Description of Brigitte Huber's 2010 CFS Research Project:

 HERVK-18 AS RISK FACTOR FOR CFIDS

DESCRIPTION (provided by applicant): The etiology of Chronic Fatigue Syndrome (CFS) is far from understood and is likely due to multiple genetic components. Infection with EBV and treatment with IFN-a have been implicated in the pathogenesis. Our laboratory has shown that EBV-infection, and exogenous IFN-a?, activate transcription of the env gene of a Human Endogenous Retrovirus, HERV-K18. This provirus is normally silent, but when induced it encodes a superantigen (SAg), which is a class of proteins that is capable of deregulating the immune system. Three alleles of HERV-K18 env have been documented, K18.1, K18.2, K18.3, whose gene products have SAg activity, but are predicted to differ biochemically and functionally. Our working hypothesis is that HERV-K18 is a risk factor for CFS. In a pilot study, the allele and genotype distributions of the HERV-K18 env gene were compared between various groups of CFS patients and healthy controls. Although only a limited number of samples were available in the various cohorts, the odds ratios that were obtained were statistically significant. The most intriguing interpretation of these data are that they provide genetic evidence for the unique etiology of at least one group of CFS patients. Thus, it may be possible to delineate different subtypes of CFS, depending on the clinical history of the patients. It is now proposed to substantiate these pilot results, using a much larger cohort of 400 CFS patients associated with EBV that has been assembled by the co-investigator, Dr. Renee Taylor. Dr. Ben Katz, board certified in both Pediatrics and Pediatric Infectious Diseases, will clinically evaluate the patient cohort, and Dr. Inga Peter, a genetic epidemiologist and biostatistician, will oversee the statistical analyses. In addition, the expression pattern of the HERV-K18 SAg during active disease versus intermission will be measured. Furthermore, T cell stimulatory activity of this SAg, expressed on peripheral blood lymphocytes of patients during the course of the disease, will be tested ex vivo, using a T cell hybridoma reporter assay that has been developed in our lab. Since SAg-activated T cells produce massive quantities of chemokines, lymphokines and neurokines, the expression of the HERV-K18 SAg could influence not only the immune system, but other organs as well. A positive association between CFS and either HERV-K18 alleles or expression patterns would open new avenues for the development of clinical treatments of this chronic disease. CFS is a disease that affects a significant number of people worldwide, yet the underlying mechanism(s) of pathogenesis remains unclear. The herpesvirus EBV and IFN-a have been suggested to be associated with CFS, although these concepts are far from accepted. We propose a novel genetic aspect in the EBV/ CFS association, namely the presence of certain HERV-K18 alleles that differ in their superantigen activity
 http://projectreporter.nih.gov/project_info_description.cfm?projectnumber=5R01AR053821-04

Popular Posts in the Last 7 Days

Oral Kaposi's Sarcoma looks like the Crimson Crescents in Chronic Fatigue Syndrome patients.

An op-ed about CFS and AIDS written by Perplexity A.I.

Does inflammation cause the reactivation of endogenous retroviruses, some with pathological potential?

From Perplexity A.I.

Perplexity A.I. creates "Nosology Man"

Popular Post in the Last 30 Days

" A new study finds that prior herpesvirus infections are linked to a faster age-related increase in blood biomarkers associated with dementia, even in cognitively healthy women. Researchers measured five key biomarkers in 167 women and found that seropositivity for HHVs doubled the rate of biomarker accumulation compared to those without prior infection. The strongest viral associations were seen for Epstein-Barr virus and HHV6, with amyloid-beta and phosphorylated tau levels most affected. These findings support the hypothesis that chronic viral infections may accelerate neurodegeneration and raise dementia risk independently of genetic factors."

Oral Kaposi's Sarcoma looks like the Crimson Crescents in Chronic Fatigue Syndrome patients.

Pigs with ASFV also develop hypovolemia?

A satirical story about in which AIDS activists get involved in promoting and defending science that turns out to be totally wrong and backfires on them

Perplexity A.I. creates "Nosology Man"

Popular Posts from the Last Year

Oral Kaposi's Sarcoma looks like the Crimson Crescents in Chronic Fatigue Syndrome patients.

Dr. Rebecca Culshaw Smith's book is discussed on Twitter

A fictional discussion of AIDS between Senator Rand Paul and Rebecca Culshaw Smith

Ablashi discusses HHV-6, AIDS, Alzheimer's, and Chronic Fatigue Syndrome

Doctors discuss using Chloroquine for COVID-19

Is African Swine Fever a threat to human health in Congo?

All Time Most Popular Posts

Dr. Bhupesh Prusty and Professor Thomas Rudel discuss their HHV-6 research

Anthony Fauci was part of the gang that silenced and destroyed Judy Mikovits.

Was Judy Mikovits destroyed because her XMRV work would have ultimately shown HIV is a total fraud?

Is Chronic Fatigue Syndrome the other AIDS epidemic in the gay community?