CDC on chronic EBV causing fatigue via mitochondrial dysfunction
Preliminary evidence of mitochondrial dysfunction associated with post-infective fatigue after acute infection with Epstein Barr virus.
"Those who developed post-infective fatigue had gene expression profiles indicative of an altered host response during acute mononucleosis compared to those who recovered uneventfully. Several genes including ISG20 (interferon stimulated gene), DNAJB2 (DnaJ [Hsp40] homolog and CD99), CDK8 (cyclin-dependent kinase 8), E2F2 (E2F transcript
ion factor 2), CDK8 (cyclin-dependent kinase 8), and ACTN2 (actinin, alpha 2), known to be regulated during EBV infection, were differentially expressed in post-infective fatigue cases. Several of the differentially expressed genes affect mitochondrial functions including fatty acid metabolism and the cell cycle."
"CONCLUSION: These preliminary data provide insights into alterations in gene transcript
s associated with the varied clinical outcomes from acute infectious mononucleosis."
www.ncbi.nlm.nih.gov/pubmed/16448567 And the CDC admits in this same report, full text, that it has been known for 50 years that Chronic EBV is associated with Chronic Fatigue:
"However, some individuals exhibit prolonged illness with fatigue, mood changes and cognitive impairment. Such prolonged illness following infectious mononucleosis has been recognized for at least half a century [9]."
www.ncbi.nlm.nih.gov/pmc/articles/PMC1373655/?tool=pubmedNIH, in the NYTimes once again, Lyme activates the herpes:
When Lyme Disease Lasts and Lasts – Jane Brody
"Complicating the picture is the fact that some people with PTLDS symptoms apparently never had Lyme disease in the first place, Dr. Marques said in an interview. There are other infectious organisms — Epstein-Barr virus, for example — that can produce similar symptoms and may be the real culprits."
well.blogs.nytimes.com/2013/07/08/when-lyme-disease-lasts-and-lasts/Clinical pathologic correlations of Lyme disease.
"Immature B cells can also be seen in the spinal fluid. These cells can appear quite atypical- not unlike those of transformed or neoplastic lymphocytes." --
www.ncbi.nlm.nih.gov/pubmed/2814170 Full Text: http://www.actionlyme.org/IDSA_CLINIPATH_DURAY.htm
1992, Paul Duray, in Lyme Disease: Molecular and Immunologic Approaches. – 1992 book.
"On occasion, these atypical-appearing large lymphocytes have been misinterpreted in biopsy by several laboratories as cells of a malignant lymphoma or leukemia. Bb antigens, then, may stimulate growth of immature lymphocytic suibsets in some target organs, as well as in the cerebrospinal fluid (Szyfelbein and Ross 1988). Usual bacterial infections do not produce such lymphocytic infiltrates in tissue. These immunoblastoid cells in Bb infections at times resemble those found in Epstein-Barr virus infections. Does Bb reactivate latent virus infections in tissues? Do some tick inocula harbor simultaneous infectious agents (ixodid ticks can harbor Rickettsiae, Babesia microti, and Ehrlichia bacteria, in addition to Bb), producing multi-agent infections in some hosts? Further studies can clarify these issues by mans of tissue-based molecular probe analysis." -
Paul Duray, NCI, NIH, Ft. Detrick, at the 1992 ALDF Cold Spring Harbor Conference
www.amazon.com/Lyme-Disease-Immunologic-Approaches-Communications/dp/0879693770Post Edited By Moderator (Traveler) : 9/19/2016 4:15:59 PM (GMT-6)