Abstract
Background and Objectives. The importance of mitochondria in inflammatory pathologies, besides providing energy, is associated with the release of mitochondrial damage products, such as mitochondrial DNA (mt-DNA), which may perpetuate inflammation. In this review, we aimed to show the importance of mitochondria, as organelles that produce energy and intervene in multiple pathologies, focusing mainly in COVID-19 and using multiple molecular mechanisms that allow for the replication and maintenance of the viral genome, leading to the exacerbation and spread of the inflammatory response. The evidence suggests that mitochondria are implicated in the replication of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), which forms double-membrane vesicles and evades detection by the cell defense system. These mitochondrion-hijacking vesicles damage the integrity of the mitochondrion’s membrane, releasing mt-DNA into circulation and triggering the activation of innate immunity, which may contribute to an exacerbation of the pro-inflammatory state. Conclusions. While mitochondrial dysfunction in COVID-19 continues to be studied, the use of mt-DNA as an indicator of prognosis and severity is a potential area yet to be explored.
Highlights
Coronavirus disease 19, (COVID-19) is a disease caused by the infection of the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), which was identified for the first time in the city of Wuhan, in the Hubei Province, China in December 2019, causing a global epidemic that has presented a significant threat to the health of the world’s population
Based on these models and in the identification of an open reading frame (ORF), the SARS-CoV-2 viral genome has been identified in mitochondria, indicating that mitochondrial residency could be required for double-membrane vesicle formation, which is critical for the unstoppable replication of coronavirus, as it evades cellular defense [7]
Knowing more about the pathogenesis and molecular mechanisms involved in this viral infection will allow for the detection of alternative ways to address this virus in treatment, and in the evaluation of its prognosis and severity in infected patients
Summary
Coronavirus disease 19, (COVID-19) is a disease caused by the infection of the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), which was identified for the first time in the city of Wuhan, in the Hubei Province, China in December 2019, causing a global epidemic that has presented a significant threat to the health of the world’s population. SARS-CoV-2 enters host cells by the mechanism of viral spike protein binding to the surface receptor for angiotensin-converting enzyme 2 (ACE-2), which mostly allows for the entry of the virus into type II pneumocytes in the lung of the host [4] This induces a local inflammatory process and promotes the release of multiple cytokines, such as tumor necrosis factor alpha (TNF-a) or interleukin-1 beta (IL-1B) and IL-6, which recruit circulatory leukocytes and amplify the systemic inflammation [5]. We aimed to show the importance of mitochondria, as organelles that, in addition to producing energy necessary for the survival of eukaryotic cells, intervene in the pathological process of multiple pathologies, including COVID-19 This intervention occurs through multiple unfamiliar molecular mechanisms that allow for the entry, replication, and maintenance of the viral genome, causing mitochondrial dysfunction and membrane damage and releasing mitochondrial DNA into circulation, which spread and exacerbate the inflammatory response. All these cells are characterized by a high metabolism and mitochondrial volume, along with being the most affected cells of the inflammatory and fibrotic processes typical of COVID-19
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