Did Etienne de Harven inadvertently reveal the retroviral connection between Chronic Fatigue Syndrome and AIDS?

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Human Endogenous Retroviruses and AIDS Research: Confusion, Consensus, or Science?

https://jpands.org/vol15no3/deharven.pdf

HHV-6

 If the endogenous retrovirus HERV-K18 is causing Chronic Fatigue Syndrome, this ALS antiretroviral therapy could be a promising treatment. It could also be a treatment for all illnesses linked to HHV-6 and the endogenous retrovirus that it "induces."

Editor's Note: We may be getting closer to a time when HHV-6 and HERV-K18 make it clear that Chronic Fatigue Syndrome and AIDS are part of the same epidemic.

HERV-K Suppression Using Antiretroviral Therapy in Volunteers With Amyotrophic Lateral Sclerosis (ALS)

https://www.clinicaltrials.gov/ct2/show/NCT02437110



HERV-K and HERV-W transcriptional activity in Myalgic Encephalomyelitis/ Chronic Fatigue Syndrome

Abstract

Chronic Fatigue Syndrome/Myalgic Encephalomyelitis (CFSMS) is an incapacitating chronic disease that dramatically compromise the life quality. The CFS/ME pathogenesis is multifactorial, and it is believed that immunological, metabolic and environmental factors play a role. It is well documented an increased activity of Human endogenous retroviruses (HERVs) from different families in autoimmune and neurological diseases, making these elements good candidates for biomarkers or even triggers for such diseases. Here the expression of Endogenous retroviruses K and W (HERVK and HERVW) was determined in blood from moderately and severely affected ME/CFS patients. HERVK was overexpressed only in moderately affected individuals and HERVW showed no difference. This is the first report about HERVK differential expression in moderate ME/CFS.
https://www.biorxiv.org/content/10.1101/693465v1?rss=1

HHV-6A infection induces expression of HERV-K18-encoded superantigen

Albert K. Taia, Janos Lukab, Dharam Ablashic, Brigitte T. Huber
published online 08 June 2009.

Abstract

Background

The human endogenous retrovirus K-18 (HERV-K18) encodes a superantigen that causes deregulation of the immune system. This provirus is transcriptionally silent, but can be induced by Epstein–Barr virus (EBV) infection and IFN-α treatment.

Objectives

Since the herpesvirus EBV induces HERV-K18 expression in human B cells, it was of interest to determine if other herpesviruses would have similar HERV-K18 transactivation properties. Human herpesvirus (HHV)-6A, a neurotropic virus associated with multiple sclerosis, was a logical candidate for these studies.

Study design

HSB2 cells (HHV-6-negative control), HSB2-ML cells (containing latent HHV-6A genome) and HSB2/HHV-6A cells (HSB-2 cells productively infected with HHV-6A) were compared for their level of HERV-K18 transcription, using quantitative RT-PCR.

Results

Latently infected HSB2-ML cells showed a significant increase in HERV-K18 RNA compared to the control cells. HERV-K18 expression was even greater in HSB2 cells productively infected with HHV-6A for 78h.

Conclusion

These results imply that HHV-6A, either in latent form or during acute infection, directly transactivates HERV-K18. This HERV-K18 induction may be mediated through IFN-α that is produced by the HHV-6A-infected cells. The functional implications of superantigen expression are discussed.

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