Varnit Chauhan
School of Biotechnology, Gautam Buddha University, Greater NOIDA, India Email ID: varnitchauhan238@gmail.com, 17ibt042@gbu.ac.in
ABSTRACT
At the end of December 2019, Wuhan – a Chinese city – triggers an epidemic of extremely infectious coronavirus(SARS CoV-2). This disease has created mayhem on a global scale and endangered public health. The lungs are the primary site of destruction when this infection is contaminated. It causes lung lesions that result in injury to the lungs and respiratory diseases. Many tests have shown that it affects several other tissues, along with the lungs. Studies on the consequences of infection on male genitalia have demonstrated that SARS CoV-2 decreases male fertility directly and indirectly because of the co-expression of the receptors on the testes responsible for the viral infection. Recent research shows that harm done by SARS CoV-2 not only decreases fertility but also creates autoimmune reactions. This article has outlined the ways in which Infection affects male reproductivity.
KEYWORDS: SARS CoV-2, Male fertility, CoVID-19, and fertility.
INTRODUCTION:
SARS CoV-2 is one of the 30 members of a Coronavirus family and is one of the largest positive-stranded RNA viruses. In recent years, several RNA virus participants like MERS-CoV and SARS CoV have created worldwide health issues. The main molecule for transmission of SARS CoV-2, which are co-expressed in the testis and genital tract, is angiotensin I conversion enzyme 2(ACE 2) — a viral receptor — and transmembrane serine protease 2(TMPRSS 2), a protein S priming receptor. Studies have shown that viral load is detected in testicles of extremely infected persons following post-mortem tests that indicate that the breaching of blood-testis boundary by the virus. The following symptoms were found in a recent demographic sample for deceased(6) and contaminated persons(23): Histopathological analysis of severely ill revealed significant thinning of seminiferous tubules and an increase in apoptotic cells.
Semen sample testing of mild and normal cases showed oligospermia when compared to same-age control.
In deceased patients, a high concentration of T-cells and macrophages was seen which indicates orchitis and epididymitis.
Another important thing observed in 4 of 6 deceased cases was the deposition of IgG in seminiferous tubules.
IgG’s deposition was accompanied by the auto-immune response due to the release of IL6, TNF-α, MCP-1 with direct and indirect damage done upon infection of SARS CoV-2.
DIRECT EFFECTS
Cytopathic effect:
As it is common knowledge, ACE2 is an entry receptor for SARS CoV-2 and has substantial tissue expression in testes, the concern of viral invasion is increased. In spermatogonia, another major molecule in viral transmission – TMPRSS – has also been expressed. In the male reproductive tract, some other viruses, such as HEV and ZIKV, were seen to replicate and cause male infertility. Co-expression ACE2 and TMPRSS2 also raise the likelihood of the male reproductive tract viral invasion that may contribute to decreased male fertility.
Direct damage of the testis:
SARS CoV 2 can damage the testis directly in various ways like creating lesions resulting in spermatogonial necrosis upon replication, damaging Ledig cells as these are highly expressing the ACE2 receptor along with alternative receptors, a decrease in testosterone level as a result of Leydig cell damage, destruction of seminiferous tubules and loss of basement membrane destroying the microenvironment of spermatogenesis.
Direct damage of the epididymis
Epididymal stone formation is observed in the animal model infected with SARS CoV-2. Epididymal stones can reduce sperm fertility and function like sperm motility, acrosomal reaction, etc as epididymis is the crucial region of sperm maturation.
INDIRECT EFFECTS
Cytokine- mediated
High cytokine concentrations in people infected by SARS CoV-2 could result in sexual dysfunction and lower serum testosterone, which can lead to decreased fertility. The elevated IL 6 content in CoVID 19 patients is also found in relation to the destruction of the integrity of the blood-testes membrane, which induces indirect viral damage and spermatogenic rejection.
Antibody-mediated
In degraded Sertoli cells and germ cells, a large amount of G(IgG) Immunoglobulin is shown, which suggests excessive IgG harm. Fertilization can also interfere with the development of antiphospholipid antibodies – anti-sperm antibodies.
High fever mediated
At a temperature lower than 37.8ºC germ cell development occur at a normal pace but higher temperature can lead to the meiotic arrest of germ cells resulting in irreversible damage and high fever being one of the major symptoms of CoVID 19 raising the concern of meiotic arrest of germ cells.
DISCUSSION
Studies have conducted SWOT(strengths, weaknesses, opportunities, threats) analysis to understand the available data(fig.).
A variety of theories and prevention steps are suggested after the study. The appearance of the virus in semen also induces an infection hypothesis during sex, and during cryopreservation procedures, there is a great chance of cross-contamination. Prior to performing ART (Assisted Reproductive Techniques) risk management and reduction methods are recommended to ensure the highest degree of protection.
CONCLUSION
The studies indicate that SARS CoV-2 infection affects the fertility of males by the direct causation of lesions and damage of Leydig cells, and by releasing cytokine and anti-sperm antibodies, which contribute to autoimmune orchitis and epididymitis, indirectly. High release of proinflammatory cytokine and chemokines can also be shown to lead to an uncontrolled inflammation of the testes, which manifest immune pathogenesis through cytokine storm and micro circular dysfunction. Indirect as well as direct effects can be countered by the regulation of the immune response, as immune modulation contributes to a reduction in IgG, cytokine, and chemokine secretion. By controlling cytokine storm SARS CoV-2 can be controlled which in turn will reduce the further damage of Leydig cells and testes. It can be concluded by stating that until the arrival of any vaccine immune modulation can be considered to counter the effects of SARS CoV-2 on male fertility.
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