Literature DB >> 10871797

Molecular evidences for a role of HSV-1 in multiple sclerosis clinical acute attack.

P Ferrante1, R Mancuso, E Pagani, F R Guerini, M G Calvo, M Saresella, L Speciale, D Caputo.   

Abstract

To verify the possible role of human herpesviruses as triggering or aggravating factors in relapsing-remitting multiple sclerosis (RRMS) clinical acute attack, we studied the prevalence of some herpesviruses in the peripheral blood mononuclear cells (PBMCs) collected from 22 MS patients during an MS relapse and in a stable phase and from 18 healthy controls (HC). DNA belonging to Herpes simplex virus type 1 (HSV-1) and type 2 (HSV-2), Human cytomegalovirus (HCMV), Epstein-Barr virus (EBV) and Human Herpes virus 6 (HHV-6) has been searched by specific nested polymerase chain reaction (n-PCR). EBV and HHV6 DNA has been detected with high frequency in acute and stable MS and in healthy controls without significant differences. HCMV DNA was observed both in acute and stable MS but not in HC, and, more interestingly, HSV-1 DNA was only found in 13% of acute MS, while both stable MS and healthy controls were negative. On the basis of these results we focused on HSV-1, and to confirm them and to demonstrate that HSV-1 is actively replicating in MS patients during clinical relapse, we searched both messenger RNA (mRNA) and DNA of HSV-1 in the PBMCs of 15 acute MS patients and 15 healthy controls. We found HSV-1 mRNA and DNA in a significant number of acute MS patients but not in the control group. On the whole these data indicate that HSV-1 reactivate in the peripheral blood of MS patients during clinical acute attack and probably play a role in the triggering of MS relapses.

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Year:  2000        PMID: 10871797

Source DB:  PubMed          Journal:  J Neurovirol        ISSN: 1355-0284            Impact factor:   2.643


  19 in total

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6.  High susceptibility of a human oligodendroglial cell line to herpes simplex type 1 infection.

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Review 10.  HSV-1 and Endogenous Retroviruses as Risk Factors in Demyelination.

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