Expression of SARS-CoV-2 entry molecules ACE2, NRP1, TMPRSS2, and FURIN in the reproductive tissues of male macaques

Ryutaro Moriyama1, Sho Nakamura2,3, Ikki Mitsui2

  • 1Department of Life Science, Kindai University, Higashiosaka, Osaka, 577-8502, Japan. mory@life.kindai.ac.jp.

PubMed

Insights

Severe acute respiratory syndrome-coronavirus-2 (SARS-CoV-2) may not directly impact primate spermatogenesis. However, its presence in Leydig cells suggests potential effects on testosterone production in males infected with COVID-19.

Area of Science:

  • Reproductive biology
  • Virology
  • Endocrinology

Background:

  • Coronavirus disease 2019 (COVID-19) is linked to male reproductive dysfunction, including impaired spermatogenesis and reduced testosterone.
  • The direct or indirect mechanisms of severe acute respiratory syndrome-coronavirus-2 (SARS-CoV-2) on male reproductive health remain unclear.

Purpose of the Study:

  • To investigate the expression of SARS-CoV-2 cell entry molecules (ACE2, NRP1, TMPRSS2, FURIN) in primate male reproductive organs.
  • To determine if SARS-CoV-2 can directly infect male reproductive tissues and affect spermatogenesis or testosterone production.

Main Methods:

  • RT-PCR analysis of testes and accessory gonads in macaques to detect gene expression of ACE2, NRP1, TMPRSS2, and FURIN.
  • Immunohistochemical staining of macaque testis tissue to localize the expression of these molecules in specific cell types.

Main Results:

  • All four SARS-CoV-2 cell entry molecules were detected in macaque testes, but not all in the same cells.
  • ACE2, NRP1, and FURIN were found in Leydig cells, Sertoli cells, and germ cells, while TMPRSS2 was not observed.
  • The co-expression of all four molecules, necessary for direct viral entry and replication via the known pathway, was not found in primate gonads.

Conclusions:

  • SARS-CoV-2 is unlikely to directly infect primate seminiferous tubules and impair spermatogenesis through the ACE2-mediated route.
  • The expression of ACE2, NRP1, and FURIN in Leydig cells suggests a potential impact of SARS-CoV-2 infection on testosterone synthesis and secretion in male primates.