Unfortunately, these public health efforts have had, at best, mixed success in curbing the spread of the pandemic. Meanwhile, extensive efforts to date have been appropriately focused on screening, identification and containment, through the collaboration and coordination between global and local health and governmental agencies. Many potential therapies have been proposed, with a subset currently undergoing investigation. It is hypothesised that current efforts will take time to develop, and may or may not be efficacious for this or future coronavirus pandemics. The similar renin–angiotensin–aldosterone–SARS-CoV (RAAS–SCoV) axis interactions shared by the two coronaviruses provide an opportunity to further our understanding of this unique interplay in our pursuit of treatment options.Įarly attempts to develop safe and effective vaccines for SARS or MERS have been unsuccessful. Following the SARS outbreak, extensive research advanced our knowledge of highly morbid coronavirus infections. The association between ACE2 and COVID-19 is rooted in two concepts: the mechanism of SARS-CoV-2 infection and the regulatory role of ACE2 during RAAS overactivation. Following virus binding, ACE2 activity is downregulated through multiple mechanisms, preventing it from performing its usual function in states of health, as will be further discussed later in this review. SARS-CoV-2 mimics SARS-CoV's mechanism of infection, which utilises angiotensin-converting enzyme (ACE) 2, part of the renin–angiotensin–aldosterone system (RAAS). Despite these differences, the shared genome translates into common clinical, microbiological and biochemical phenotypes. The genetic variations between SARS-CoV and SARS-CoV-2 translate into differences in infectivity and immune response. Genetic studies found that SARS-CoV-2 shares almost 80% and 50% sequence identity with SARS-CoV and Middle East respiratory syndrome coronavirus (MERS-CoV), respectively. This novel coronavirus is closely related to the severe acute respiratory syndrome coronavirus (SARS-CoV), which caused an outbreak of disease (SARS) in 2003. Learning from prior pandemics and related viruses can focus our efforts to control spread and treat those infected. As many countries are struggling with the onset of their epidemics, pharmacotherapeutics remain lacking. COVID-19-related hospitalisations are mostly due to the need for respiratory support and progressively higher levels of care, with respiratory failure being the underlying aetiology of COVID-19-related deaths. Infectivity ( R 0) is estimated at 2.24 to 3.58. While early estimates vary and true values remain uncertain, mortality is estimated between 0.4% and 3.4% with initial morbidity and mortality disproportionally affecting older patients. At the time of writing, reported COVID-19 cases exceeded 700 000, with more than 30 000 deaths. In December 2019, Wuhan, China, was identified as the epicentre of this outbreak. This review explores the current state of knowledge regarding the RAAS–SCoV axis (informed by prior studies of SARS-CoV), how this relates to our currently evolving pandemic, and how these insights might guide our next steps in an evidence-based manner.Ĭoronavirus disease 2019 (COVID-19), the infectious disease caused by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), has left over 180 countries and territories grappling with a devastating pandemic.
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There exists significant controversy and confusion surrounding how anti-hypertensive agents might function along this pathway. Importantly, SARS-CoV-2 utilises and interrupts this pathway directly, which could be described as the renin–angiotensin–aldosterone–SARS-CoV (RAAS–SCoV) axis.
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The renin–angiotensin–aldosterone system (RAAS) is crucial to the homeostasis of both the cardiovascular and respiratory systems. The window of opportunity to mitigate downstream morbidity and mortality is narrow but remains open. As many countries are grappling with the onset of their epidemics, pharmacotherapeutics remain lacking. Coronavirus disease 2019 (COVID-19), the disease caused by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), has been declared a global pandemic with significant morbidity and mortality since first appearing in Wuhan, China, in late 2019.