Antiretroviral therapy with protease inhibitors in human immunodeficiency virus type 1- and human herpesvirus 8-coinfected patients

Milito, Angelo De; Catucci, Marinunzia; Venturi, Giulietta; Romanò, Laura; Incandela, Laura; Valensin, Pier Egisto; Zazzi, Maurizio

doi:10.1002/(sici)1096-9071(199902)57:2<140::aid-jmv9>3.0.co;2-y

Cited by 34 publications

(11 citation statements)

References 16 publications

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“…These findings are in agreement with the effects of HAART that has been shown to act on peripheral blood HIV RNA levels, as well as increasing CD4 ϩ T cells (26,33), and might also affect HHV-8 viremia (15,24,28,35).…”

Section: Discussionsupporting

confidence: 89%

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Viral Load of Human Herpesvirus 8 in Peripheral Blood of Human Immunodeficiency Virus-Infected Patients with Kaposi's Sarcoma

et al. 2001

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Kaposi's sarcoma (KS)-associated herpesvirus or Human herpesvirus 8 (HHV-8) (13), is a ␥-herpesvirus now widely established as a necessary cause of KS and also associated with body cavity-based lymphoma and multicentric Castleman's disease (5). These diseases were previously rare but are now brought to prominence by the AIDS pandemic. Detection of HHV-8 DNA in peripheral blood mononuclear cells (PBMCs) from human immunodeficiency virus type 1 (HIV-1)-infected persons is associated with an increased risk of subsequent development of KS (30,43) and with KS clinical stage (10, 11).Highly active antiretroviral therapy (HAART) is effective for inhibiting HIV replication, increasing CD4 cell counts, and delaying AIDS-associated opportunistic infections (26, 33). Case reports suggest that HAART may also be of benefit against AIDS-related KS as well as in eliminating detectable HHV-8 DNA from PBMCs of HIV carriers (15,24,28,35).Previous studies about the relationship between peripheral blood HHV-8 load and KS pathogenesis have been limited by the use of qualitative or semiquantitative estimates of HHV-8 load. Reproducible, sensitive, and specific quantitative techniques are needed to assess the HHV-8 DNA load and its correlation with different clinical conditions.We have therefore developed a highly sensitive and specific real-time PCR assay for the quantification of the HHV-8 genomes in peripheral blood. The present study wished to evaluate the consistency over time of HHV-8 viral DNA loads among KS patients receiving treatment for HIV-1 infection. We also sought to determine whether HHV-8 DNA viral load was correlated with HIV RNA viral load, CD4 cell counts, and/or serological reactivity to HHV-8. MATERIALS AND METHODSPatients. Fourteen HIV-infected patients with histologically confirmed KS (13 male and one female; range of ages, 28 to 56 years) were monitored at the Department of Oncology & AIDS, Centro di Riferimento Oncolgico of Aviano, Aviano, Italy, over the period 1997 to 2000. All patients but one had advanced clinical stages of KS disease, with visceral and/or lymph node involvement. According to the Krown staging system (21), 13 patients were at stage T1, 7 patients were at stage I1, and 8 patients were at stage S1.After informed consent was given by each patient, blood samples were collected at consecutive visits and HIV RNA viral load, CD4 T-cell count, HHV-8 serology for lytic and latent viral antigens and HHV-8 DNA viral load in peripheral blood were assessed. For each patient, one blood sample was collected before starting HAART, and then two or more samples were taken, depending on the number of control visits after the therapy had been initiated.Thirteen patients were receiving combination therapy with one protease inhibitor and two nucleoside reverse transcriptase inhibitors; one patient was receiving one nonnucleoside reverse transcriptase inhibitor and two nucleoside reverse transcriptase inhibitors.During the follow-up, three patients had also been treated with local radiotherapy; one patient had ...

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Section: Discussionsupporting

confidence: 89%

“…Case reports suggest that HAART may also be of benefit against AIDS-related KS as well as in eliminating detectable HHV-8 DNA from PBMCs of HIV carriers (15,24,28,35).…”

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confidence: 99%

Viral Load of Human Herpesvirus 8 in Peripheral Blood of Human Immunodeficiency Virus-Infected Patients with Kaposi's Sarcoma

et al. 2001

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“…Protease inhibitors have direct antiproliferative and antiangiogenic effects in vitro, and inhibit the development of KS-like lesions in animal models by blocking an enzyme required for the production of infectious HHV-8 particles (Pati et al, 2002;Sgadari et al, 2002Sgadari et al, , 2003. In clinical trials, PI-containing regimens led to full remission from KS in approximately 50% of patients, and conferred an added survival benefit (Burdick et al, 1997;Aboulafia, 1998;Krischer et al, 1998;Cattelan et al, 1999;De Milito et al, 1999;Paparizos et al, 2002;Leitch et al, 2003;Sgadari et al, 2003).…”

