Article Text

Lack of association between hepatitis G virus and multiple sclerosis
  1. S SAULEDA
  1. Liver Unit, Department of Medicine
  2. Unit of Clinical Neuroimmunology, Department of Neurology
  3. Liver Unit, Department of Medicine, Hospital General, Universitari Vall d’Hebron, Barcelona, Spain
  1. Dr J Río, Unitat de Neuroimmunologia Clinica, Escola d’Enfermeria 5ª planta, Hospital Universitario Vall d’Hebron, Psg. Vall d′Hebron 119–129, 08035 Barcelona, Spain. Fax 0034 3 4274700; email: jrio{at}ar.vhebron.es
  1. J RIO,
  2. X MONTALBAN,
  3. E MARTINEZ-CACERES
  1. Liver Unit, Department of Medicine
  2. Unit of Clinical Neuroimmunology, Department of Neurology
  3. Liver Unit, Department of Medicine, Hospital General, Universitari Vall d’Hebron, Barcelona, Spain
  1. Dr J Río, Unitat de Neuroimmunologia Clinica, Escola d’Enfermeria 5ª planta, Hospital Universitario Vall d’Hebron, Psg. Vall d′Hebron 119–129, 08035 Barcelona, Spain. Fax 0034 3 4274700; email: jrio{at}ar.vhebron.es
  1. JI ESTEBÁN,
  2. J GUARDIA
  1. Liver Unit, Department of Medicine
  2. Unit of Clinical Neuroimmunology, Department of Neurology
  3. Liver Unit, Department of Medicine, Hospital General, Universitari Vall d’Hebron, Barcelona, Spain
  1. Dr J Río, Unitat de Neuroimmunologia Clinica, Escola d’Enfermeria 5ª planta, Hospital Universitario Vall d’Hebron, Psg. Vall d′Hebron 119–129, 08035 Barcelona, Spain. Fax 0034 3 4274700; email: jrio{at}ar.vhebron.es

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The aetiology of multiple sclerosis is still not fully understood. Infectious agents have been postulated as causes of the disease for over a century. A theory proposes that an exogenous stimulus initiates an immune response against endogenous CNS proteins. Supporting this hypothesis, some epidemiological studies strongly implicate an environmental factor in the development of multiple sclerosis.1 Several common human viruses have been implicated in the pathogenesis of multiple sclerosis. However, despite data obtained from epidemiological, serological, and animal studies, no virus has been consistently isolated, or viral material uniquely identified, from patients with multiple sclerosis.2Hepatitis G virus (HGV), a novel potentially hepatotrophic flavilike virus, has recently been identified but little is known about the relation of this virus to chronic viral hepatitis and other chronic diseases.3-4

To investigate the relation between multiple sclerosis and HGV, we have studied the presence of HGV RNA, a marker of ongoing infection, and anti-E2 HGV antibodies, a marker of exposure and recovery of infection, in serum of patients with multiple sclerosis.5

We tested serum from 99 consecutive patients (68 females, mean age 35.2 (SD 11.9) years) with definite multiple sclerosis seen at our hospital. Fifty five patients had a relapsing-remitting, 17 a secondary progressive, and 27 a primary progressive disease. As controls, we included 1000 consecutive blood donors who had tested negative for HCV, HBV, and HIV markers. HGV RNA was determined by reverse transcription/polymerase chain reaction with specific primers of the 5’ and NS5 regions (Boehringer Mannheim) and anti-E2 antibodies were detected from 10μl serum by μPLATE anti-HGenv (Boehringer Mannheim).

Results in patients with multiple sclerosis did not differ significantly from those in healthy blood donors (table). Two patients with multiple sclerosis had ongoing HGV infection, normal liver tests, and were negative for anti-E2 antibodies. None of the patients with HGV exposure (RNA or anti-E2 positive) had received blood transfusions and were not intravenous drug users or healthcare workers. No differences in age, sex, duration of disease, and clinical forms were found among patients with multiple sclerosis. Although the only two patients positive for HGV RNA were primary progressive patients, this finding must be interpreted with caution.

Number of patients and controls positive for HGV RNA and anti-E2 antibodies

In conclusion, the prevalence of HGV infection is not higher in our population of patients with multiple sclerosis than in our controls. Our results do not therefore support any causative role for HGV in the pathogenesis of multiple sclerosis.

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