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

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.

Keywords: T cells; T-helper 17; cytokine storm; immune system; interferon; pandemic respiratory infection; pityriasis rosea; severe acute respiratory syndrome coronavirus 2; telemedicine; viral reactivation.

Publication types

  • Review

MeSH terms

  • COVID-19*
  • Chemokines
  • Cytokine Release Syndrome
  • Cytokines
  • Humans
  • Interferons
  • Interleukin-17
  • Interleukin-6
  • Janus Kinases
  • Ligands
  • Macrophage Inflammatory Proteins
  • Pityriasis Rosea*
  • Receptors, Cytokine
  • SARS-CoV-2
  • Tumor Necrosis Factors

Substances

  • Chemokines
  • Cytokines
  • Interleukin-17
  • Interleukin-6
  • Ligands
  • Macrophage Inflammatory Proteins
  • Receptors, Cytokine
  • Tumor Necrosis Factors
  • Interferons
  • Janus Kinases