Risk of sporadic amyotrophic lateral sclerosis associated with seropositivity for herpesviruses and echovirus-7

Cermelli, Claudio; Beretti, Francesca; Pietrini, Vladimiro; Nacci, Grazia; Pietrosemoli, Paola; Bartoletti, Anna Maria; Guidetti, Donata; Sola, Patrizia; Bergomi, Margherita; Vivoli, Gianfranco; Portolani, Marinella

doi:10.1023/a:1023067728557

Cited by 46 publications

(30 citation statements)

References 17 publications

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“…Starting from the pioneer study by Bowery [1] showing the neurodegenerative effects produced by tetanus toxin in rats, a significant emerging body of literature suggests the possibility that CNS infections may play a cofactorial role in inducing neurodegenerative diseases [2]. Serological studies suggest a potential involvement of enteroviruses (EV) and human herpesviruses (HHV) in the aetiology of ALS, a fatal neurodegenerative disease selectively affecting motor neurons [3]. A viral origin of PD has also been proposed on the basis of the close similarity between the clinical symptoms of PD and those of Japanese encephalitic virus [4].…”

Section: Introductionmentioning

confidence: 99%

Infectious Agents and Neurodegeneration

Chiara

Marcocci

Sgarbanti³

et al. 2012

Mol Neurobiol

201

172

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A growing body of epidemiologic and experimental data point to chronic bacterial and viral infections as possible risk factors for neurodegenerative diseases, including Alzheimer’s disease, Parkinson’s disease and amyotrophic lateral sclerosis. Infections of the central nervous system, especially those characterized by a chronic progressive course, may produce multiple damage in infected and neighbouring cells. The activation of inflammatory processes and host immune responses cause chronic damage resulting in alterations of neuronal function and viability, but different pathogens can also directly trigger neurotoxic pathways. Indeed, viral and microbial agents have been reported to produce molecular hallmarks of neurodegeneration, such as the production and deposit of misfolded protein aggregates, oxidative stress, deficient autophagic processes, synaptopathies and neuronal death. These effects may act in synergy with other recognized risk factors, such as aging, concomitant metabolic diseases and the host’s specific genetic signature. This review will focus on the contribution given to neurodegeneration by herpes simplex type-1, human immunodeficiency and influenza viruses, and by Chlamydia pneumoniae.

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Section: Introductionmentioning

confidence: 99%

Infectious Agents and Neurodegeneration

Chiara

Marcocci

Sgarbanti³

et al. 2012

Mol Neurobiol

201

172

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“…In a study of Gulf War veterans there was a significant association between systemic mycoplasmal infections and ALS (Nicolson et al, 2002), although it was not established if mycoplasma plays a role in the pathogenesis of ALS or if ALS patients are more susceptible to ALS. The results of another study suggested an association between the risk of ALS and infection with certain enteroviruses and herpes virus (Cermelli et al, 2003).…”

Section: Amyotrophic Lateral Sclerosismentioning

confidence: 96%

Infectious agents and age-related neurodegenerative disorders

Mattson

2004

Ageing Research Reviews

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chlamdAs with other organ systems, the vulnerability of the nervous system to infectious agents increases with aging. Several different infectious agents can cause neurodegenerative conditions, with prominent examples being human immunodeficiency virus (HIV-1) dementia and prion disorders. Such infections of the central nervous system (CNS) typically have a relatively long incubation period and a chronic progressive course, and are therefore increasing in frequency as more people live longer. Infectious agents may enter the central nervous system in infected migratory macrophages, by transcytosis across blood-brain barrier cells or by intraneuronal transfer from peripheral nerves. Synapses and lipid rafts are important sites at which infectious agents may enter neurons and/or exert their cytotoxic effects. Recent findings suggest the possibility that infectious agents may increase the risk of common age-related neurodegenerative disorders such as Alzheimer's disease (AD) and Parkinson's disease (PD), amyotrophic lateral sclerosis (ALS) and stroke. While scenarios can be envisioned whereby viruses such as Chlamydia pneumoniae, herpes simplex and influenza promote damage to neurons during aging, there is no conclusive evidence for a major role of these pathogens in neurodegenerative disorders. In the case of stroke, blood vessels may be adversely affected by bacteria or viruses resulting in atherosclerosis.

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“…Arguably one of the most studied and most conflicting series of results is that regarding the potential viral aetiology of ALS [82][83][84]. Suspected culprits include polioviruses [85], enteroviruses [85][86][87][88][89][90], herpesviruses (HHV-6, HHV-7, HHV-8 [91][92][93]), echoviruses (ECHO6 and ECHO7 [92,94]), and even human endogenous retroviruses [95]. This line of inquiry is likely spurred by the continued findings of reverse transcriptase activity in patients with ALS [96,97] and reversible ALS-like symptoms that are sometimes observed in HIV patients [98][99][100][101].…”

Section: Amyotrophic Lateral Sclerosismentioning

confidence: 99%

Putative biofilm-forming organisms in the human vasculature: expanded and review of the literature

Fry¹,

Ellis²,

Shabilla³

et al. 2014

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Objectives: New technologies, particularly in the field of clinical metagenomics, have opened up new avenues to explore microbial involvement in illnesses where disease initiation is poorly understood. Here we present a series of six patients suffering from diseases with potential microbial involvement: systemic lupus erythematosus, chronic fatigue syndrome, fibromyalgia, multiple sclerosis, amyotrophic lateral sclerosis, and arteriosclerosis. Material and methods: Peripheral blood (first five cases) and suction debris from carotid percutaneous angioplasty (arteriosclerosis) were refrigerated and transported to the site of analysis. DNA was extracted using the standard QIAamp DNA Blood Mini and Protozoal Extraction kits. Bacterial-specific DNA sequences were amplified and subsequently barcoded for DNA sequencing with 16S rRNA-directed primers flanking the variable regions 1 and 2 and variable regions 4 and 5, respectively. Protozoal-specific DNA sequences were amplified and subsequently barcoded for DNA sequencing using low stringency conditions and primers directed to variable regions in the 18S rRNA gene. Results: We found previously unreported mixed bacterial and protozoal biofilm communities in all samples. In all six disease types we revealed protozoa, being close relatives to known aquatic-based protozoa, such as: Oblongichytrium, Chrysocapsa vernalis, Ochromonas, and Perkinsus qugwadi. In a blood sample from the patient with lupus erythematosus DNA stains and culture studies revealed an unknown protozoan exhibiting profound biofilm-forming capability: candidatus Protomyxzoa rheumatica. Conclusions: Discovery of these potentially pathogenic protozoa in human blood may be of great clinical relevance. However, our preliminary results should be confirmed by independent researchers, and the role of biofilm-forming protozoa in human disease should be elucidated.

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Risk of sporadic amyotrophic lateral sclerosis associated with seropositivity for herpesviruses and echovirus-7

Cited by 46 publications

References 17 publications

Infectious Agents and Neurodegeneration

Infectious Agents and Neurodegeneration

Infectious agents and age-related neurodegenerative disorders

Putative biofilm-forming organisms in the human vasculature: expanded and review of the literature

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