The roles of viruses in brain tumor initiation and oncomodulation

Abstract

While some avian retroviruses have been shown to induce gliomas in animal models, human herpesviruses, specifically, the most extensively studied cytomegalovirus, and the much less studied roseolovirus HHV-6, and Herpes simplex viruses 1 and 2, currently attract more and more attention as possible contributing or initiating factors in the development of human brain tumors. The aim of this review is to summarize and highlight the most provoking findings indicating a potential causative link between brain tumors, specifically malignant gliomas, and viruses in the context of the concepts of viral oncomodulation and the tumor stem cell origin.

Prevalence of Neurotropic Viruses in Malignant Glioma and Their Onco-Modulatory Potential

“…HCMV is relatively widespread in immunocompromised patients (11). The clinical relevance of HCMV infection in GBM pathogenesis has been investigated since 2002 (16,25), but there has been no evidence to date for a role of HCMV in gliomagenesis.…”

“…A metaanalysis of 16 reports by Salomon et al (25) confirmed the concept that there is no clear-cut evidence for a role of HCMV in GBM tumorigenesis. Similarly, specific roles of other herpes viruses in glioma initiation have not been demonstrated to date (11,(26)(27)(28)(29)(30).…”

Comprehensive polymerase chain reaction assay for detection of pathogenic DNA in lymphoproliferative disorders of the ocular adnexa

“…HHV-6 and HHV-7 are established oncogenic viruses that can induce tumors in an animal model through the inactivation of p53 and deregulation of nuclear factor kappa-B1718. Known malignant tumors typically linked with HHV-6 include T-cell lymphoma and Hodgkin’s lymphoma.…”

1410 Absence of human cytomegalovirus infection in childhood brain tumors

“…Some viral genes are involved in the pathogenesis of cancer in vivo, codifying for proteins having an oncomodulatory effect and therefore able to modulate malignant phenotype [12]. Actually, the most accepted theory supports the hypothesis that HCMV could act as oncomodulator.…”