Volgens Medveczky (Morsani College of Medicine van de Universiteit van Florida), Montoya e.a.

is bij een deel van de ME/CVS (?)-patiënten, vaak met neurologische problemen, sprake van

overerving van HHV6 via het DNA van de moeder ("chromosomale integratie") en

werd bij die patiënten m.b.v. PCR vaak een actieve HHV6-infectie vastgesteld,

week de actieve HHV6-variant af van de overefde variant, wijzend op een nieuwe infectie, en

kan langdurige behandeling met valgancyclovir uitkomst brengen door virus-replicatie te stoppen.

HHV6 veroorzaakt de zesde ziekte bij kinderen en voor het derde levensjaar is 95% geinfecteerd.

bij de meeste mensen zal het (neurotrope * en lymfotrope **) virus slapend/latent aanwezig blijven,

bij mensen met immundysfunctie kan het virus reactiveren (een nieuwe infectie veroorzaken)

HHV6-infecties kunnen leiden tot neurologische problemen, longontsteking en encefalomyelitis (!)

*   neurotroop: in staat het zenuwstelsel te infecteren of de werking ervan te beinvloeden.

** lymfotroop: in staat om lymfocyten (witte bloedcellen: T cellen, B cellen en NK cellen)

     te infecteren of de werking daarvan te beïnvloeden.

De bevindingen zijn zeer interessant en hoopgevend,

al blijft de vraag voor ME/CVS-patienten natuurlijk:

is een (nieuwe/reactiverende) HHV6-infectie oorzaaak of gevolg?

Klik op onderstaande afbeelding om een lezing van Medveczky over overerfde HHV6-infecties

(6e internationale HHV6 en 7-conferentie, Baltimore, Maryland, 2008) te bekijken:

Persbericht:

USF-led study suggests some patients with chronic fatigue-like illness may benefit from anti-herpesvirus drug treatment

Tampa, FL (July 25, 2013) –

Many experts believe that chronic fatigue syndrome (CFS) has several root causes including some viruses.

...

Over 95 percent of the population is infected with HHV-6 by age 3, but in those with normal immune systems the virus remains inactive. HHV-6 causes fever and rash (or roseola) in infants during early childhood, and is spread by saliva. In immunocompromised patients, it can reactivate to cause neurological dysfunction, encephalitis, pneumonia and organ failure.

"The good news reported in our study is that antiviral drugs improve the severe neurological symptoms, including chronic pain and long-term fatigue, suffered by a certain cohort of patients with an inherited form of HHV-6," said Medveczky, who is a professor of molecular medicine at USF Health and the study’s principal investigator. "An estimated 15,000 to 20,000 patients with this CFS-like disease in the United States alone may ultimately benefit from the application of this research including antiviral drug therapy."

...

The link between HHV-6 infection and CFS-like illnes is quite complex. After the first encounter, or "primary infection," all nine known human herpesviruses become silent, or "latent," but may reactivate and cause diseases upon immunosuppression or during aging. A previous study from the Medveczky laboratory showed that HHV-6 is unique among human herpesviruses; during latency, its DNA integrates into the structures at the end of chromosomes known as telomeres.

Furthermore, this integrated HHV-6 genome can be inherited from parent to child, a condition commonly referred to as "chromosomally integrated HHV-6," or CIHHV-6. By contrast, the "latent" genome of all other human herpesviruses converts to a circular form in the nucleus of the cell, not integrated into the chromosomes, and not inheritable by future generations.

...

Medveczky’s team discovered that untreated CIHHV-6 patients with CFS symptoms showed signs that the HHV-6 virus was actively replicating: determined by the presence of HHV-6 messenger RNA (mRNA), a substance produced only when the virus is active. The team followed these patients during treatment, and discovered that the HHV-6 mRNA disappeared by the sixth week of antiviral therapy with valganciclovir, a drug used to treat closely related cytomegalovirus (HHV-5). Of note, the group also found that short-term treatment regimens, even up to three weeks, had little or no impact on the HHV-6 mRNA level.

...

http://hscweb3.hsc.usf.edu/blog/2013/07/25/usf-led-study-suggests-some-chronic-fatigue-syndrome-patients-may-benefit-from-anti-herpesvirus-drug-treatment/

Persistent human herpesvirus-6 infection in patients with an inherited form of the virus.

Journal of Medical Virology.

J Med Virol. 2013 Jul 25. doi: 10.1002/jmv.23685.

Pantry SN, Medveczky MM, Arbuckle JH, Luka J, Montoya JG, Hu J, Renne R, Peterson D, Pritchett JC, Ablashi DV, Medveczky PG.

Keywords:

human herpesvirus 6;

HHV-6;

antiviral drug treatment;

chronic fatigue syndrome;

integration

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.

Some CIHHV-6 patients are suffering from neurological symptoms,

while others remain asymptomatic.

Four patients with CIHHV-6 and CNS dysfunction

were treated with valganciclovir or foscarnet.

HHV-6 replication was detected

by reverse transcriptase polymerase chain reaction amplification of a late envelope glycoprotein.

In this study we also compared the inherited and persistent HHV-6 viruses by DNA sequencing.

The prevalence of CIHHV-6 in this cohort of adult patients from the USA

suffering from a wide range of neurological symptoms including long-term fatigue

were found significantly greater than the reported 0.8% in the general population.

Long-term antiviral therapy inhibited HHV-6 replication

as documented by loss of viral mRNA production.

Sequence comparison of the mRNA and the inherited viral genome

revealed that the transcript is produced by an exogenous virus.

In conclusion, the data presented here document that

some individuals with CIHHV-6 are infected persistently with exogenous HHV-6 strains

that lead to a wide range of neurological symptoms;

the proposed name for this condition is inherited herpesvirus 6 syndrome or IHS.

PMID: 23893753

http://onlinelibrary.wiley.com/doi/10.1002/jmv.23685/abstract