Does autoimmune vitiligo protect against COVID‐19 disease?

Abstract

The SARS‐CoV‐2 pandemic has evolved to a global health problem with a dramatic morbidity and mortality rate impacting our daily life and those of many patients. While there is evidence that some diseases are associated with an increased risk for development of a more severe course of COVID‐19, little is known on protective conditions. Importantly, clearance of viral infection and protection against disease manifestation crucially depends on functional innate and adaptive immunity and the interferon signalling axis. Here, we hypothesize that patients with non‐segmental vitiligo (NSV), an autoimmune skin (and mucosal) disorder, may clear SARS‐CoV‐2 infection more efficiently and have a lower risk of COVID‐19 development. Conversely, in case of COVID‐19 development, vitiligo autoimmunity may influence the cytokine storm‐related disease burden. In addition, immune activation during SARS‐CoV‐2 infection or COVID‐19 disease might increase vitiligo disease activity. Our hypothesis is based on the shift of the immune system in NSV towards adaptive type 1 (IFNγ and CD8 T cells) and innate immune responses. Identified susceptibility genes of NSV patients may further confer increased antiviral activity. To validate our hypothesis, we suggest an international consortium to perform a retrospective data registry and patient‐reported study on a large number of NSV patients worldwide during the COVID‐19 pandemic.

New‐onset vitiligo following COVID‐19 disease

“…9 Of note, immune activation during COVID-19 disease might increase vitiligo disease activity through a shift towards adaptive type 1 immunity (CD8 T cells and IFNγ). 9 Also, Pfizer-BioNTech vaccine BNT162b2 (Cominarty) has already been linked to upregulation of Th1 response, causing increased levels of IL-2, IFN-γ and TNFα. These inflammatory cytokines have been associated to lichen planus reactivation and may also be involved in the pathogenesis of other autoimmune skin diseases, such as vitiligo.…”

“…It can be classified considering the clinical involvement as segmental (localized) or non-segmental (generalized) and considering disease activity as stable or progressing. 7,9 The aetiopathogenesis of vitiligo is still debated, but there is evidence of a possible T CD8+ cell-mediated autoimmune process, triggered by oxidative stress. 9 Of note, immune activation during COVID-19 disease might increase vitiligo disease activity through a shift towards adaptive type 1 immunity (CD8 T cells and IFNγ).…”

“…7,9 The aetiopathogenesis of vitiligo is still debated, but there is evidence of a possible T CD8+ cell-mediated autoimmune process, triggered by oxidative stress. 9 Of note, immune activation during COVID-19 disease might increase vitiligo disease activity through a shift towards adaptive type 1 immunity (CD8 T cells and IFNγ). 9 Also, Pfizer-BioNTech vaccine BNT162b2 (Cominarty) has already been linked to upregulation of Th1 response, causing increased levels of IL-2, IFN-γ and TNFα.…”

Risk of COVID‐19 related complications in vitiligo patients: A database study

“…Vitiligo is known to be associated with a poor-quality life, numerous autoimmune disorders, and comorbid diseases such as metabolic syndrome, which may increase the risk of worse COVID-19 outcomes [1][2][3][4]. Conversely, it has also been hypothesized that vitiligo may provide protection against severe COVID-19 outcomes based on the propensity of the disorder to induce interferon signaling [5][6][7]. Therefore, the goal of this study is to investigate the effect of vitiligo on COVID-19-related outcomes.…”

“…This study found that vitiligo may confer protective effects against worse outcomes in a severe course for patients infected with SARS-CoV-2. While the pathophysiological reasoning is unclear, a previous review hypothesized that non-segmental vitiligo (NSV), the most common form of vitiligo in around 90 % of cases, shifts the body's immune system to a more adaptive type 1 (IFN-γ and CD8 + T cells) and that innate immune responses increase interferon (IFN) signaling [5][6][7][8]. Other related coronaviruses such as SARS-CoV and MERS-CoV are known to disrupt interferon (IFN) signaling via Orf6 and Orf3b [9].…”