Exploring the interplay between Kaposi's sarcoma and SARS‐CoV‐2 infection: A case series and systematic review

Author:

Pietroluongo Erica1ORCID,Luciano Angelo1,Peddio Annarita1,Buonaiuto Roberto1,Caltavituro Aldo1,Servetto Alberto1,De Angelis Carmine1,Arpino Grazia1,Palmieri Giovannella1,Veneziani Bianca Maria2,De Placido Sabino1,Bianco Roberto1,De Placido Pietro34,Giuliano Mario1

Affiliation:

1. Department of Clinical Medicine and Surgery University Federico II Naples Italy

2. Department of Molecular Medicine and Medical Biotechnologies University of Naples “Federico II Naples Italy

3. Department of Advanced Biomedical Sciences University Federico II Naples Italy

4. Department of Medical Oncology Dana‐Farber Cancer Institute Boston MA USA

Abstract

AbstractKaposi's sarcoma (KS) is an angio‐proliferative disease with a viral etiology and a multifactorial pathogenesis that results from immune dysfunction. In patients affected by latent viral infections such as herpesviruses, SARS‐CoV‐2 infection may result in lytic cycle reactivation in host cells. A robust immune system response is crucial for eliminating pathogens and resolving both latent and non‐latent viral infections. We report a case series of KS characterized by tumor progression after SARS‐CoV‐2 infection. We performed a systematic literature review of the PubMed/MEDLINE and EMBASE databases. The keyword terms included “SARS‐CoV‐2,” “HHV‐8,” “Kaposi's sarcoma,” “IL‐6,” and “COVID‐19.” English language restriction was applied. Items not covered by our study were excluded. KS is a complex disease linked to an impaired immune system. Conditions that result in temporary or permanent immunodeficiency can trigger viral reactivation or exacerbate an existing disease. It is feasible that the increase in cytokine levels in COVID‐19 patients, coupled with lymphocyte downregulation and treatment that induces herpesvirus lytic reactivation, may contribute to the progression of KS after SARS‐CoV‐2 infection. These observations suggest that patients with KS should be clinically monitored both during and after SARS‐CoV‐2 infection. Nevertheless, prospective data should be collected to validate this hypothesis and enhance our understanding of the mechanisms implicated in the onset or progression of KS.

Publisher

Wiley

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