HHV-6 & Cancer

HHV-6 induced immune dysregulation puts patients with chronic active infections at risk for autoimmune disease and certain lymphoproliferative disorders. Both beta herpesviruses (cytomegalovirus, HHV-6 and HHV-7) and gamma herpesviruses (Epstein Barr Virus and HHV-8) have been recently identified as risk factors for some types of cancer.  EBV has been implicated in several types of lymphoma and HHV-8 has been implicated in Kaposi's sarcoma. Beta herpesviruses may serve as   a possible cofactor in certain tumors. A recent study (Chun Lu, 2005) found that Kaposi's sarcoma will not develop without a co-infection of HHV-6. There has been some suggestive evidence for CMV or HHV-6 contributing to the development of cervical cancer and Hodgkin's disease .

HHV-6 is frequently present in patients with various lymphoproliferative disorders including acute lymphoblastic leukemia, multiple myeloma, Hodgkin's disease   and myeloproliferative syndromes. HHV-6 has also been linked to oral cancer. Further studies are required, however, to elucidate the causal relationship   to the pathogenesis of such diseases. It is difficult to study the disease associations in tissue by PCR given the high level of HHV-6 latent virus in the cells.
 
HHV-6 may contribute to cancer indirectly through immune suppression. HHV-6   can directly infect CD4+ T-cells and induce their death (apoptosis).. HHV-6 can also infect thymic epithelial cells, hematopoietic stem cells   and natural killer cells, which are critical immune maturation and for the protection against cancer and   viral infections. Thus active HHV-6 infection can contribute to the pathologic effects of other viral infections.
 
Kashanki (1997) found that HHV-6 genes have malignant transforming activity and the "ORF-1 oncogene" binds to p53, the tumor suppressor protein and inactivates it. This is not proof that an active HHV-6 infection is oncogenic (increases your chance of getting cancer) but it raises the level of suscpicion. In addition, there exist apparently other mechanisms such as of genomic transactivation (e.g. by NF-?B activation) by HHV-6 that can enhance the pathogenesis of diseases by various causes.

Krueger GRF, Schonnebeck T, Braun M: Enhanced cell membrane receptor expression folloing infection with human herpesvirus-6. FASEB J 4: A343, 1990

Schonnebeck M, Krueger GRF, Braun M, Fischer M, Koch B, Ablashi DV, Balachandran N: Human herpesvirus-6 infection may predispose to suprinfection by other viruses. In Vivo 5: 255-264, 1991

Gies M, Jalali Z, Wagner M, Krueger GRF: Modulation of nuclear factor kappa B (NF-?B) activity in human herpes virus-6 (HHV-6) infection and its sequellae for cell function: effects of antisense DNA treatment. Rev Med Hospital Gen Mexico 61: 218-225, 1998

        HHV-6 & MS
        HHV-6 & CFS
        HHV-6 & Cancer