Abstract: A paradigm linking herpes-virus immediate-early gene expression apoptosis and myalgic encephalomyelitis chronic fatigue syndrome – Source: Virus Adaptation and Treatment, Feb 21, 2011
[Note: To read the full text of this article reviewing a 72-month study which reported that 79 of 106 ME/CFS patients who were treated with long-term valacyclovir for EBV ME/CFS subsets, or long-term valganciclovir for HCMV or HHV6 ME/CFS subsets (but not subsets with tick-borne infections) "now continue normal lives" – with a theory suggesting how the antivirals may work in this respect, CLICK HERE.]
There is no accepted science to relate herpesviruses (Epstein–Barr virus [EBV], human cytomegalovirus [HCMV], and human herpesvirus 6 [HHV6]) as causes of myalgic encephalomyelitis (ME)/chronic fatigue syndrome (CFS). ME/CFS patients have elevated serum immunoglobulin (Ig)G serum antibody titers to EBV, HCMV, and HHV6, but there is no herpesvirus DNA-emia, herpesvirus antigenemia, or uniformly elevated IgM serum antibody titers to the complete virions.
We propose that herpesvirus EBV, HCMV, and HHV6 immediate-early gene expression in ME/CFS patients leads to host cell dysregulation and host cell apoptosis without lytic herpesvirus replication.
Specific antiviral nucleosides, which alleviate ME/CFS, namely:
• Valacyclovir for EBV ME/CFS
• And valganciclovir for HCMV/HHV6 ME/CFS…
…inhibit herpesvirus DNA polymerases and/or thymidine kinase functions, thus inhibiting lytic virus replication.
New host cell recruitment thus ceases. In the absence of new herpesvirus, nonpermissive herpesvirus replication stops, and ME/CFS recovery ensues.
Source: Virus Adaptation and Treatment, Feb 2011;2011(3)pp 19-24. Lerner AM, Begaj S. Department of Medicine, William Beaumont Hospital, Royal Oak, Michigan; 2DCL Medical Laboratories, Indianapolis, Indiana, USA.[Email: firstname.lastname@example.org]