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