Viral Infection of the Reproductive System in Times of COVID-19

Viral Infection of the Reproductive System in Times of COVID-19

Khaled Kahloula, Djallal Eddine Houari Adli, Nadia Zouhairi, Kaddour Ziani, Miloud Slimani, Wafaa Arabi, Abdelmohcine Aimrane, Soraia El Baz, Ahmed Draoui, Mohamed Echchakery, Abdelali Bitar
DOI: 10.4018/978-1-7998-8225-1.ch011
OnDemand:
(Individual Chapters)
Available
$37.50
No Current Special Offers
TOTAL SAVINGS: $37.50

Abstract

Coronavirus (SARS-COV2) caused several deaths worldwide. This virus infects the target cell by binding to angiotensin-converting enzymes 2 (ACE2) receptor through its receptor-binding domain (RBD) and replicates. Thus, a high level of ACE2 expression is detected in the testicular cells so that the testis is believed to count as a potential target for direct damage by COVID-19. Moreover, the possibility of testicular damage may be caused by either direct viral invasion through interaction with ACE2 receptors or because of inflammatory response. Similarly, in women, literature reported the distribution and function of ACE2 in the female reproductive system, which is widely expressed in the ovary, uterus, vagina, and placenta. It regulates follicular development and ovulation, modulates luteal angiogenesis and degeneration, and influences regular changes in endometrial tissue and embryo development. Taking these functions into account, COVID-19 may disturb the female reproductive functions through regulating ACE2, resulting in infertility, menstrual disorder, and fetal distress.
Chapter Preview
Top

Cellular Entry Mechanism Of The Virus

A novel CoV emerged in December 2019, termed SARS-CoV-2 by the International Virus Taxonomy Committee (Gorbalenya et al., 2020) due to its genetic similarities to the SARS-CoV-1 virus (79.5%) (Guo et al., 2020). The infection has been termed “COVID-19” (coronavirus disease-19), as this is a CoV-related disease that was discovered originally in 2019 (Ashour et al., 2020; Guarner, 2020) SARS-CoV-2 has been identified as a member of the β-coronavirus subgroup, with a positive-sense single-strand RNA, located within a nucleocapsid contained in an envelope Ashour et al., 2020; Lu et al., 2020; Zhou, 2020). The viral structure includes characteristic spike (S) proteins that are projected from the virion surface and assist viral cell entry, membrane (M) and envelope (E) proteins that assist in viral assembly, and the N protein which forms the nucleocapsid (Ashour et al., 2020). The S protein mediates viral transfer into host cells and is composed of two unique subunits, S1 and S2. The S1 domain functions in virus binding to the host cell membrane, while the S2 domain is responsible for the fusion of the virus to host cell membranes to facilitate the viral genome in entering the host cell. Viral S proteins undergo proteolytic priming by the transmembrane protease, serine 2 (TMPRSS2) (Hoffmann et al., 2020). Many receptors on the human cell membrane are identified which are involved in S1 protein binding to host cells (Ashour et al., 2020). The SARS-CoV-2 may gain access to host cells through the angiotensin-converting enzyme 2 (ACE2) receptor, with a higher affinity than reported in SARS-CoV-1 (Ashour et al., 2020; Gheblawi et al., 2020) (Fig.1). These receptors are widely expressed in the lungs (particularly type II pneumocytes and macrophages), cardiovascular system, gastrointestinal system, kidneys, neurological tissues, and the testes (Guo et al., 2020, Verdecchia et al., 2020; Fu et al., 2020). Here, the viruses replicate within the cells, releasing mature virions, which in turn infect new target cells (Margone et al., 2020).

Complete Chapter List

Search this Book:
Reset