HHV-6 University

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12115999&dopt=Abstract J Med Virol. 2002 Aug;67(4):528-33. Related Articles, Links HHV-6 infects human aortic and heart microvascular endothelial cells, increasing their ability to secrete proinflammatory chemokines. Caruso A, Rotola A, Comar M, Favilli F, Galvan M, Tosetti M, Campello C, Caselli E, Alessandri G, Grassi M, Garrafa E, Cassai E, Di Luca D. Institute of Microbiology, University of Brescia Medical School, Italy. Endothelial cells are important targets for herpesvirus infection. To evaluate the biological effects of human herpesvirus-6 (HHV-6) infection, adult heart microvascular and aortic endothelial cells were examined for in vitro susceptibility to HHV-6 and for the alterations induced by viral infection on the production of monocyte chemoattractant protein-1 (MCP-1) and interleukin-8 (IL-8). Analysis by reverse transcription-polymerase chain reaction and b

Here's what Robert Gallo had to say about HHV-6 in an NIH interview in 1995: Have we ever argued for a possible cofactor? Yes, with the qualification I just told you, that it is obvious that some things will promote progression and some things will inhibit progression. One of those things may be the genetics of me versus you. We can say dose is a factor that can lead to progression, or lack of it, and at a greater or lesser rate. But we have argued for certain herpesviruses as possibly being a factor in promoting AIDS progression. Several groups have argued for cytomegalovirus because it does do things and it does activate more HIV in some subtle settings. In the middle of the 1980s, we became aware that the lymphomas that were associated with HIV infection were perhaps one-third of the time EBV-positive. Epstein-Barr virus, as you know, can immortalize some B cells and, when you have EBV-positive lymphomas, generally they are the kind of lymphomas that, more

In a recent Co-Cure posting on CFIDS, Rich Van Konynenburg writes "we know that many PWCs have mild diabetes insipidus." The following appeared on the Aegis site which is devoted to AIDS research: Int Conf AIDS 1994 Aug 7-12; 10:196 (abstract no. PB0797) Harris P, Curry R; AIDS Clinical Research Center of Washington, DC 20009. OBJECTIVE: Ten of 200 patients have complained over the last year of polyuria, polydipsia and nocturia. We were interested in whether diabetes insipidus (DI) may be directly associated with this infection. METHODS: We measured urine and serum osmolalities, serum antidiuretic hormone (ADH), serum sodium, BUN, glucose and potassium levels; calculated serum osmolalities; evaluated CD4 and CD8 counts, Beta-2 microglobulin and HIV P-24 antigen levels; assessed recent brain scans; reviewed clinical pictures and noted current medications. RESULTS: ADH levels were less than 1 pg/ml, serum osmolalities 295-312 mos/kg H2O, CD4 levels 3-

http://www.thedoctorsdoctor.com/bodysites/tonsils.htm If HHV-6 is the real cause of AIDS, here are some of the implications: 1. HIV is a massive scientific fraud. Something akin to a Ponzi scheme. Scientists who challenged the HIV theory of AIDS (the ones who have been thuggishly censored and silenced) turn out to be on the money. 2. Chronic Fatigue Syndrome and Autism (and many other so-called HHV-6 related mysterious epidemics) are part of the so-called AIDS epidemic.  Chronic Fatigue Syndrome and Autism both are clearly the results of the ravages of HHV-6. 3. AIDS and Chronic Fatigue Syndrome has been artificially and politically separated into two epidemics. We are living in a period of CFS/AIDS apartheid. So-called AIDS patients have to sit in the back of the HHV-6 epidemic bus while the befuddled HHV-6/CFS patients and HHV-6/Autism victims sit up front. Nobody is well-served. 4. AIDS is not a sexually transmitted disease. That paradigm has set a scapego