The coronavirus SARS-CoV-2 causes the COVID-19 disease and affects primarily the lungs, but also other organs, causing accelerated cell aging. One of main pathways involved in aging is telomere attrition,… Click to show full abstract
The coronavirus SARS-CoV-2 causes the COVID-19 disease and affects primarily the lungs, but also other organs, causing accelerated cell aging. One of main pathways involved in aging is telomere attrition, which ultimately leads to defective tissue regeneration and organ dysfunction. Indeed, short telomeres in aged people aggravate the COVID-19 symptoms and, COVID-19 survivors showed shorter telomeres in blood cells. The SARS-CoV-2 has been detected in testis, but the ovaries, which express the viral entry factors, have not been fully explored. Our objective was the analysis of telomeres and reproductive outcomes in women who had COVID-19 and controls. In this prospective cohort study, granulosa cells (GCs) and blood were collected from 65 women. Telomere length (TL) was measured by high-throughput in situ hybridization. Mean TL of GCs and peripheral blood mononuclear cells (PBMCs) was alike in control and mild cases. However, mean TL of GCs was lower in severe cases compared to controls (p=0.017). Control and COVID groups had similar ovarian reserve and number of total oocytes after puncture. However, the oocyte maturation rate was lower in severe cases (p= 0.018). Interestingly, a positive correlation between the oocyte maturation rate and TL of GCs was found in the control group (p=0.024). Our findings point to a potential impact of the coronavirus infection on telomeres and reproductive outcomes in severe cases. This might be considered upon possible new SARS-CoV threats, to favor treatments that enhance oocyte maturation in women severely affected by coronavirus undergoing ART.
               
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