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The article presents a study aimed at analyzing the prevalence of anti-John Cunningham (JC) virus antibodies, the conversion rate and the influence of anti-JC virus antibody status on the clinical course in a pediatric multiple sclerosis (MS) cohort. It notes the use of serum samples within six months of disease onset and during the course of the disease to proceed with the analysis. It reveals the lack of evidence that seropositivity for anti-JC virus antibodies influences the clinical course.

Monocytes represent a heterogeneous population of primary immune effector cells. At least three different subsets can be distinguished based on expression of the low-affinity FcγRIII: CD14++CD16- classical monocytes, CD14++CD16+ intermediate monocytes, and CD14+CD161 non-classical monocytes. Whereas CD16- classical monocytes are considered key players in multiple sclerosis (MS), little is known on CD16+ monocytes and how they contribute to the disease. In this study, we examined the frequency and phenotype of monocyte subpopulations in peripheral blood, cerebrospinal fluid (CSF), and brain biopsy material derived from MS patients and controls. Furthermore, we addressed a possible monocyte dysfunction in MS and analyzed migratory properties of monocyte subsets using human brain microvascular endothelial cells. Our ex vivo studies demonstrated that CD16+ monocyte subpopulations are functional but numerically reduced in the peripheral blood of MS patients. CD16+ monocytes with an intermediate-like phenotype were found to be enriched in CSF and dominated the CSF monocyte population under noninflammatory conditions. In contrast, an inversed CD16+ to CD16- CSF monocyte ratio was observed in MS patients with relapsing-remitting disease. Newly infiltrating, hematogenous CD16+ monocytes were detected in a perivascular location within active MS lesions, and CD16+ monocytes facilitated CD4+ T cell trafficking in a blood-brain barrier model. Our findings support an important role of CD16+ monocytes in the steady-state immune surveillance of the CNS and suggest that CD16+ monocytes shift to sites of inflammation and contribute to the breakdown of the blood-brain barrier in CNS autoimmune diseases. [ABSTRACT FROM AUTHOR]

Background: Because of the emergence of novel therapies for multiple sclerosis (MS) and the associated increased risk of progressive multifocal leukoencephalopathy, John Cunningham (JC) virus infection has become a focus of interest for neurologists. However, little is known about JC virus infection in pediatric MS to date., Objective: We aimed to analyze the prevalence of anti-JC virus antibodies, the conversion rate and the influence of the anti-JC virus antibody status on the clinical course in a large pediatric MS cohort., Methods: Anti-JC virus antibodies were analyzed in serum samples within six months of disease onset and during the course of the disease. Clinical data were extracted from a pediatric MS databank., Results: A total of 51.6% of 256 patients were found to be positive for anti-JC virus antibodies at onset of disease. No correlation between antibody status and clinical course was seen. Analyzing 693 follow-up serum samples revealed high titer stability, and an annual conversion rate of 4.37% was seen., Conclusion: No evidence was found that seropositivity for anti-JC virus antibodies influences the clinical course. Surprisingly, seroprevalence for anti-JC virus antibodies was more than twice as high as anticipated in this age group, raising the question of whether the infection increases the risk of MS development., (© The Author(s), 2014.)