SARS-CoV-2 belongs to the genus Beta of the Coronaviridae family of enveloped single-stranded, positive-sense ribonucleic acid (RNA) with a genome length of 30,000bp. The virion is composed of various non-structural (RNA dependent RNA polymerase also known as RdRp) and structural proteins such as Spike (S), Nucleocapsid (N), Matrix (M), and Envelope (E) proteins.

When immune cells are activated, they undergo metabolic change in order to have sufficient energy to function effectively. The Krebs cycle is one of the most important pathways involved in this response and citrate, a critical component of this pathway, regulates carbohydrate and lipid metabolism.

Inflammation can be caused by various environmental factors, including microbial infection and toxic chemical exposure. In response to inflammation, immune cells like macrophages, B and T lymphocytes, fibroblasts, endothelial cells, and various stromal cells secrete soluble polypeptide cytokine Tumor Necrosis Factor Alpha (TNF?)

At the beginning of Covid-19 pandemic, we proposed to use hydroxychloroquine (HCQ) and intranasal interferon (IFN) a-2b spray to prevent SARS-CoV-2. Since then, clinical trials testing these two drugs separately for the treatment and prophylaxis have been reported. A consensus is forming that HCQ and IFNs are not effective in treating severe Covid-19. However, the pathogenesis of Covid-19 suggests that early intervention could reduce the infection and prevent the progression from mild to severe Covid-19.

We review here the evidence for participation of mitochondrial autoimmunity in BC inception and progression and propose a new paradigm that may challenge the prevailing thinking in oncogenesis by suggesting that mitochondrial autoimmunity is a major contributor to breast carcinogenesis and probably to the inception and progression of other solid tumors. It has been shown that MNRR1 mediated mitochondrial-nuclear function promotes BC cell growth and migration and the development of metastasis and constitutes a proof of concept supporting the participation of mitochondrial autoimmunity in breast carcinogenesis.