cancers Article Viral and Immunological Analytes are Poor Predictors of the Clinical Treatment Response in Kaposi’s Sarcoma Patients Salum J. Lidenge 1,2,3,4 , For Yue Tso 1,2 , Yasaman Mortazavi 1,2 , John R. Ngowi 3 , Danielle M. Shea 1 , Julius Mwaiselage 3,4 , Charles Wood 1,2,5, * and John T. West 1,5, * 1 Nebraska Center for Virology, Lincoln, NE 68583, USA; sjlidenge@yahoo.co.uk (S.J.L.); ftso2@unl.edu (F.Y.T.); yass.mortazavi@yahoo.com (Y.M.); danielle.shea@unl.edu (D.M.S.) 2 School of Biological Sciences, University of Nebraska-Lincoln, Lincoln, NE 68588, USA 3 Department of Academics and Research, Ocean Road Cancer Institute, P. O. Box 3592 Dar es Salaam, Tanzania; jrngowi146@gmail.com (J.R.N.); jmwaiselage@yahoo.com (J.M.) 4 Department of Clinical Oncology, Muhimbili University of Health and Allied Sciences, P. O. Box 65001 Dar es Salaam, Tanzania 5 Department of Biochemistry, University of Nebraska-Lincoln, Lincoln, NE 68588, USA * Correspondence: cwood1@unl.edu (C.W.); jwest2@unl.edu (J.T.W.); Tel.: +1-402-202-472-4550 (C.W.); +1-402-202-472-4550 (J.T.W.) Received: 17 May 2020; Accepted: 12 June 2020; Published: 16 June 2020   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. Keywords: Kaposi’s sarcoma; immune responses; neutralizing antibody; cytokine; T-cells; treatment response; HIV-1; KSHV; sub-Saharan Africa 1. Introduction 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 [2–4]. Before the AIDS epidemic, HIV negative African-endemic KS (EnKS) comprised 4–10% of African adult cancers [5,6]. With the ongoing HIV/AIDS epidemic, Cancers 2020, 12, 1594; doi:10.3390/cancers12061594 www.mdpi.com/journal/cancers