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Review
. 2021 Jan:99:65-70.
doi: 10.1016/j.reprotox.2020.11.012. Epub 2020 Nov 26.

SARS-COV-2 (Covid-19) and male fertility: Where are we?

Affiliations
Review

SARS-COV-2 (Covid-19) and male fertility: Where are we?

Temidayo S Omolaoye et al. Reprod Toxicol. 2021 Jan.

Abstract

Severe acute respiratory syndrome coronavirus 2 (SARS-COV-2), a single-stranded RNA virus, was found to be the causal agent of the disease called coronavirus disease. During December 2019, China informed the World Health Organization (WHO) of an outbreak of cases of pneumonia of unknown etiology, which caused severe-acute respiratory distress. The disease was termed coronavirus disease 2019 (Covid-19). Due to alarming levels of spread and severity, on the 11th of March 2020, the WHO declared the outbreak as a global pandemic. As of September 14, 2020, more than 29 million cases have been reported, with over 900,000 deaths globally. Since the outbreak, although not conclusive, discoveries have been made regarding the understanding of the epidemiology, etiology, clinical features, clinical treatment, and prevention of the disease. SARS-COV-2 has been detected in saliva, respiratory fluids, blood, urine, and faeces. Findings are however controversial regarding its presence in the semen or the testis. Hence, this review aimed to further analyse the literature concerning (i) the effects of previously identified human coronaviruses on male fertility (ii) the impact of Covid-19 on male fertility and (iii) the implication for general health in terms of infection and transmission.

Keywords: Covid-19; MERS−COV; Male fertility; SARS−COV; SARS−COV-2.

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Conflict of interest statement

Declaration of Competing Interest The authors have no conflicts of interest to declare.

Figures

Fig. 1
Fig. 1
Summary of search outcome.
Fig. 2
Fig. 2
Summary of SARS−COV-2 entry into the cell. The spike (S) proteins have two subunits, namely S1 and S2 subunits. Binding of S1 leads to a conformational change in S2, hence the primary function of S1 is to bind, while that of S2 is to fuse. For viral entry, the N-terminal of S (S1) binds ACE2 receptor. Binding of S1 to ACE2 leads to a conformational change in S2. During the conformational change, viral protein cleavage occurs, which is mediated by receptor transmembrane protease serine 2 (TMPRSS2). Following protein cleavage, fusion between viral and cellular membrane occurs, which subsequently result in the entry of the virus into the cell, thereby releasing its content.

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