Viral and Immunological Analytes are Poor Predictors of the Clinical Treatment Response in Kaposi’s Sarcoma Patients

Authors

Salum J. Lidenge, Nebraska Center for Virology & University of Nebraska-Lincoln & Ocean Road Cancer Institute & Muhimbili University of Health and Allied SciencesFollow
For Yue Tso, University of Nebraska-LincolnFollow
Yasaman Mortazavi, University of Nebraska - LincolnFollow
John R. Ngowi, Ocean Road Cancer InstituteFollow
Danielle M. Shea, Nebraska Center for VirologyFollow
Julius Mwaiselage, Ocean Road Cancer InstituteFollow
Charles Wood, Nebraska Center for Virology & University of Nebraska - LincolnFollow
John T. West, Nebraska Center for Virology & University of Nebraska-LincolnFollow

ORCID IDs

https://orcid.org/0000-0002-4256-1530

Date of this Version

2020

Citation

2020 by the authors

Comments

Cancers 2020, 12, 1594; doi:10.3390/cancers12061594 www.mdpi.com/journal/cancers

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.