Abstract
Kaposi’s sarcoma-associated herpes virus (KSHV) is the etiologic agent for Kaposi’s sarcoma (KS). The prognostic utility of KSHV and HIV-1 (human immunodeficiency virus) viremia as well as immunological parameters in clinical management of participants with KS is unclear. The objective of this study was to investigate viral and immunological parameters as predictors of KS treatment responses in participants with KS from sub-Saharan Africa (SSA). Plasma KSHV-DNA, HIV-1 viral load, total anti-KSHV antibody, KSHV-neutralizing antibody (nAb), cytokine/chemokine levels, and T-cell differentiation subsets were quantified before and after KS treatment in 13 participants with KS and in 13 KSHV-infected asymptomatic control individuals. One-way analysis of variance and the Mann-Whitney t-test were used to assess differences between groups where p-values < 0.05 were considered significant. Subjects with patch and plaque KS lesions responded more favorably to treatment than those with nodular lesions. Pre-treatment and post-treatment levels of plasma KSHV-DNA, HIV-1 viral load, KSHV-Ab responses, cytokines, and T-cell populations did not predict the KS treatment response. Elevated KSHV-humoral and cytokine responses persisted in participants with KS despite a clinical KS response. While patch and plaque KS lesions were more common among treatment responders, none of the analyzed viral and immunological parameters distinguished responders from non-responders at baseline or after treatment.
Highlights
Kaposi’s sarcoma (KS), which is a multifocal angio-proliferative sarcoma commonly found on skin and mucosal surfaces, is caused by the Kaposi’s sarcoma-associated herpes virus (KSHV) or human herpes virus-8 (HHV-8) [1]
The two control groups were comparable in age, gender, CD4 count, and KSHV status (Table 1)
While the comparison of CD4 count did not reveal significant differences between groups of controls and participants with KS, KS non-responders had significantly lower CD4 count when compared to normal controls (HIV-1− ) (p = 0.03)
Summary
Kaposi’s sarcoma (KS), which is a multifocal angio-proliferative sarcoma commonly found on skin and mucosal surfaces, is caused by the Kaposi’s sarcoma-associated herpes virus (KSHV) or human herpes virus-8 (HHV-8) [1]. KSHV infection is endemic in sub-Saharan Africa (SSA) with prevalence as high as 90% in some countries [2,3,4]. Before the AIDS epidemic, HIV negative African-endemic. AIDS-associated/epidemic KS (EpKS) has become the most common cancer in HIV-1 infected African individuals [7,8]. Anti-retroviral therapy (ART) has led to significant decline in KS incidence in HIV-1 infected individuals, even though recent reports demonstrate that KS still occurs in individuals with reconstituted CD4+ T-cell counts and a suppressed HIV-1 plasma viral load [9,10,11,12,13]. A similar decline in KS incidence has not been observed in SSA where KS remains one of the top five cancers despite of increased ART coverage, uptake, and adherence [9,14,15]. Lack of early disease recognition, advanced presentation, and lack of effective treatments all contribute to high KS morbidity and mortality [16,17,18]
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