P4-105: HSV-1 Specific IGG Subclasses in Individuals with Alzheimer’s Disease

2016 ◽  
Vol 12 ◽  
pp. P1052-P1053 ◽  
Author(s):  
Roberta Mancuso ◽  
Simone Agostini ◽  
Elena Calabrese ◽  
Ambra Hernis ◽  
Raffaello Nemni ◽  
...  
2018 ◽  
Vol 63 (1) ◽  
pp. 131-138 ◽  
Author(s):  
Simone Agostini ◽  
Roberta Mancuso ◽  
Ambra Hernis ◽  
Andrea Saul Costa ◽  
Raffaello Nemni ◽  
...  

2020 ◽  
Vol 18 (1) ◽  
Author(s):  
Andrea Saul Costa ◽  
Simone Agostini ◽  
Franca Rosa Guerini ◽  
Roberta Mancuso ◽  
Mario Clerici ◽  
...  

2019 ◽  
Vol 39 (8) ◽  
pp. 1217-1221
Author(s):  
Simone Agostini ◽  
Andrea Saul Costa ◽  
Roberta Mancuso ◽  
Franca Rosa Guerini ◽  
Raffaello Nemni ◽  
...  

2006 ◽  
Vol 2 ◽  
pp. S150-S150
Author(s):  
Anita M. Geppert ◽  
Maria Koczorowska ◽  
Robert Knas ◽  
Magdalena Myga ◽  
Anna Gozdzicka-Jozefiak ◽  
...  

2004 ◽  
Vol 73 (4) ◽  
pp. 605-611 ◽  
Author(s):  
Isamu Mori ◽  
Yoshinobu Kimura ◽  
Hironobu Naiki ◽  
Rokuro Matsubara ◽  
Tohru Takeuchi ◽  
...  

2018 ◽  
Author(s):  
Nisha Rathore ◽  
Sree Ranjani Ramani ◽  
Homer Pantua ◽  
Jian Payandeh ◽  
Tushar Bhangale ◽  
...  

AbstractPaired Immunoglobulin-like Type 2 Receptor Alpha (PILRA) is a cell surface inhibitory receptor that recognizes specific O-glycosylated proteins and is expressed on various innate immune cell types including microglia. We show here that a common missense variant (G78R, rs1859788) of PILRA is the likely causal allele for the confirmed Alzheimer’s disease risk locus at 7q21 (rs1476679). The G78R variant alters the interaction of residues essential for sialic acid engagement, resulting in >50% reduced binding for several PILRA ligands including a novel ligand, complement component 4A, and herpes simplex virus 1 (HSV-1) glycoprotein B. PILRA is an entry receptor for HSV-1 via glycoprotein B, and macrophages derived from R78 homozygous donors showed significantly decreased levels of HSV-1 infection at several multiplicities of infection compared to homozygous G78 macrophages. We propose that PILRA G78R protects individuals from Alzheimer’s disease risk via reduced inhibitory signaling in microglia and reduced microglial infection during HSV-1 recurrence.


2020 ◽  
Vol 09 (03) ◽  
pp. 57-75
Author(s):  
Brian T. Reiss ◽  
Meade C. Eggleston ◽  
Arah C. Godbole ◽  
Julia A. Marut ◽  
Cecelia M. McCann ◽  
...  

2022 ◽  
Vol 12 ◽  
Author(s):  
Yuwei Zhang ◽  
Jiaojiao Qu ◽  
Li Luo ◽  
Zhongshun Xu ◽  
Xiao Zou

In recent years, the herpes virus infectious hypothesis for Alzheimer’s disease (AD) has gained support from an increasing number of researchers. Herpes simplex virus (HSV) is a potential risk factor associated with AD. This study assessed whether HSV has a causal relationship with AD using a two-sample Mendelian randomization analysis model. Six single-nucleotide polymorphisms (SNPs) associated with HSV-1 and thirteen SNPs associated with HSV-2 were used as instrumental variables in the MR analysis. We estimated MR values of relevance between exposure and the risk of AD using inverse-variance weighted (IVW) method, MR-Egger regression (Egger), and weighted median estimator (WME). To make the conclusion more robust and reliable, sensitivity analyses and RadialMR were performed to evaluate the pleiotropy and heterogeneity. We found that anti-HSV-1 IgG measurements were not associated with risk of AD (OR, 0.96; 95% CI, 0.79–1.18; p = 0.736), and the same was true for HSV-2 (OR, 1.03; 95% CI, 0.94–1.12; p = 0.533). The findings indicated that any HSV infection does not appear to be a genetically valid target of intervention in AD.


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