Jenkins (5) responded to the report by Rezza (3)) by suggesting that KS in HIV 1-negative transplant re-cipientss cannot be formally compared with KS in HIV 1-positivee individuals in regard to the impact of

immunosuppressionn on the rate of progression of HHV 8 infectionn to KS. We agree with the comments of Jacobson andjenkinss and wish to point out that, in oir original report (1),, CD4 cell count, not HIV-1 virus load, was an independ-entt risk factor for KS. In our view, it is therefore more likely thatt HIV related immunodeficiency, rather than steadv-statcc levels of HIV in blood, and, bv inference, levels of HIV-11 Tat or inflammatory cytokines increase the risk for KS. .

References s

11 Renvick N , I lalabv T, Weverling ( i | , </<//. Seroconversion for hu-mann herpesvirus 8 is highly predictive of Kaposi's sarcoma. .-UD\ 1998;12:2481-8. .

22 Jacobson 1.1', Jenkins FJ, Springer (I, et al. Interaction of human immunodeficienevv virus type 1 and human herpesvirus type 8 in-fectionss on the incidence or Kaposi's sarcoma. / Infect Pis 2000;181:1940-9. .

33 Re/za (). Immunosuppression, timing of human herpesvirus 8 in tection,, and risk of Kaposi's sarcoma among human immunodefi-ciencyy virus rvpc 1-infected persons and transplant recipients. / 7«/rt7/)/.r2lMM);|| 82:1809.

44 Parravacini C, ()lsen SI, Capra M, ft al. Risk of Kaposi's sar-coma-associatedd herpes virus transmission from donor allograft amongg Italian posttransplant Kaposi's sarcoma patients. /WW

]] 997.91 ):2H21-9.

55 Jacobson LP, Jenkins FJ. Reply. / Infect Dis 2000; 182:1809-ld.

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