SARS-CoV-2 effect on male infertility and its possible pathophysiological mechanisms.

First case of COVID-19 was reported in Wuhan, China in December 2019. As of now, May 2021, a total of 164,189,004 people were infected, and 3,401,990 deaths have occurred caused by SARS-CoV-2. As SARS-CoV-2 virus cell entry mainly depends on the ACE2 and TMPRSS2 proteins, the presence of high expression levels of both ACE2 and TMPRSS2 in testes highlights the possible vulnerability of men to the virus. Other RNA viruses frequently induce orchitis and result in male infertility. This review evaluates the decline in male fertility and a total of 48 original articles were included for the analysis. We investigated the effects of COVID-19 on male reproductive health and male fertility.  There is a strong association between the high number of ACE2 receptors in the testes and the COVID-19 viral loads. SARS-CoV-2 infection negatively affects the male reproductive tract. Human biological tissues, including body fluids and excretions, tissues, and organs showed positive results tests for SARS-CoV-2. A disruption in the balance of male reproductive system hormones is also observed. Male gonads may be potentially vulnerable to SARS-CoV-2 infection, suggesting caution to follow-up and evaluate infected men that have plans to conceive. Further studies are required to determine if this impairment is temporary or permanent, elucidate SARS-CoV-2's entrance strategies into the testis and how it can affect the semen quality and quantity. We recommend a post-infection follow-up, especially in male patients of reproductive age already having fertility issues.

High mortality co-infections of COVID-19 patients: mucormycosis and other fungal infections.

Severe COVID-19 disease is associated with an increase in pro-inflammatory markers, such as IL-1, IL-6, and tumor necrosis alpha, less CD4 interferon-gamma expression, and fewer CD4 and CD8 cells, which increase the susceptibility to bacterial and fungal infections. One such opportunistic fungal infection is mucormycosis. Initially, it was debated whether a person taking immunosuppressants, such as corticosteroids, and monoclonal antibodies will be at higher risk for COVID-19 or whether the immunosuppresive state would cause a more severe COVID-19 disease. However, immunosuppressants are currently continued unless the patients are at greater risk of severe COVID-19 infection or are on high-dose corticosteroids therapy. As understood so far, COVID-19 infection may induce significant and persistent lymphopenia, which in turn increases the risk of opportunistic infections. It is also noted that 85% of the COVID-19 patients' laboratory findings showed lymphopenia. This means that patients with severe COVID-19 have markedly lower absolute number of T lymphocytes, CD4+T and CD8+ T cells and, since the lymphocytes play a major role in maintaining the immune homeostasis, the patients with COVID-19 are highly susceptible to fungal co-infections. This report is intended to raise awareness of the importance of early detection and treatment of mucormycosis and other fungal diseases, such as candidiasis, SARS-CoV-2-associated pulmonary aspergillosis, pneumocystis pneumonia and cryptococcal disease, in COVID-19 patients, to reduce the risk of mortality.