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dc.contributor.authorMcFarland, AJ
dc.contributor.authorYousuf, MS
dc.contributor.authorShiers, S
dc.contributor.authorPrice, TJ
dc.date.accessioned2021-07-05T01:04:24Z
dc.date.available2021-07-05T01:04:24Z
dc.date.issued2021
dc.identifier.issn2471-2531
dc.identifier.doi10.1097/PR9.0000000000000885
dc.identifier.urihttp://hdl.handle.net/10072/405646
dc.description.abstractSARS-CoV-2 is a novel coronavirus that infects cells through the angiotensin-converting enzyme 2 receptor, aided by proteases that prime the spike protein of the virus to enhance cellular entry. Neuropilin 1 and 2 (NRP1 and NRP2) act as additional viral entry factors. SARS-CoV-2 infection causes COVID-19 disease. There is now strong evidence for neurological impacts of COVID-19, with pain as an important symptom, both in the acute phase of the disease and at later stages that are colloquially referred to as “long COVID.” In this narrative review, we discuss how COVID-19 may interact with the peripheral nervous system to cause pain in the early and late stages of the disease. We begin with a review of the state of the science on how viruses cause pain through direct and indirect interactions with nociceptors. We then cover what we currently know about how the unique cytokine profiles of moderate and severe COVID-19 may drive plasticity in nociceptors to promote pain and worsen existing pain states. Finally, we review evidence for direct infection of nociceptors by SARS-CoV-2 and the implications of this potential neurotropism. The state of the science points to multiple potential mechanisms through which COVID-19 could induce changes in nociceptor excitability that would be expected to promote pain, induce neuropathies, and worsen existing pain states.
dc.description.peerreviewedYes
dc.languageen
dc.publisherOvid Technologies (Wolters Kluwer Health)
dc.relation.ispartofpagefrome885
dc.relation.ispartofissue1
dc.relation.ispartofjournalPain Reports
dc.relation.ispartofvolume6
dc.subject.fieldofresearchClinical sciences
dc.subject.fieldofresearchcode3202
dc.titleNeurobiology of SARS-CoV-2 interactions with the peripheral nervous system: Implications for COVID-19 and pain
dc.typeJournal article
dc.type.descriptionC1 - Articles
dcterms.bibliographicCitationMcFarland, AJ; Yousuf, MS; Shiers, S; Price, TJ, Neurobiology of SARS-CoV-2 interactions with the peripheral nervous system: Implications for COVID-19 and pain, Pain Reports, 2021, 6 (1), pp. e885
dcterms.licensehttps://creativecommons.org/licenses/by/4.0/
dc.date.updated2021-07-05T00:11:34Z
dc.description.versionVersion of Record (VoR)
gro.rights.copyright© 2021 The Author(s). Published by Wolters Kluwer Health, Inc. on behalf of The International Association for the Study of Pain. This is an open access article distributed under the Creative Commons Attribution License 4.0 (CCBY), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
gro.hasfulltextFull Text
gro.griffith.authorMcFarland, Amelia J.


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