Abstract
Measles virus (MV) is a member of the paramyxovirus family of enveloped RNA viruses and one of the most infectious viral pathogens identified. Despite initial optimism that vaccination programs would eventually eradicate measles, reduced vaccination coverage against measles continues to result in outbreaks of measles. Mild or asymptomatic measles infections are common among measles-immune persons exposed to measles cases and may be the most common manifestation of measles during outbreaks in highly immune populations. Persistent, asymptomatic MV infections commonly persist in apparently healthy individuals. MV has been detected in several malignancies, including lung, breast, and endometrial cancers, as well as Hodgkin’s lymphoma. The presence of MV in these tumors was associated with distinct clinico-pathological characteristics: in lung cancer, older ages of patients and over expression of Pirh2, and in breast cancer, age less than 50 years, lower histological grade, and over expression of p53. Nectin-4 is the MV receptor in epithelial cells and is highly expressed in certain epithelial tumors. MV-associated tumorigenesis may be linked to the effect of MV-phosphoprotein on Pirh2, an E3 ubiquitin ligase of p53. By way of MV interaction with Nectin-4 and Pirh2, persistent MV infection may co-act with other factors in transforming cells to become malignant.
Highlights
Viruses have long been implicated as a cause of cancer [1], their relevance to human cancer development has often been debated
Epstein-Barr virus (EBV), human papilloma virus (HPV), hepatitis B virus (HBV), [3] human herpes virus-8 (HHV8) [4], and the recently identified Merkel cell Polyomavirus (MCPyV) [5] are DNA viruses that are capable of causing the development of human cancers
This review summarizes the data supporting a role played by measles virus (MV) in the development of several types of cancers
Summary
Viruses have long been implicated as a cause of cancer [1], their relevance to human cancer development has often been debated. Whereas for most of the tumor viruses the viral genome persists in an integrated or episomal form with a subset of viral genes expressed in the tumor cells, HCV is not inherently oncogenic, but infection leads to transformation of cells by indirect means. For some malignancies such as Burkitt’s lymphoma, EBV appears to serve as a cofactor.
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