Tag Archives: human herpes virus-6

ME/CFS: the human herpesviruses are back!

Posted on 02/03/2021 by wames

Myalgic Encephalomyelitis/Chronic Fatigue Syndrome: the human herpesviruses are back! by  Maria Eugenia Ariza in Biomolecules 2021, 11(2), 185; 29 January 2021 [doi.org/10.3390/biom11020185]  (This article belongs to the Special Issue Epstein-Barr Virus Disease Mechanisms and Stress Responses)   Review abstract: Myalgic … Continue reading →

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Human Herpesvirus-6 reactivation, mitochondrial fragmentation, & the coordination of antiviral & metabolic phenotypes in ME/CFS

Posted on 04/27/2020 by wames

Human Herpesvirus-6 reactivation, mitochondrial fragmentation, and the coordination of antiviral and metabolic phenotypes in Myalgic Encephalomyelitis/ Chronic Fatigue Syndrome, by Philipp Schreiner, Thomas Harrer, Carmen Scheibenbogen, Stephanie Lamer, Andreas Schlosser, Robert K Naviaux and Bhupesh K Prusty in ImmunoHorizons April … Continue reading →

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ME/CFS as a hyper-regulated immune system driven by an interplay between regulatory T cells & chronic human herpesvirus infections

Posted on 11/22/2019 by wames

Myalgic Encephalomyelitis/Chronic Fatigue Syndrome as a hyper-regulated immune system driven by an interplay between regulatory T cells and chronic human herpesvirus infections, by Nuno Sepúlveda,  Jorge Carneiro,  Eliana M Lacerda and  Luis C Nacul in Front. Immunol. 21 Nov 2019 … Continue reading →

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Human herpesvirus 6 and 7 are biomarkers for fatigue

Posted on 08/05/2016 by wames

Research highlights: Salivary HHV-6 and HHV-7 can be used for assessment of physiological fatigue. Activation and differentiation of macrophages are needed for viral reactivation. Salivary HHV-6 and HHV-7 do not increase with pathological fatigue. Salivary HHV-6/7 can distinguish between physiological … Continue reading →

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Human herpesvirus-6 infection can be inherited

Posted on 08/18/2013 by wames

HHV-6 has been found in people with ME. Abstract Human herpesvirus-6 (HHV-6)A and 6B are ubiquitous betaherpesviruses viruses with lymphotropic and neurotropic potential. As reported earlier, these viruses establish latency by integration into the telomeres of host chromosomes. Chromosomally integrated … Continue reading →

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