Neuropediatrics 2016; 47(02): 112-114
DOI: 10.1055/s-0035-1565272
Short Communication
Georg Thieme Verlag KG Stuttgart · New York

Age-Dependent Seroprevalence of JCV Antibody in Children

Eva Maria Hennes
1   Olgahospital – Pediatrics, Kriegsbergstraße, Stuttgart 70174, Germany
,
Barbara Kornek
2   Medical University Vienna, Neurology, Vienna, Austria
,
Peter Huppke
3   Medical University Göttingen, Pediatric Neurology, Göttingen, Germany
,
Markus Reindl
4   Medical University of Innsbruck, Neurology, Innsbruck, Austria
,
Kevin Rostasy
5   Vestische Kinderklinik Datteln, Pediatric Neurology, Datteln, Germany
,
Thomas Berger
6   Medical University of Innsbruck, Neurology, Innsbruck, Austria
› Author Affiliations
Further Information

Publication History

14 May 2015

01 September 2015

Publication Date:
19 October 2015 (online)

Abstract

Progressive multifocal leukoencephalopathy (PML) is an opportunistic central nervous system infection, caused by the John Cunningham virus (JCV). PML may occur during treatment with immunosuppressive agents or monoclonal antibodies such as natalizumab. The JCV seroprevalence increases with age with a seropositivity of 60% in the adult human population. In this study, we analyzed sera from 109 pediatric multiple sclerosis (MS) patients (mean age 14 years) as well as sera from 162 patients with a wide range of suspected neurologic disorders (mean age 6.3 years). Our results showed a considerably lower seroprevalence for JCV in our pediatric cohort with 33.3% and equal distribution in both subgroups, compared with reported seropositivity in adult population. This could result in a lower risk for drug-induced PML in pediatric patients compared with adult patients and can influence the indication for natalizumab therapy in pediatric MS patients.

 
  • References

  • 1 Ferenczy MW, Marshall LJ, Nelson CD , et al. Molecular biology, epidemiology, and pathogenesis of progressive multifocal leukoencephalopathy, the JC virus-induced demyelinating disease of the human brain. Clin Microbiol Rev 2012; 25 (3) 471-506
  • 2 Iacobaeus E, Ryschkewitsch C, Gravell M , et al. Analysis of cerebrospinal fluid and cerebrospinal fluid cells from patients with multiple sclerosis for detection of JC virus DNA. Mult Scler 2009; 15 (1) 28-35
  • 3 White MK, Khalili K. Pathogenesis of progressive multifocal leukoencephalopathy—revisited. J Infect Dis 2011; 203 (5) 578-586
  • 4 Warnke C, Dehmel T, Posevitz-Fejfár A , et al. Anti-JC-virus antibody prevalence in a German MS cohort. Mult Scler 2012; 18 (7) 1054-1055
  • 5 Kean JM, Rao S, Wang M, Garcea RL. Seroepidemiology of human polyomaviruses. PLoS Pathog 2009; 5 (3) e1000363
  • 6 Gorelik L, Lerner M, Bixler S , et al. Anti-JC virus antibodies: implications for PML risk stratification. Ann Neurol 2010; 68 (3) 295-303
  • 7 Knowles WA, Pipkin P, Andrews N , et al. Population-based study of antibody to the human polyomaviruses BKV and JCV and the simian polyomavirus SV40. J Med Virol 2003; 71 (1) 115-123
  • 8 Polo C, Pérez JL, Mielnichuck A, Fedele CG, Niubò J, Tenorio A. Prevalence and patterns of polyomavirus urinary excretion in immunocompetent adults and children. Clin Microbiol Infect 2004; 10 (7) 640-644
  • 9 Viscidi RP, Rollison DE, Sondak VK , et al. Age-specific seroprevalence of Merkel cell polyomavirus, BK virus, and JC virus. Clin Vaccine Immunol 2011; 18 (10) 1737-1743
  • 10 Huppke P, Hummel H, Ellenberger D , et al. JC virus antibody status in a pediatric multiple sclerosis cohort: prevalence, conversion rate and influence on disease severity. Mult Scler 2015; 21 (4) 382-387