Abstract
Simple SummaryThe aim of this article is to review the complex interactions of bacteria with Kaposi’s sarcoma-associated herpesvirus (KSHV) infection and KSHV-induced cancers. KSHV is causally associated with multiple cancers including Kaposi’s sarcoma (KS) and primary effusion lymphoma. Among patients coinfected by HIV and KSHV, patients with KS have a distinct oral microbiome compared to patients without KS. Moreover, KSHV patients have increased levels of salivary bacterial pathogen-associated molecular patterns compared to KSHV-negative patients. KSHV-associated bacterial species can increase KSHV replication and dissemination, and enhance cell proliferation of KSHV-transformed cells. The analysis of bacterial biomarkers associated with KSHV may help improve our understanding of the mechanisms driving KSHV-induced oncogenesis and identify novel targets for improving therapies of KSHV-related cancers.The objective of this article is to review the current status of the bacteria-virus interplay in Kaposi’s sarcoma-associated herpesvirus (KSHV) infection and KSHV-driven cancers. KSHV is the etiological agent of several cancers, including Kaposi’s sarcoma (KS) and primary effusion lymphoma. Due to immunosuppression, patients with KSHV are at an increased risk for bacterial infections. Moreover, among patients coinfected by HIV and KSHV, patients with KS have distinct oral microbiota compared to non-KS patients. Bacterial biomarkers associated with KSHV-driven cancers can provide insights in discerning the mechanisms of KSHV-induced oncogenesis. For example, pathogen-associated molecular patterns and bacterial products of certain bacterial species can regulate the expression of KSHV lytic and latent genes, thereby affecting viral replication and dissemination. In addition, infection with distinct opportunistic bacterial species have been associated with increased cell proliferation and tumorigenesis in KSHV-induced cancers through activation of pro-survival and -mitogenic cell signaling pathways. By elucidating the various mechanisms in which bacteria affect KSHV-associated pathogenesis, we will be able to pinpoint therapeutic targets for KSHV infection and KSHV-related cancers.
Highlights
The utilization of bacterial markers to determine cancer pathology has progressed tremendously in recent years
S. aureus medium downregulated expression of cyclin D1 and other host proteins responsible for processing cellular miRNAs, including Dicer, and Argonaut 1 and 2. These results suggested that the S. aureus medium might induce Kaposi’s sarcoma-associated herpesvirus (KSHV) reactivation through the cyclin D1-Dicer-viral miRNAs axis in KSHV-infected oral cell lines [67]
This study shows that it is necessary to assess individual bacterial pathogen-associated molecular patterns (PAMPs) on the activation of cell signaling pathways in order to more effectively elucidate molecules involved in inflammation and identify the potential therapeutic targets for KSHV-induced cancers
Summary
The utilization of bacterial markers to determine cancer pathology has progressed tremendously in recent years. Microbiome analyses using generation sequencing report that the colonization of pathogenic bacterial species is increased in cancer patients and exacerbates cancer pathogenesis [1]. Pathogenic bacteria such as Fusobacterium nucleatum and Helicobacter pylori have been extensively studied for their carcinogenic effects, as they can produce toxins and effector proteins that induce host cell damage and alter cell signaling pathways involved in cell survival and proliferation [2]. Recent studies have shown that bacteria can interact with cancer-causing viruses to promote viral replication and the progression of viral cancers [4]. To thoroughly comprehend the interactions between bacteria and KSHV-induced cancers, it is necessary to begin with a brief overview of the general interactions between the microbiome, immune response, and cancer
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