Section: Discussionmentioning

confidence: 99%

Remission from Kaposi's sarcoma on HAART is associated with suppression of HIV replication and is independent of protease inhibitor therapy

et al. 2006

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Highly active antiretroviral therapy (HAART) reduces the incidence and improves the prognosis of Kaposi's sarcoma (KS). This study was designed to identify factors associated with KS clinical responses in HIV-infected patients during HAART. We reviewed the files of 138 HIV-1-infected patients with KS. Epidemiologic and HIV-related clinical and biological parameters were recorded at KS diagnosis (baseline) and every 6 months thereafter. In a subset of 73 antiretroviral-naive patients, we compared the clinical outcome of KS according to the use or nonuse of protease inhibitors (PI). After 6 months of follow-up, KS remission was more frequent in patients who were naive of HAART and who were at ACTG stage S0 at baseline (P ¼ 0.03 and 0.02). Undetectable HIV viral load was strongly associated with KS remission (Pp0.004 at all time points), while CD4 cell count was not. Among the 73 antiretroviralnaive patients at baseline, and who were studied for 24 months, KS outcome did not differ between patients who were prescribed PIcontaining and PI-sparing regimens. Intercurrent multicentric Castleman's disease was associated with poor outcome after 60 months of follow-up (Pp0.0001). Fourteen deaths occurred after a median follow-up of 37.5 months, eight of which were KS related. Suppression of HIV replication appears to be crucial to control KS. Non-PI-based regimens were equivalent to PI-based regimens as regards the clinical and virological outcome of antiretroviral-naive HIV-infected patients with KS.

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“…Preliminary data from case reports suggest that protease inhibitors may help induce remission of HIV-related KS 125,[138][139][140][141][142][143] and clearance of HHV-8 DNA from PBMCs 138,139,141,143,145 . Moreover, HAART in 2 HIV-positive patients with BCBL resulted in HHV-8 DNA being undetected in their pleural effusions 146 .…”

Section: Antiviral Therapymentioning

confidence: 99%

Human herpesvirus 8 (HHV-8) and the etiopathogenesis of Kaposi's sarcoma

Leão¹,

Caterino–de–Araujo

Porter

et al. 2002

Rev. Hosp. Clin.

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OBJECTIVE: To review the current literature on human herpesvirus 8 with particular attention to the aspects related to the etiopathogenesis of Kaposi's sarcoma. MATERIALS AND METHODS: The authors searched original research and review articles on specific aspects of human herpesvirus 8 infection, including virology, epidemiology, transmission, diagnosis, natural history, therapy, and Kaposi's sarcoma etiopathogenesis. The relevant material was evaluated and reviewed. RESULTS: Human herpesvirus 8 is a recently discovered DNA virus that is present throughout the world but with major geographic variation. In the Western world, the virus, transmitted mainly by means of sexual contact, is strongly associated with Kaposi's sarcoma and body cavity-based lymphoma and more controversially with multiple myeloma and other non-proliferative disorders. There is no specific effective treatment, but HIV protease inhibitors may play an indirect role in the clearance of human herpesvirus 8 DNA from peripheral blood mononuclear cells of HIV-infected patients. Human herpesvirus 8 DNA is present in saliva, but there are as yet no documented cases of nosocomial transmission to health care workers. The prevalence of human herpesvirus 8 among health care workers is probably similar to that in the general population. CONCLUSION: Human herpesvirus 8 appears to be, at least in Western Europe and United States, restricted to a population at risk of developing Kaposi's sarcoma. Human herpesvirus 8 certainly has the means to overcome cellular control and immune responses and thus predispose carriers to malignancy, particularly Kaposi's sarcoma. The wide diffusion of Human herpesvirus 8 in classic Kaposi's sarcoma areas appears to represent an important factor in the high incidence of the disease. However, additional co-factors are likely to play a role in the development of Kaposi's sarcoma.

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Antiretroviral therapy with protease inhibitors in human immunodeficiency virus type 1- and human herpesvirus 8-coinfected patients

Cited by 34 publications

References 16 publications

Viral Load of Human Herpesvirus 8 in Peripheral Blood of Human Immunodeficiency Virus-Infected Patients with Kaposi's Sarcoma

Viral Load of Human Herpesvirus 8 in Peripheral Blood of Human Immunodeficiency Virus-Infected Patients with Kaposi's Sarcoma

Remission from Kaposi's sarcoma on HAART is associated with suppression of HIV replication and is independent of protease inhibitor therapy

Human herpesvirus 8 (HHV-8) and the etiopathogenesis of Kaposi's sarcoma

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