Abstract
The SARS-CoV-2, the virus that causes COVID-19, has infected millions of people worldwide. The symptoms of this disease are primarily due to pulmonary involvement, uncontrolled tissue inflammation, and inadequate immune response against the invader virus. Impaired interferon (IFN) production is one of the leading causes of the immune system’s inability to control the replication of the SARS-CoV-2. Mitochondria play an essential role in developing and maintaining innate cellular immunity and IFN production. Mitochondrial function is impaired during cellular stress, affecting cell bioenergy and innate immune responses. The mitochondrial antiviral-signaling protein (MAVS), located in the outer membrane of mitochondria, is one of the key elements in engaging the innate immune system and interferon production. Transferring healthy mitochondria to the damaged cells by mesenchymal stem cells (MSCs) is a proposed option for regenerative medicine and a viable treatment approach to many diseases. In addition to mitochondrial transport, these cells can regulate inflammation, repair the damaged tissue, and control the pathogenesis of COVID-19. The immune regulatory nature of MSCs dramatically reduces the probability of an immune rejection. In order to induce an appropriate immune response against the SARS-CoV-2, we hypothesize to donate mitochondria to the host cells of the virus. We consider MSCs as an appropriate biological carrier for mitochondria. Besides, enhancing the expression of MAVS protein in MSCs and promoting the expression of SARS-CoV-2 viral spike protein as a specific ligand for ACE2+ cells will improve IFN production and innate immune responses in a targeted manner.
Highlights
The novel coronavirus disease 2019 (COVID-19), caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), has caused a serious worldwide pandemic that has influenced different aspects of people’s lives
It is demonstrated that SARS-CoV-2 carries a protein gene called open reading frame-9b (ORF-9b) that inhibits the interferon response in the infected cells by inhibiting mitochondria and the mitochondrial antiviral-signaling protein (MAVS) signalosome
Considering the crucial role of mitochondria in inducing innate and adaptive immune responses by promoting IFN production and activating antiviral pathways, we suggested that transferring healthy mitochondria will improve innate immune response and prevent the distribution of the infection in the body
Summary
The novel coronavirus disease 2019 (COVID-19), caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), has caused a serious worldwide pandemic that has influenced different aspects of people’s lives. Type I interferons (IFNs), a group of innate immune cytokines, are secreted from virally infected cells and act on more than 7,000 genes that regulate critical cellular processes, including metabolism, survival, migration, and inhibition of virus replication and assembly (Wang and Fish, 2019). Many studies have proven the pivotal roles of IFNs in effective innate and adaptive immune responses against viral infections.
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