JC Virus Seroprevalence and JCVAb Index in Polish Multiple Sclerosis Treatment-Naïve Patients.

Robert Bonek,Konrad Rejdak,Radosław Zajdel,Anna Litwin,Robert Jałowiński,Wojciech Guenter,Anna Karbicka,Veronique Petit,Maciej Maciejowski

doi:10.3390/jcm9123867

Abstract

Multiple sclerosis (MS) treatment with new agents is associated with the risk of the development of progressive multifocal leukoencephalopathy (PML). The seropositivity and a high index of anti-John Cunningham virus (JCV) antibodies are some of the risk factors for PML development. The aim of this study was to assess the seroprevalence of anti-JCVAb and JCVAb index (AI), as well as its correlations with demographic and clinical characteristics in treatment-naïve Polish MS patients. This is a multicenter, prospective, and cross-sectional study involving 665 MS patients. The overall prevalence of anti-JCVAb was 65.3%, while 63.1% of seropositive patients had an index level of >1.5. The seroprevalence was shown to increase along with the patient’s age. Except for age, the prevalence of anti-JCVAb was not associated with demographic or clinical data. No correlations between the index levels and the demographic or clinical data were observed. In Poland, the seroprevalence of anti-JCVAb in treatment-naïve MS patients is one of the highest in Europe. The majority of seropositive patients had an anti-JCV antibody level denoting a high-risk category. This means that we need further studies to be conducted on the individualization of MS treatment in order to provide patients with an appropriate therapeutic safety level.

Highlights

The John Cunningham virus (JCV/JCPyV) is an omnipresent and species-specific, human DNA virus belonging to the Polyomaviridae family
The unique aspect of the study is the fact that it was conducted in the treatment-naïve multiple sclerosis (MS) patients, which allowed us to exclude the effect of MS therapies on the JCV antibodies (JCVAb) seroprevalence or index levels
It was found that the duration of natalizumab exposure was a risk factor for the higher prevalence of JCVAb potentially resulting from an asymptomatic JC virus reactivation [15], while the treatment time correlated with an antibody index (AI) increase [25]

Summary

Introduction

The John Cunningham virus (JCV/JCPyV) is an omnipresent and species-specific, human DNA virus belonging to the Polyomaviridae family. In the majority of cases, exposure to JCV occurs in childhood without causing any clinical manifestation. The JCV seropositivity rate in the general population ranges from 33% to 91% [1,2]. JCV is an etiological agent of progressive multifocal leukoencephalopathy (PML). This is a rare, but frequently fatal, demyelinating disease of the central nervous system (CNS), during which lytic oligodendrocyte injuries are observed. The first cases of PML were reported in 1958 in three patients with chronic lymphocytic leukemia (CLL) and Hodgkin’s disease. In 1971, the JCV was isolated from the brain of a Hodgkin’s disease patient as the first of the 13 currently known polyomaviruses [3,4,5]

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