Abstract
Kaposi’s sarcoma-associated herpesvirus (KSHV) modulates the immune response to allow the virus to establish persistent infection in the host and facilitate the development of KSHV-associated cancer. The complement system has a central role in the defense against pathogens. Hence, KSHV has adopted an evasion strategy for complement attack using the viral protein encoded by KSHV open reading frame 4. However, despite this defense mechanism, the complement system appears to become activated in KSHV-infected cells as well as in the region surrounding Kaposi’s sarcoma tumors. Given that the complement system can affect cell fate as well as the inflammatory microenvironment, complement activation is likely associated with KSHV pathogenesis. A better understanding of the interplay between KSHV and the complement system may, therefore, translate into the development of novel therapeutic interventions for KSHV-associated tumors. In this review, the mechanisms and functions of complement activation in KSHV-infected cells are discussed.
Highlights
Kaposi’s sarcoma-associated herpesvirus (KSHV), known as human herpesvirus 8(HHV-8), is the etiologic agent of Kaposi’s sarcoma (KS), primary effusion lymphoma (PEL), and multicentric Castleman’s disease (MCD) [1,2,3]
Antibodies against KSHV ORF4 were detected in KSHV-infected individuals; these antibodies did not inhibit the regulatory function of complement activation [48]
We found that the alternative pathway is activated in various eukaryotic cells, which can cause cell injury; not all cells die as a result [11,50,69,70]
Summary
Kaposi’s sarcoma-associated herpesvirus (KSHV), known as human herpesvirus 8. The interplay between the virus and immune responses during KSHV infection significantly impacts the clinical outcomes of KSHV-associated disease. The association of the complement system with the pathogenesis of KSHV infection has been recognized [11], this area of research has received only minimal attention far. The function and activation mechanisms of the complement system in the pathogenesis of KSHV infection remain poorly understood. It is, essential to advance these areas of research to inform the development of novel approaches for KSHV prevention and treatment. KSHV, (3) the activation of the complement system in KSHV‐infected cells, and (4) the role of the complement system in KSHV infection
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