Impact of COVID-19 on the reproductive health of men and women
The outbreak of coronavirus disease 2019 (COVID-19) caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) was declared a global pandemic by the World Health Organization (WHO) on March 11, 2020 .
To study: Potential Effects of COVID-19 on Reproductive Health: A Mini Review. Image Credit: Rost9/Shutterstock
The entry of the virus inside the host cell is done by binding the viral spike protein (S) present at the level of the cell membrane to the human angiotensin converting enzyme 2 (ACE2). After that, the Orf1a/B gene at the 5′ end is translated by a cellular protein translation system. An RNA polymerase complex is produced which further produces a positive and negative chain using the viral genome.
During the early stages of infection, patients have normal or reduced white blood cell counts, elevated C-reactive protein levels, reduced lymphocyte counts, normal procalcitonin levels, and positive blood test results. imagery. Severely infected patients showed increased levels of pro-inflammatory cytokines and features of cytokine storm. However, information on the impact of COVID-19 on reproductive health is scarce.
Recent studies have reported that in germ cells, Leydig cells and Sertoli cells of the testes and ovaries, the ACE2 receptor can be expressed. This suggests that the testes may serve as a possible target of SARS-CoV-2.
A new review article published in the American Journal of Translational Research investigated the relationship between SARS-CoV-2 infection and reproductive health.
Molecular basis of testicular damage caused by SARS-CoV-2
Although ACE2 is important in viral entry, alone it is insufficient to induce viral infection in host cells. ACE2 requires the help of other receptors and co-receptors to mediate host cell invasion, such as a transmembrane serine protease 2 (TMPRSS2) on the cell membrane.
ACE2 are also expressed by Sertoli cells, spermatogonial cells in human testicular tubules and Leydig cells in the interstitial region. High levels of ACE2 are expressed by supporting cells, while low levels are expressed by early spermatocytes, late spermatocytes, and spermatozoa. The expression pattern of TMPRSS2 was found to be quite different from ACE2.
Moreover, the BSG, CTSL and CTSB genes associated with COVID-19 were expressed to different degrees in spermatogenic cells and stromal cells at different stages of development. The testis is therefore at risk of infection with COVID-19, but the mechanism of infection is still unclear.
Impact of COVID-19 on female reproduction
Several studies indicate that the Ang(1-7)-MAS-ACE2 receptor axis exists in human ovaries, as well as the presence of ACE2 markers at all levels in the follicles. ACE2 was expressed by granulosa cells and endometrial epithelial cells, but not so much by stromal cells. The expression level of ACE2 has been reported to change with the menstrual cycle.
SARS-CoV-2 is believed to affect the follicular membrane and granulosa cells of the ovary, influence follicle growth and oocyte quality, decrease ovarian reserve function, and cause infertility or pregnancy loss. It can also damage endometrial epithelial cells which affect early embryo implantation. Several studies have suggested that SARS-CoV-2 may indirectly affect fetal growth in pregnant women. Therefore, monitoring of fetal growth, especially during the second half of pregnancy, is important in women infected with SARS-CoV-2.
However, studies regarding the impact of COVID-19 on pregnancy outcomes are scarce. The potential for vertical transmission between mother and child is also extremely low. Some recent studies have indicated changes in breast milk protein and metabolism associated with COVID-19. Changes in the composition of breast milk can affect the early development of immune defenses in newborns.
Impact of COVID-19 on male reproduction
Studies have reported that all men infected with SARS-CoV-2 had orchitis at autopsy. ACE2 expression in males is mainly located in renal tubule cells, testicular stromal cells, and spermatogenic cells, while TMPRSS2 expression was in spermatozoa and spermatogonial cells.
Expressions of genes related to virus reproduction and transmission were up-regulated in ACE2-positive spermatogonial cells, while genes related to spermatogenesis were down-regulated. Expressions of intercellular connection genes and genes related to the immune system increased in ACE-positive mesenchymal cells and supporting cells, while expression of genes related to reproduction decreased.
Studies also suggest that ACE2 expression in testicular cells is associated with age. The highest expression was reported in the 30-year-old age group, while the lowest was reported in the 60-year-old group. COVID-19 infection could lead to more severe testicular damage in young men than in older men. SAR-CoV-2 infections in men have also been associated with a higher risk of male infertility.
Semen analysis results from patients in the recovery period and in the acute phase suggested that the positivity rate was 26.7% in the acute phase and 8.7% in the recovery period. Semen analysis also reported that patients with moderate infection had lower sperm concentration, lower total sperm count per ejaculate, motile sperm, and progressively motile sperm than healthy individuals.
Additionally, serum luteinizing hormone (LH) levels were significantly increased in men infected with SARS-CoV-2, along with a decrease in testosterone (T) to LH and follicle-stimulating hormone (FSH) ratios. ) to LH.
Recent studies show that both female and male reproductive systems have a molecular basis to support viral attachment. COVID-19 has several negative impacts on the reproductive system and can lead to infertility. However, further research is needed to disclose the relationship of infection with the novel coronavirus and fertility deficiency. Healthcare professionals should also assess a patient’s fertility needs, disease status, and psychological state so that they can help provide appropriate fertility counseling and counseling.