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Infectious Diseases - Neurological Disorders - Pathology - Public Health and Epidemiology - Urology

Association between IgM Anti-Herpes Simplex Virus and Plasma Amyloid-Beta Levels
Published: Wednesday, December 28, 2011
Author: Catherine Féart et al.

by Catherine Féart, Catherine Helmer, Hervé Fleury, Yannick Béjot, Karen Ritchie, Philippe Amouyel, Susanna Schraen-Maschke, Luc Buée, Jean-Charles Lambert, Luc Letenneur, Jean-François Dartigues


Herpes simplex virus (HSV) reactivation has been identified as a possible risk factor for Alzheimer's disease (AD) and plasma amyloid-beta (Aß) levels might be considered as possible biomarkers of the risk of AD. The aim of our study was to investigate the association between anti-HSV antibodies and plasma Aß levels.


The study sample consisted of 1222 subjects (73.9 y in mean) from the Three-City cohort. IgM and IgG anti-HSV antibodies were quantified using an ELISA kit, and plasma levels of Aß1–40 and Aß1–42 were measured using an xMAP-based assay technology. Cross-sectional analyses of the associations between anti-HSV antibodies and plasma Aß levels were performed by multi-linear regression.


After adjustment for study center, age, sex, education, and apolipoprotein E-e4 polymorphism, plasma Aß1–42 and Aß1–40 levels were specifically inversely associated with anti-HSV IgM levels (ß?=?-20.7, P?=?0.001 and ß?=?-92.4, P?=?0.007, respectively). In a sub-sample with information on CLU- and CR1-linked SNPs genotyping (n?=?754), additional adjustment for CR1 or CLU markers did not modify these associations (adjustment for CR1 rs6656401, ß?=?-25.6, P?=?0.002 for Aß1–42 and ß?=?-132.7, P?=?0.002 for Aß1–40; adjustment for CLU rs2279590, ß?=?-25.6, P?=?0.002 for Aß1–42 and ß?=?-134.8, P?=?0.002 for Aß1–40). No association between the plasma Aß1–42-to-Aß1–40 ratio and anti-HSV IgM or IgG were evidenced.


High anti-HSV IgM levels, markers of HSV reactivation, are associated with lower plasma Aß1–40 and Aß1–42 levels, which suggest a possible involvement of the virus in the alterations of the APP processing and potentially in the pathogenesis of AD in human.