Abstract

There has been significant concern regarding fertility and reproductive outcomes during the SARS-CoV2 pandemic. Recent data suggests a high concentration of SARS-Cov2 receptors, ACE2 or TMPRSS2, in nasal epithelium and cornea, which explains person-to-person transmission. We investigated the prevalence of SARS-CoV2 receptors among reproductive tissues by exploring the single-cell sequencing datasets from uterus, myometrium, ovary, fallopian tube, and breast epithelium. We did not detect significant expression of either ACE2 or TMPRSS2 in the normal human myometrium, uterus, ovaries, fallopian tube, or breast. Furthermore, none of the cell types in the female reproductive organs we investigated, showed the co-expression of ACE2 with proteases, TMPRSS2, Cathepsin B (CTSB), and Cathepsin L (CTSL) known to facilitate the entry of SARS2-CoV2 into the host cell. These results suggest that myometrium, uterus, ovaries, fallopian tube, and breast are unlikely to be susceptible to infection by SARS-CoV2.

Highlights

  • The coronavirus disease 2019, commonly known as COVID-19 is caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV2)

  • We investigated the presence of the angiotensin-converting enzyme 2 (ACE2), TMPRSS2, Cathepsin B (CTSB), and Cathepsin L (CTSL) in the human ovary cell types derived from single-cell sequencing [9]

  • Since ACE2 requires the co-expression of protease TMPRSS2 or CTSB/L to facilitate its entry into the host cell by priming the S protein on its surface, our data suggest that SARS-CoV2 is unlikely to infect the ovarian cells

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Summary

Introduction

The coronavirus disease 2019, commonly known as COVID-19 is caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV2). SARS-CoV2 is a single-stranded positive sense RNA virus first detected in Wuhan, China in late 2019 [1, 2]. In the absence of TMPRSS2, SARS-CoV2 is known to use cathepsins, CTSB and CTSL as an alternate to enter the host cells [3]. These proteases are required for the priming of the S protein after it binds to the ACE2 receptor for its entry into the host cell [3, 5]

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