# Type I Interferons in SARS-CoV-2 Cutaneous Infection: Is There a Role in Antiviral Defense?

## TL;DR

This study explores how the skin of COVID-19 patients responds to SARS-CoV-2, focusing on the role of type I interferons in antiviral defense.

## Contribution

The study identifies specific molecular changes in the skin of deceased COVID-19 patients and highlights the role of type I interferons in antiviral defense.

## Key findings

- SARS-CoV-2 was detected in the skin of deceased COVID-19 patients using electron microscopy and RT-qPCR.
- Type I interferons were elevated in epidermal cells, suggesting a role in modulating the skin's response to the virus.
- Microvascular changes and altered cytokine expression were observed in skin samples from affected patients.

## Abstract

SARS-CoV-2, a β-coronavirus, primarily affects the lungs, with non-specific lesions and no cytopathic viral effect in the skin. Cutaneous antiviral mechanisms include activation of TLR/IRF pathways and production of type I IFN. We evaluated the antiviral mechanisms involved in the skin of COVID-19 patients, including skin samples from 35 deceased patients who had contracted COVID-19 before the launch of the vaccine. Detection of SARS-CoV-2 in the skin was performed using transmission electron microscopy and RT-qPCR. Microscopic and molecular effects of the virus in skin were evaluated by histopathology, RT-qPCR, and immunohistochemistry (IHC). The results revealed the presence of SARS-CoV-2 and microscopic changes, including microvascular hyaline thrombi, perivascular dermatitis, and eccrine gland necrosis. There was increased transcription of TBK1 and a reduction in transcription of TNFα by RT-qPCR in the COVID-19 group. IHC revealed reduced expression of ACE2, TLR7, and IL-6, and elevated expression of IFN-β by epidermal cells. In the dermis, there was decreased expression of STING, IFN-β, and TNF-α and increased expression of IL-6 in sweat glands. Our results highlight the role of type I IFN in the skin of COVID-19 patients, which may modulate the cutaneous response to SARS-CoV-2.