VCV at relapse

TwistedHelix · Post by **TwistedHelix** » Fri Feb 29, 2008 8:02 am

I thought this was interesting since this virus has come up before, and this study seems to show that reactivation coincides almost perfectly with relapses. I'd like to understand how and why this reactivation occurs – anyone know?

Ann Neurol. 2008 Feb 27 [Epub ahead of print]
Related Articles

Varicella-zoster virus in cerebrospinal fluid at relapses of multiple sclerosis.

Sotelo J, Martínez-Palomo A, Ordoñez G, Pineda B.

Neuroimmunology Unit, National Institute of Neurology and Neurosurgery, Center for Research and Advanced Studies, Mexico City, Mexico.

OBJECTIVE: Recent studies in peripheral blood mononuclear cells (PBMCs) have indicated that exacerbations of multiple sclerosis (MS) could be associated with the reactivation of latent varicella-zoster virus (VZV). METHODS: Ultrastructural observations for viral particles were made by electron microscopy in cerebrospinal fluid (CSF) from 15 MS patients during relapse, 19 MS patients during remission, and 28 control subjects. Initial findings were reproduced in a confirmation cohort. In addition, DNA from VZV was quantified by real-time polymerase chain reaction in PBMCs and CSF from a large number of MS patients (n = 78 ). RESULTS: We found by electron microscopy the presence of abundant viral particles identical to VZV in CSF obtained from MS patients within the first few days of an acute relapse. In contrast, viral particles were not seen in CSF samples from MS patients in remission or from neurological control subjects. Also, DNA from VZV was present in CSF and in PBMCs during relapse, disappearing in most patients during remission. The mean viral load was 542 times greater in CSF at relapse than in CSF at remission and 328 times greater in CSF at relapse than in PBMCs at relapse. INTERPRETATION: The ultrastructural finding of viral particles identical to VZV, together with the simultaneous presence of large quantities of DNA from VZV in the subarachnoid space, almost restricted to the periods of exacerbation, as well as its steady diminution and eventual disappearance from clinical relapse to clinical remission are surprising and constitute the strongest evidence to support the participation of VZV in the pathogenesis of MS. Ann Neurol 2008.

PMID: 18306233 [PubMed - as supplied by publisher]

dignan · Post by **dignan** » Fri Feb 29, 2008 1:19 pm

More interesting virus news, thanks Dom. I think the theory that one of the herpes viruses (VZV, EBV, HHV6a, HSV-1) combined with a retrovirus can cause relapses/progression is getting more compelling all the time.

Loobie · Post by **Loobie** » Fri Feb 29, 2008 1:29 pm

I think that of all the "connections" to the cause that are the most prominent (Herpes, no sun, Vit. D def, and EBV) this one hits home the most to me. I have had cold sores since I was young, but now I almost always feel very "MS'y" after I have an outbreak.

CureOrBust · Post by **CureOrBust** » Sat Mar 01, 2008 3:53 pm

The one thing that raises a question in my mind is that they haven't explicitly discussed (and I certainly don't know) how the immune system acts (or specifically malfunctions) during a relapse.

If we accept that the immune system is acting awry, then maybe its expected that dormant virus become active and multiply almost uncontrollably near the point of relapse.

I don't know, its more a question.

Loobie · Post by **Loobie** » Sat Mar 01, 2008 4:03 pm

That sounds logical. It almost stands to reason also from the point of view that every time one of us gets a nasty infection, we seem to follow up with a relapse.