The clinical and immunological features of alopecia areata following SARS-CoV-2 infection or COVID-19 vaccines

ABSTRACT

Introduction

Alopecia areata (AA) is an autoimmune disease induced by viral infection or vaccination. With the increased incidence of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), the incidence of AA has also increased. Recently the incidence was found to be 7.8% from a previously reported rate of 2.1%. The physical and psychological damage caused by AA could seriously affect patients’ lives, while AA is a challenging dermatological disease owing to its complex pathogenesis.

Areas covered

This paper presents a comprehensive review of the prevalence, pathogenesis and potential therapeutic targets for AA after infection with SARS-CoV-2 or SARS-CoV-2 vaccine.

Expert opinion

The treatment of AA remains challenging because of the complexity of its pathogenesis. For patients with AA after SARS-CoV-2 infection or vaccination, the use of sex hormones and alternative regenerative therapies may be actively considered in addition to conventional treatments. For preexisting disease, therapeutic agents should be adjusted to the patient’s specific condition.

KEYWORDS:

• Alopecia areata
• viral infection
• vaccination
• SARS-CoV-2
• Therapeutic targets

Article highlights

• SARS-CoV-2 infection or vaccination could induce or aggravate alopecia areata.

• The updated incidence of alopecia areata during COVID-19 pandemic was fourfold higher than previously reported.

• Etiological factors, including genes, autoimmunity, coagulation, and psychological stress account for alopecia areata associated with SARS-CoV-2.

• Besides conventional treatments, sex hormone replacement therapies and regenerative therapies are alternative options.

List of abbreviations

SARS-CoV-2	=	severe acute respiratory syndrome coronavirus 2
AA	=	alopecia areata
HF	=	hair follicle
IP	=	immune privilege
COVID-19	=	coronavirus disease 2019
TMPRSS2	=	transmembrane protease serine 2
ACE2	=	angiotensin-converting enzyme 2
Th1 cells	=	T helper-1 cells
IL	=	interleukin
IFN	=	interferon
Th2 cells	=	T helper-2 cells
DCs	=	dendritic cells
TNF	=	tumor necrosis factor
NK cells	=	natural killer cells
DNA	=	deoxyribonucleic acid
mRNA	=	messenger RNA
RNA	=	ribonucleic acid
TLRs	=	toll-like receptors
NF-kB	=	nuclear factor-k-gene binding
JAK	=	Janus tyrosine kinase
HFSCs	=	hair follicle stem cells
pDC	=	plasmacytoid dendritic cell
NLRP3	=	pyrin domain of the NOD-like receptor containing three inflammasomes
ASIA	=	autoimmune/inflammatory syndrome induced by adjuvants

Declaration of interest

The authors have no relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript. This includes employment, consultancies, honoraria, stock ownership or options, expert testimony, grants or patents received or pending, or royalties.

Reviewer disclosures

Peer reviewers on this manuscript have no relevant financial or other relationships to disclose.

Additional information

Funding

This manuscript was funded by Zhejiang Provincial Natural Science Foundation of China under Grant [NO LY23H110001], Science and Technology Major Project of Zhejiang Province and the State Administration of Traditional Chinese Medicine [NO GZY-ZJ-KJ-23035].