Abstract
Background: Serious adverse drug reactions of disease-modifying drugs in multiple sclerosis (MS) therapy may include enhanced susceptibility to reactivation of neurotropic herpes viruses like varicella-zoster virus (VZV) and the John Cunningham (JC) polyomavirus. Objective: Because symptomatic reactivation of these viruses are rare events, we determined the incidence of rises in anti-VZV IgG antibody levels as a potential marker for enhanced susceptibility to subclinical and symptomatic reactivation of neurotropic viruses. Methods: Anti-VZV IgG levels were measured in paired serum samples taken 6-8 months apart from natalizumab-treated MS patients, healthy blood donors and human immunodeficiency virus (HIV) infected patients. Results: The incidence of significant rises in anti-VZV IgG levels in natalizumab-treated MS patients was 4.26 per 100 person-years, which was significantly higher than in healthy blood donors. Retrospective evaluation of the available medical records of patients with rises of anti-VZV IgG levels did not reveal herpes zoster (i.e. shingles) manifestations. Conclusions: The increased incidence of significant rises of anti-VZV IgG levels in natalizumab-treated MS patients might indicate an association of natalizumab treatment of MS with an elevated risk of a subclinical VZV reactivation and/or reinfection events. Whether this is predictive of an increased risk of herpes zoster or even symptomatic reactivation of other neurotropic viruses remains to be determined in larger prospective studies.
Original language | English |
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Pages (from-to) | 1823-1832 |
Number of pages | 10 |
Journal | Multiple Sclerosis Journal |
Volume | 21 |
Issue number | 14 |
DOIs | |
State | Published - 1 Dec 2015 |
Externally published | Yes |
Keywords
- Adverse events
- JC virus
- antibodies
- autoimmune disease
- blood donors
- herpes zoster
- human immunodeficiency virus
- immunosuppression
- multiple sclerosis
- natalizumab
- neurotropic virus
- risk factors
- subclinical reactivation
- varicella-zoster virus
- virus reactivation