HHV-6 Latent Infection Identified in Patients with Glioma

In All, Cancer, News by hhv6foundation

HHV-6 Latent Infection Identified in Patients with Glioma

Investigators from Nanjing Medical University led by Dr. Kun Yao have found HHV-6 latent infection in glioma tissues, and have isolated a strain of HHV-6A from the glioma cyst, supporting earlier studies that suggest the involvement of HHV-6 in the pathogenesis of adult and pediatric gliomas.

Using nested PCR and immunohistochemistry (IHC), Dr. Yao’s team identified HHV-6 DNA and protein in tissue from 42.5% of gliomas compared to 7.7% of normal brain tissue. In addition, elevated levels of several cytokines that were specifically promoted by HHV-6 infection in astrocyte cultures (including IL-6, IL-8, and TGF-beta) were also observed in HHV-6-positive cyst fluid samples from glioma tissues.

CMV has also been implicated as a potential factor in gliomas in several studies (Lucas 2011, others); with CMV proteins found in approximately half of glioblastoma multiforme samples. Dr. Yao’s team reports 20% of their glioma tissues were positive for CMV via nested PCR analysis, compared with 0% of controls. The same percentages were observed for EBV as well. However, only the presence of HHV-6 was found to be significantly correlated with the development of glioma in this study.

An earlier paper by NINDS/NIH investigators (Crawford 2009) found that both early (p41) and late (gp116/64/54) HHV-6 viral antigens were detected three times more frequently in adult glial tumors compared to control brain tissues. An additional study by this group utilized nested PCR, in situ hybridization (ISH), and IHC to detect HHV-6 in pediatric brain tumors, and demonstrated that HHV-6 viral antigens were significantly correlated with low grade-glioma tissues compared to controls (Crawford 2009).

The authors note that “proinflammatory cytokines induced by HHV-6 infection might provide a chronic inflammatory environment that facilitates the development of glioma” by altering the properties of the infected cell and inducing proinflammatory cytokine secretion—as has been documented previously (Yoshikawa 2002)–HHV-6 may directly facilitate the pathogenesis of glioma. In addition, the authors suggest that selective immunosuppression caused by HHV-6 infection can lead to the disruption of key immune activation pathways, perhaps further contributing to the pathogenesis of glioma.

For more information, read the abstract, and visit the HHV-6 Foundation’s webpage on HHV-6 & Cancer.