Overview of the pathogenesis of COVID-19 (Review)

Abstract

At present, the pathogenesis of the novel coronavirus disease 2019 (COVID-19) has not been fully elucidated. Clinical and experimental findings from studies investigating COVID-19 have suggested that the immune-inflammatory response has a crucial role in severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection. The present article aimed to systematically review the available literature on the pathogenesis of COVID-19. Severe COVID-19 is characterized by organ dysfunction, hypercytokinemia and lymphopenia. It is assumed that the direct cytopathological damage of host cells and the dysregulated immune response caused by SARS-CoV-2 may be the primary underlying mechanisms of COVID-19. Based on the published literature, this review attempts to provide an integrated view of the immunological mechanisms and the potential pathogenesis of COVID-19, providing an in-depth summary of the host-pathogen interaction and host immune responses. It is of great importance to elucidate the possible pathogenesis of COVID-19 to determine the direction of future research.

Keywords: coronavirus disease 2019; cytokine storm; immunity; pathogenesis; severe acute respiratory syndrome coronavirus 2.

Figure 1

Hypothetical pathogenesis of COVID-19. Severe acute respiratory syndrome coronavirus 2 targets cells through the S protein that binds to the ACE2 receptor, replicating and assembling in target cells before being released extracellularly. Inflammatory signaling molecules are released by infected cells and may induce organ injury through innate and acquired immunity. COVID-19, coronavirus disease 2019; S, spike; ACE2, angiotensin converting enzyme 2.

Figure 2

Schematic diagram of the proposed role of angiotensin II and ACE2 in the development of ARDS. Angiotensin II may be involved in the pathophysiological processes of pulmonary inflammation, pulmonary edema, pulmonary fibrosis and parenchymal cell apoptosis in ARDS. SARS-CoV2 spike proteins may result in downregulated expression of ACE2, therefore increasing local angiotensin II levels and aggravating lung injury. ACE2, angiotensin-converting enzyme 2; ARDS, acute respiratory distress syndrome; SARS-CoV2, severe acute respiratory syndrome coronavirus 2.