Was Susan Sontag a Victim of the Politics of HHV-6?
My mother, Susan Sontag, lived almost her entire 71 years believing that she was a person who would beat the odds. Even during the last nine months of her life, after she was discovered to have myelodysplastic syndrome, or M.D.S., a particularly virulent blood cancer, she continued to persevere in the belief that she would be the exception. M.D.S. is technically a precursor to acute myeloid leukemia.--David Rieff, "Illness as More Than Metaphor," New York Times, December 4, 2005.
Lymphotropic human herpesviruses: Epstein-Barr (EBV), 6 y 7 (HHV-6 and HHV-7) in the pathogenia of myelodysplastic (MDS) and mieloproliferative diseases (MPS)
Myelodysplasic and myeloproliferative alterations have been observed in patients with lymphoproliferative diseases associated to lymphotropic human herpes viruses. Screening studies were done to eventually demonstrate the reactivation of these viruses and their possible implication in the pathogenesis and course of the myelodisplastic and myeloproliferative syndromes (MDS/MPS). We investigated 74 bone marrow biopsies and sera from patients with MDS and 49 bone marrow biopsies and 36 sera from patients with chronic myelogenous leukemia (CML), in 13 Mexican cases serologic studies were not done. Diagnosis and classification of the diseases followed the FAB (French-American-Britain) guidelines. The patients were serologically tested for antibodies (Ab) against virus capsid antigen (VCA) and the early antigen (EA) from the EBV (ELISA and IFA-immunofluorescence) and HHV-6 and HHV-7 (IFA). The immunohistology was done by the APAAP technique and with the monoclonal Ab against the proliferation cell nuclear antigen (PCNA). IgG titers anti-EBV-EA were found in 62% of the cases of MDS and in 33% with CML, IgG titers against HHV-6 were elevated in 19% of the cases with MDS and in 9.3% with CML, HHV-7 was found in 37.8% and 13.9% respectively. IgM titers were negative for the 3 viruses. The EBV-EA expression was positive in the bone marrow in 76% of the MDS cases, 48.6% were positive to HHV-6 p41 and 37.8% were positive to HHV-7. The CML cases expressed EBV-EA in 77%, HHV-6 in 54.5% and HHV-7 in 21.8%.--Rojo J, Cruz-Ortiz H, Krueger GRF, Rev Med Hosp Gen Mex 2000; 63 (1): 18-24
"And because the government will not admit that HHV-6 is the cause of AIDS, it is spreading all over our country and causing all kinds of diseases that go way beyond AIDS. We should be talking about HHV-6 disease rather than AIDS."--Charles Ortleb The Closing Argument: A Courtroom Novella
A virus that has been considered for several years a possible cause of Chronic Fatigue Syndrome is Human Herpes Virus 6 (HHV-6). This virus was first discovered in AIDS and cancer patients in the mid-1980s at the National Cancer Institute. It was subsequently found that people with Chronic Fatigue Syndrome, like people with AIDS, can have extremely high levels of antibodies to HHV-6.
As more is learned about HHV-6, its ability to attack the immune system -- and perhaps other parts of the body, like the nervous system -- has been documented in more and more frightening ways. Even more alarmingly, the most recent research on HHV-6 suggests that it, and not HIV, is the primary infection that destroys an important part of the immune system in AIDS.
That part of the immune system is the natural killer (NK) cells. NK cells are crucial to the immune system's front-line defense against both viruses and cancer, because they attack and kill any cells they perceive to be foreign. If the NK cells aren't working properly -- which they aren't, in both AIDS and CFS -- this very important protection is knocked out.
The research team that discovered the existence of HHV-6, working with Dr. Robert C. Gallo at the National Cancer Institute, announced in early April 1993 that HHV-6 is the only virus known to be able to infect and kill NK cells.--Neenyah Ostrom America's Biggest Cover-Up: 50 More Things Everyone Should Know About The Chronic Fatigue Syndrome Epidemic And Its Link To AIDS
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. --The HHV-6 Foundation