The Impact of COVID-19 on Adipose Tissue The synergism between obesity and its associated comorbidities makes it difficult to discern the maladies specifically attributed to corpulence [80]. the coronavirus family has been the origin of Cinchonine (LA40221) multiple highly infectious global outbreaks. The most significant ones were the 2003 Severe Acute Cinchonine (LA40221) Respiratory Syndrome coronavirus-1 (SARS-CoV-1) outbreak in China, and the 2012 Middle East Respiratory Syndrome coronavirus (MERS-CoV) outbreak in Saudi Arabia [1,2]. The most recent coronavirus outbreak developed in December 2019 is mainly characterized by signs of acute hypoxic respiratory failure and severe pneumonia [3]. Further genomic sequencing analysis revealed that the causative pathogenic agent of this outbreak is a positive-sense single-stranded RNA virus, which was later identified in February 2020 as the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) by the International Virus Classification Commission [4]. The disease caused by SARS-CoV-2 is known as coronavirus disease 2019 (COVID-19) and has since become a global pandemic [5]. COVID-19-related deaths have exceeded its two predecessors, SARS-CoV-1 and MERS-CoV, combined [6]. The number of identified cases is steadily increasing, and the outbreak has rapidly spread to 222 countries over a short period of time [6]. As of 24 August 2021, 213 million cases and 4.4 million deaths have been documented worldwide [6]. Therefore, understanding the clinical complications of SARS-CoV-2 infection is pivotal. The clinical presentation of SARS-CoV-2 infection could range from asymptomatic or subclinical infection to severe pneumonia with respiratory failure and even death [7]. Around 80% of COVID-19 patients have mild to moderate disease, 15% develop severe disease, and about 5% end up in a critical condition that requires hospitalization [8]. Specifically, elderly patients with underlying chronic conditions such as cardiovascular complications, diabetes, and emphysema are more vulnerable to the development of severe disease condition, as well as death [9]. Most of COVID-19 patients are typically presented with fever, dry cough, dyspnea, sore throat, and fatigue [10]. Additionally, abdominal pain, vomiting, and diarrhea are considered less commonly reported symptoms [10]. However, some COVID-19 patients might experience nonspecific or atypical symptoms, leading to a delay in testing, diagnosis, and isolation [9]. The pathophysiology behind these atypical presentations is still poorly understood, but the possibility of experiencing these atypical symptoms increases with advanced age and pre-existing comorbidities [11]. The interaction between the SARS-CoV-2 spike protein (S) and angiotensin-converting enzyme 2 (ACE2) receptors facilitates viral entry into host cells [10]. Theoretically, any organ-system expressing ACE2 receptors is potentially susceptible to SARS-CoV-2 direct invasion, including the central nervous system, the gastrointestinal tract, the kidneys, the heart, and the reproductive system [12]. Besides, there are various indirect mechanisms of SARS-CoV-2 infection that may result in multiple organ-system consequences, such as systemic inflammation, hypercoagulability state, and dysregulation of the reninCangiotensinCaldosterone system Rabbit Polyclonal to NSF (RAAS) [13]. The clinical manifestations of COVID-19 should be carefully monitored in clinical settings, in Cinchonine (LA40221) order to mitigate and prevent multiple organ-system complications by implementing organ-specific therapeutic approaches. In this review article, we discuss the pathophysiology and clinical impact of SARS-CoV-2 infection on various organ-systems, to provide a perspective on the major extra-pulmonary consequences of this viral infection. 2. Immunological Complications SARS-CoV-2 is a pathogen with morphologically distinct crown-like projections [14,15]. It enters the host via fomite exposure, respiratory droplets, and infective aerosols [14,16]. Once inside the body, transmembrane serine protease 2 (TMPRSS2), furin, and cathepsin B/L cleave the spike proteins, thereby acquiescing ACE2 receptor binding [14,15,17]. These concerted processes facilitate viral fusion with the host cell membrane [15,17]. Ensuing, SARS-CoV-2 replicates until the.