https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7355084/#!po=6.81818
.... "Introduction
The global outbreak of coronavirus disease (COVID-19) caused by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) represents an unprecedented challenge for healthcare. Despite social distancing and isolation measures, the number of affected patients is growing daily. Hyperinflammation and immunosuppression are prominently featured in COVID-19 [1, 2], resulting in a cytokine storm [3] ultimately leading to development of micro-thrombosis and disseminated intravascular coagulation (DIC). This cytokine storm is strongly associated with the development of interstitial pneumonia (IP) [4]; however, although lungs are the primarily targeted organs, the cardiovascular system is globally affected. Evidence in this regard supports the notion that the exaggerated production of early response proinflammatory cytokines, such as tumor necrosis factor (TNF), interleukin-1β, -6, and -10 (IL-1β, IL-6, and IL-10, respectively), increases the risk of vascular hyperpermeability, possibly progressing to multiple organ failure and, ultimately, death [3]. The presence of vascular dysfunction at multiple levels, including pulmonary embolisms, alveolar hemorrhage, microangiopathy and vasculitis has been ascertained in post-mortem examination [5, 6]. Additionally, both venous and arterial thromboembolic complications, including endothelial inflammation, have been reported [7, 8]. Indeed, a growing body of evidence seems to support the theory that the endothelium is targeted by the SARS-CoV-2 [9]; most importantly, the endothelium expresses the protein angiotensin-converting enzyme 2 (ACE2) [10, 11], through which the virus can access host cells [12]. Endothelial dysfunction is, therefore, a pivotal determinant of COVID-19 symptoms [13, 14].
As of June 12th, 2020, more than 7.5 million COVID-19 cases have been confirmed worldwide, with more than 420,000 lives lost due to the disease [15]. More than 3.5 million subjects have recovered from COVID-19; however, the long-term consequences of the disease are still largely unknown. Data from 2002–2004 epidemics of SARS suggest that cardiovascular sequelae, such as microangiopathy, cardiomyopathy and impaired endothelial function, are to be expected also in COVID-19 patients [5, 16]. However, while similarities with SARS have been identified, COVID-19 is largely more prevalent due to its high transmissibility, and its consequences, even for recovered patients, are likewise more worrying. Additionally, new evidence is suggesting that autoimmune conditions, such as type 1 diabetes mellitus, might be triggered by the onset of COVID-19 [17], therefore, worsening the risk profile for survivors.
These findings can be extremely relevant for male sexual health: indeed, based on these premises, there is quite enough evidence to hypothesize that consequences of COVID-19 can extend to sexual and reproductive health. We investigated the current literature to understand the long-term clinical complications for COVID-19 survivors, aiming to provide adequate information for clinicians to plan adequate and timely intervention measures."...(more)
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