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新型冠状病毒病 2019 与玫瑰糠疹:免疫关联的综述。

Coronavirus disease 2019 and pityriasis rosea: A review of the immunological connection.

机构信息

Section Of Dermatology, Department of Clinical and Experimental Medicine, University of Messina, Messina, Italy.

School and Operative Unit of Allergy and Clinical Immunology, University of Messina, Messina, Italy.

出版信息

J Dermatol. 2022 Oct;49(10):948-956. doi: 10.1111/1346-8138.16482. Epub 2022 Jun 8.

Abstract

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is characterized by the activation of a cytokine storm derived from an excess release of cytokine (interleukin [IL]-6, interferon [IFN] I, C-X-C motif chemokine ligand [CXCL]10, tumor necrosis factor [TNF]-α, macrophage inflammatory protein [MIP]1) due to an uncontrolled immune activation. There has been a fivefold increase in the number of cases of pityriasis rosea during the SARS-CoV-2 pandemic. Using the keywords "pityriasis" and "COVID-19", we carried out a PubMed search, including all articles in the English language published until November 2021. We aimed to investigate the possible connection between SARS-CoV-2 and pityriasis rosea (PR). Pityriasis could be considered an immunological disease due to the involvement of cytokines and chemokines. Our analysis yielded 65 articles of which 53 were not considered; the others (n = 12) concerning the association between PR and COVID-19 were included in our study. We suggest two mechanisms underlying the involvement of the skin in viral infections: (i) viruses directly affecting the skin and/or inducing host immune response thus causing cutaneous manifestations; and (ii) viruses as a possible inducer of the reactivation of another virus. The first mechanism is probably related to a release of pro-inflammatory cytokine and infection-related biomarkers; in the second, several pathways could be involved in the reactivation of other latent viruses (human herpesviruses 6 and 7), such as a cytokine-cytokine receptor interaction, the Janus kinase-signal transducer and activator of transcription signaling pathway, and the IL-17 signaling pathway. We thus believe that a cytokine storm could be directly or indirectly responsible for a cutaneous manifestation. More investigations are needed to find specific pathways involved and thus confirm our speculations.

摘要

严重急性呼吸综合征冠状病毒 2 (SARS-CoV-2) 的特征是细胞因子风暴的激活,这是由于免疫激活失控导致细胞因子(白细胞介素 [IL]-6、干扰素 [IFN] I、C-X-C 基序趋化因子配体 [CXCL]10、肿瘤坏死因子 [TNF]-α、巨噬细胞炎症蛋白 [MIP]1)过度释放引起的。在 SARS-CoV-2 大流行期间,玫瑰糠疹的病例数增加了五倍。我们使用关键词“玫瑰糠疹”和“COVID-19”,在 PubMed 上进行了搜索,包括截至 2021 年 11 月发表的所有英文文章。我们旨在探讨 SARS-CoV-2 与玫瑰糠疹(PR)之间的可能联系。由于细胞因子和趋化因子的参与,玫瑰糠疹可被视为一种免疫性疾病。我们的分析产生了 65 篇文章,其中 53 篇不被认为相关;其余的(n=12)关于 PR 与 COVID-19 之间的关联的文章被纳入我们的研究。我们提出了皮肤参与病毒感染的两种机制:(i)病毒直接影响皮肤和/或诱导宿主免疫反应,从而导致皮肤表现;(ii)病毒可能是另一种病毒重新激活的诱导剂。第一种机制可能与促炎细胞因子和感染相关生物标志物的释放有关;在第二种机制中,几种途径可能涉及其他潜伏病毒(人类疱疹病毒 6 和 7)的重新激活,例如细胞因子-细胞因子受体相互作用、Janus 激酶-信号转导和转录激活因子信号通路以及白细胞介素-17 信号通路。因此,我们认为细胞因子风暴可能直接或间接地导致皮肤表现。需要进一步的研究来寻找涉及的特定途径,从而证实我们的推测。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7497/9347431/4453e3e89708/JDE-49-948-g002.jpg

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