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Purinergic signaling in infectious diseases of the central nervous system.
Alves, Vinícius Santos; Leite-Aguiar, Raíssa; Silva, Joyce Pereira da; Coutinho-Silva, Robson; Savio, Luiz Eduardo Baggio.
  • Alves VS; Laboratory of Immunophysiology, Biophysics Institute Carlos Chagas Filho, Federal University of Rio de Janeiro, Rio de Janeiro, Brazil.
  • Leite-Aguiar R; Laboratory of Immunophysiology, Biophysics Institute Carlos Chagas Filho, Federal University of Rio de Janeiro, Rio de Janeiro, Brazil.
  • Silva JPD; Laboratory of Immunophysiology, Biophysics Institute Carlos Chagas Filho, Federal University of Rio de Janeiro, Rio de Janeiro, Brazil.
  • Coutinho-Silva R; Laboratory of Immunophysiology, Biophysics Institute Carlos Chagas Filho, Federal University of Rio de Janeiro, Rio de Janeiro, Brazil.
  • Savio LEB; Laboratory of Immunophysiology, Biophysics Institute Carlos Chagas Filho, Federal University of Rio de Janeiro, Rio de Janeiro, Brazil. Electronic address: savio@biof.ufrj.br.
Brain Behav Immun ; 89: 480-490, 2020 10.
Article in English | MEDLINE | ID: covidwho-669660
ABSTRACT
The incidence of infectious diseases affecting the central nervous system (CNS) has been increasing over the last several years. Among the reasons for the expansion of these diseases and the appearance of new neuropathogens are globalization, global warming, and the increased proximity between humans and wild animals due to human activities such as deforestation. Neurotropism affecting normal brain function is shared by organisms such as viruses, bacteria, fungi, and parasites. Neuroinfections caused by these agents activate immune responses, inducing neuroinflammation, excitotoxicity, and neurodegeneration. Purinergic signaling is an evolutionarily conserved signaling pathway associated with these neuropathologies. During neuroinfections, host cells release ATP as an extracellular danger signal with pro-inflammatory activities. ATP is metabolized to its derivatives by ectonucleotidases such as CD39 and CD73; ATP and its metabolites modulate neuronal and immune mechanisms through P1 and P2 purinergic receptors that are involved in pathophysiological mechanisms of neuroinfections. In this review we discuss the beneficial or deleterious effects of various components of the purinergic signaling pathway in infectious diseases that affect the CNS, including human immunodeficiency virus (HIV-1) infection, herpes simplex virus type 1 (HSV-1) infection, bacterial meningitis, sepsis, cryptococcosis, toxoplasmosis, and malaria. We also provide a description of this signaling pathway in emerging viral infections with neurological implications such as Zika and SARS-CoV-2.
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Full text: Available Collection: International databases Database: MEDLINE Main subject: Central Nervous System Infections / Receptors, Purinergic P1 / Receptors, Purinergic P2X / Receptors, Purinergic P2Y Type of study: Observational study Limits: Humans Language: English Journal: Brain Behav Immun Journal subject: Allergy and Immunology / Brain / Psychophysiology Year: 2020 Document Type: Article Affiliation country: J.bbi.2020.07.026

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Full text: Available Collection: International databases Database: MEDLINE Main subject: Central Nervous System Infections / Receptors, Purinergic P1 / Receptors, Purinergic P2X / Receptors, Purinergic P2Y Type of study: Observational study Limits: Humans Language: English Journal: Brain Behav Immun Journal subject: Allergy and Immunology / Brain / Psychophysiology Year: 2020 Document Type: Article Affiliation country: J.bbi.2020.07.026