Three Big Books

Tuesday, March 03, 2015

Interview with Konnie Knox, the scientist who should receive a Nobel Prize for her work on HHV-6

Interview with Konnie Knox, the scientist who should receive a Nobel Prize for her work on HHV-6

Dr. Konstance Knox, Chief Executive Officer Dr. Knox was a co-founder of Wisconsin Viral Research Group and Viracor, infectious disease diagnostic laboratories specializing in the diagnosis of viral infections in patients with compromised systems including patients with HIV/AIDS and bone marrow/stem cell transplant and solid organ transplant recipients. Dr. Knox earned her PhD in experimental pathology from the Medical College of Wisconsin and completed her post-doctoral training in translational medicine in the Immunotherapy/Gene Therapy Division of the Cancer Program at St. Luke's Medical Center in Milwaukee, Wisconsin. Dr. Knox's research interests have focused on the role of persistent viral and prion infections in chronic diseases of animals and humans, especially as they relate to diseases of the central nervous system (CNS). She served as a Special Scientific Reviewer for the Department of Defense National Prion Research Program, and for the National Institute of Neurological Disorders and Stroke, NIH, Bethesda, Maryland. Dr. Knox is the author and co-author on 41 peer reviewed scientific publications. Currently she serves on the Scientific Advisory Board on the Chronic Fatigue Syndrome Association of Wisconsin, and is Chair of the Scientific Advisory Board for Simmaron Research Foundation, Incline Village, Nevada.

Call for Abstracts for HHV-6 Conference in Boston

The World Has a Serious HHV-6 Heart Problem

Aggravation of left ventricular dysfunction in patients with biopsy-proven cardiac human herpesvirus A and B infection.



"CONCLUSIONS:Persistence of cardiac HHV-6 B genomes was significantly associated with cardiac dysfunction, and hemodynamic parameters improved in association with HHV-6 B clearance."

Does this help explain how HHV-6 causes CFS/AIDS/Autism etc.?

GP96 interacts with HHV-6 during viral entry and directs it for cellular degradation.


CD46 and CD134 mediate attachment of Human Herpesvirus 6A (HHV-6A) and HHV-6B to host cell, respectively. But many cell types interfere with viral infection through rapid degradation of viral DNA. Hence, not all cells expressing these receptors are permissive to HHV-6 DNA replication and production of infective virions suggesting the involvement of additional factors that influence HHV-6 propagation. Here, we used a proteomics approach to identify other host cell proteins necessary for HHV-6 binding and entry. We found host cell chaperone protein GP96 to interact with HHV-6A and HHV-6B and to interfere with virus propagation within the host cell. In human peripheral blood mononuclear cells (PBMCs), GP96 is transported to the cell surface upon infection with HHV-6 and interacts with HHV-6A and -6B through its C-terminal end. Suppression of GP96 expression decreased initial viral binding but increased viral DNA replication. Transient expression of human GP96 allowed HHV-6 entry into CHO-K1 cells even in the absence of CD46. Thus, our results suggest an important role for GP96 during HHV-6 infection, which possibly supports the cellular degradation of the virus.

gp96—The immune system's Swiss army knife

HHV-6 in temporal lobe epilepsy biopsies.

HHV-6 News

Large-scale analysis of viral nucleic acid spectrum in temporal lobe epilepsy biopsies.

 "RNA viruses were virtually absent."

"... the higher virus load in TLE patients and the increased detection rate of HHV-6B DNA in patients with previous inflammatory brain reactions require further investigations."

books on kindle

Two books on amazon

Everyone needs to know what the CDC is hiding about CFS and HHV-6. NEW YORK NATIVE contains both volumes of THE CHRONIC FATIGUE SYNDROME EPIDEMIC COVER-UP. The print version is $23. Only $7.98 in Kindle.

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