Home Men Health An evaluation of the differential effect and the impact of SARS-CoV-2 infection on semen quality

An evaluation of the differential effect and the impact of SARS-CoV-2 infection on semen quality

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An evaluation of the differential effect and the impact of SARS-CoV-2 infection on semen quality

In a recent study published within the eBioMedicine Journal, researchers performed a longitudinal observational cohort study amongst 120 males in Belgium.

The study aimed to research the impact of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection on semen quality parameters, including sperm concentration, motility, and morphology.

Study: SARS-CoV-2 infection reduces quality of sperm parameters: prospective one 12 months follow-up study in 93 patients. Image Credit: Rost9/Shutterstock.com

Background

Studies have detected SARS-CoV-2 within the testis of deceased coronavirus disease 2019 (COVID-19) patients and even through the acute infection phase. Semen is uninfectious on average 21 days after SARS-CoV-2 infection; thus, the danger for sexual transmission of SARS-CoV-2 is low during this time window. 

Nevertheless, on account of a scarcity of longitudinal studies, short- and long-term effects of SARS-CoV-2 on sperm quality and subsequent effects on male fertility remain largely unknown.

Further, research has established that thousands and thousands of meiotic reduction divisions occur in men day by day, producing gametes even in an environment lacking immune protection; thus, male gametes are more liable to viral infections than female gametes. 

A perturbation within the meiotic reduction division during gametogenesis on account of a viral infection momentarily ceases spermatozoa production, leading to a compromised sperm concentration on average 43 days post-infection. Thus, one other strategy is required to guard or inactivate these gametes.

Furthermore, in men, not only during sperm production but after sperm production, some viruses, e.g., the Zika virus, could gain access to the spermatozoa, which compromises the embryo.

A recent study showed that SARS-CoV-2’s presence within the testis, even after recovery from COVID-19, could alter protein-coding genes in spermatozoa and transfer them to the embryo.

In regards to the study

In the current study, researchers recruited males aged 18 to 70 who had confirmed COVID-19 in Belgium between March 2020 and June 2020 or August 2020 and February 2021.

Of 120 patients recruited on this study, 93, 42, nine, three, and two patients had two, three, 4, five, and 6 control visits, of which 242 were post-COVID-19. During each follow-up visit, the team collected a fresh sperm and blood sample from each participant. Further, the team used the World Health Organization (WHO) criteria to evaluate sperm quality. They quantified the deoxyribonucleic acid (DNA) fragmentation index (DFI) and the high-density stainability (HDS), and IgA- and IgG-anti-sperm antibodies (ASA). 

For moving spermatozoa, the researchers used mixed antiglobulin response (MAR) tests to detect IgA and IgG. The team used light microscopy to find out the proportion of motile sperms with attached latex particles.

As well as, they recorded the placement on the spermatozoan, head, midpiece, or tail, where the latex particles attached. The researchers tested all post-COVID-19 sperm samples for SARS-CoV-2 ribonucleic acid (RNA) with the SpermCOVID test, for which the detection limit was two SARS-CoV-2 RNA copies per ml.

They graded the motility of every spermatozoon into three categories, Grade A, B, and C, where the last category of sperm was immotile. While Grade A spermatozoa showed progressive motility and moved actively, linearly, or in a big circle, Grade B sperm swam in small circles but showed no progressive motility.

The synthesis of Apale-spermatogonia that turn out to be committed to meiosis and enter lively spermatogenesis takes 16 days of the seminiferous epithelium cycle that continually releases spermatozoa. Also, a spermatogenic wave lasts 74 days, followed by an epididymal transit that lasts 12 days. 

The researchers hypothesized that a perturbation in any of those processes on account of SARS-CoV-2 infection would manifest as a reduced spermatozoa output that becomes apparent as a proportional difference between peak and bottom sperm concentration even after several days of COVID-19 onset.

This difference and other estimated sperm parameters served in its place when evaluating the impact of the SARS-CoV-2 infection on sperm parameters of all 93 patients who attended at the very least two follow-up visits.

The researchers calculated the time difference (in days) between the primary SARS-CoV-2 positive reverse transcription-polymerase chain response (RT-PCR) (day zero) and the date of ejaculation on each of the 242 visits. In addition they determined, for every participant, the variety of days post-infection when the sperm concentration was lowest or highest.

Moreover, the researchers analyzed the effect of the SARS-CoV-2 infection across different rounds of spermatogenesis, totaling to 102-days. Finally, they calculated what number of sperm parameters returned to normal, i.e., baseline values post-SARS-CoV-2 infection, and implicated these findings with the spermiogenesis cycle phase.

Results

Of all parameters, sperm concentration was depending on the spermatogenic cycle. Recovery of different sperm parameters varied between patients; nonetheless, it took greater than one-year post-SARS-CoV-2 infection in some cases and relied on the patient’s initial immune response. Also, peak progressive sperm motility post-COVID-19 relied on the patient’s antibody response. Nevertheless, the authors didn’t detect a decline in sperm concentration maxima during anytime post-COVID-19, further indicating that viral infection impacts the reduction division process. 

Every participant had a singular sperm production maximum, reflecting their efficiency in producing spermatocytes from spermatogonia. So, once the external influence declined, sperm concentrations returned to the utmost baseline value.

Patients producing each IgA/IgG-ASA had the fastest complete recovery, while patients without these antibodies couldn’t completely get better. It might be on account of a declining immunological response and its waning effect on spermatozoa.

Moreover, the study data showed that fever didn’t reduce sperm concentration post-SARS-CoV-2 infection however the immune response afterward.

Perhaps IgA and IgG recognize the SARS-CoV-2 receptor angiotensin-converting enzyme-2 (ACE2); thus, they attached themselves to the spermatozoa tail where ACE2 was present.

Conversely, lethal sIgG-N in blood only correlated with higher DFI, consistent with reports that the antibodies are either protective or harmful.

In symptomatic COVID-19 patients who recovered, lowered hepatocyte growth factor (HGF) serum levels inhibited Apale-spermatogonia divisions, crossed the blood-testis barrier, and have become spermatocytes, leading to a lower sperm concentration.

For ejaculated spermatozoa between days zero and 43 post-infection, elevated HDS and DFI rendered the spermatozoa inactive.

Journal reference:

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