Premium
Coronavirus disease 2019 and pityriasis rosea: A review of the immunological connection
Author(s) -
Borgia Francesco,
Li Pomi Federica,
Alessandrello Clara,
Vaccaro Mario,
Pioggia Giovanni,
Gangemi Sebastiano
Publication year - 2022
Publication title -
the journal of dermatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.9
H-Index - 65
eISSN - 1346-8138
pISSN - 0385-2407
DOI - 10.1111/1346-8138.16482
Subject(s) - pityriasis rosea , coronavirus , connection (principal bundle) , covid-19 , disease , virology , medicine , immunology , infectious disease (medical specialty) , pathology , engineering , outbreak , structural engineering
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.