Figure 4 | Scientific Reports

Figure 4

From: Systematic review and meta-analysis of serum total testosterone and luteinizing hormone variations across hospitalized Covid-19 patients

Figure 4

Pathogenetic hypothesis of COVID-19 infection and interplay between hypogonadism and immune response. Hypothesis 1. Sars-CoV-2 viral infection. The virus may present direct testicles cell tropism (such as for Leydig cells), some authors hypthesized a direct detrimental action on testosterone secretion, hence proposing a primary hypogonadism-like condition; Hypothesis 2. Hypogonadism may be a consequence of sexual axis involvement (hypothalamic–pituitary–adrenal axis) after Sars-CoV-2 infection. In patients presenting worse outcomes, hypogonadism may be the key to unfavourable events, encompassing altered immune response, leading to poor outcomes. Abbreviations: T testosterone; ROS Reactive Oxygen Species; NF-kB nuclear factor kappa-light-chain-enhancer of activated B cells. Created with BioRender.com.

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