COVID-19: a multi-organ perspective

Abstract

In this mini review, we explore the complex network of inflammatory reactions incited by SARS-CoV-2 infection, which extends its reach well beyond the respiratory domain to influence various organ systems. Synthesizing existing literature, it elucidates how the hyperinflammation observed in COVID-19 patients affects multiple organ systems leading to physiological impairments that can persist over long after the resolution of infection. By exploring the systemic manifestations of this inflammatory cascade, from acute respiratory distress syndrome (ARDS) to renal impairment and neurological sequelae, the review highlights the profound interplay between inflammation and organ dysfunction. By synthesizing recent research and clinical observations, this mini review aims to provide an overview of the systemic interactions and complications associated with COVID-19, underscoring the need for an integrated approach to treatment and management. Understanding these systemic effects is crucial for improving patient outcomes and preparing for future public health challenges.

Keywords: Covid-19; SARS-CoV-2; clinical outcomes; hyperinflammation; systemic effects.

Figure 1

This illustration portrays the wide array of clinical symptoms linked to the inflammatory reaction induced by COVID-19 across different organ systems. These symptoms may arise either directly from the inflammatory response or indirectly as a result of the inflammation incited following the infection and demise of the host’s cells by SARS-CoV-2.

Figure 2

Stages of lung damage through SARS-CoV-2 illustration. (1) SARS-CoV-2 infection pathway (arrows) through the upper airways, migrating mainly to the lower lung lobes. (2) Recruitment of immune cells such as macrophages, neutrophils, lymphocytes, antigen-presenting cells, natural killer cells in the presence of SARS-CoV-2 (arrow). (3) Worsening of the clinical condition, with blood hypercoagulability occurring, first generating pulmonary edema, in the second figure the defense cells entering the alveoli causing an inflammatory reaction, with a higher probability to decrease oxygen saturation and also, one of the very common outcomes accompanied by D- dimers increased, the Pulmonary Thromboembolism presentation.

Figure 3

Functioning of Angiotensinogen. This illustration demonstrates the Renin-Angiotensin System cascade, highlighting the conversion of Angiotensinogen into Angiotensin I and II, and the vasoconstrictive action of Angiotensin II. The role of ACE2 in converting Ang II into Ang 1-7, demonstrates one cycle benefit to human body, in which promotes vasodilation. The ACE2 interaction with coronavirus during COVID-19 are also represented. During the disease the ACE2 is working as the main virus receptor, reducing its work in this cycle making diminished Ang 1-9 or Ang 1-7 production. The different receptors AT1R, AT2R, AT4R, and MasR are indicated, with their functions in blood pressure regulation, fibrosis, and thrombosis. During the disease, AT4R and AT1R are the main receptors working in this cycle.