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Human herpesvirus 6 infects the central nervous system of multiple sclerosis patients in the early stages of the disease

Section of Microbiology, Department of Experimental and Diagnostic Medicine, University of Ferrara, Italy

I Merlotti

Section of Microbiology, Department of Experimental and Diagnostic Medicine, University of Ferrara, Italy

L Caniatti

Section of Neurology, Department of Medical and Surgical Disciplines, University of Ferrara, Italy

E Caselli

Section of Microbiology, Department of Experimental and Diagnostic Medicine, University of Ferrara, Italy

E Granieri

Section of Neurology, Department of Medical and Surgical Disciplines, University of Ferrara, Italy

M R Tola

Section of Neurology, Department of Medical and Surgical Disciplines, University of Ferrara, Italy

D Di Luca

Section of Microbiology, Department of Experimental and Diagnostic Medicine, University of Ferrara, Italy, dil{at}dns.unife.it

E Cassai

Section of Microbiology, Department of Experimental and Diagnostic Medicine, University of Ferrara, Italy

The presence and the replicative state of human herpesvirus 6 (HHV-6) were evaluated in clinical samples from multiple sclerosis (MS) patients at the first time of MS diagnosis. HHV-6 variant B was present in peripheral blood mononuclear cells of 5/32 (15%) patients, but persisted with a latent infection. Viral sequences were present also in cerebrospinal fluid (CSF), both free in the liquid (7/32, 22%) and latent in the cellular fraction (3/32, 9%), as shown by analysis of viral transcription. In these cases, variant A was detected. HHV-6 DNA sequences present in the CSF were associated to mature viral particles. In fact, in vitro infectious assays of CSF showed the presence of replication-competent virions. These results show that about 20% of MS patients have active foci of HHV-6 variant A infection in the early stages of the disease and suggest that viral replication takes place within the central nervous system.

Key Words: ELISA • human herpesvirus 6 • multiple sclerosis • transcription • viral infection • viral latency

Multiple Sclerosis, Vol. 10, No. 4, 348-354 (2004)
DOI: 10.1191/1352458504ms1045oa


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