key: cord-0252395-1uy1fdof authors: Mohammadpour, Hadiseh; Ziai, Ali; Sadr, Makan; Rezaei, Mitra; Marjani, Majid; Tabarsi, Payam title: A Novel Coronavirus Disease (COVID-19): a Review of Host Cell Signaling Pathways date: 2020-11-03 journal: Tanaffos DOI: nan sha: a8213248c56eae0a3354d5658e24769bf14732bf doc_id: 252395 cord_uid: 1uy1fdof Coronaviruses (CoVs) are the largest group of positive-sense RNA viruses. By increasing our understanding of the interactions between CoVs and the host innate immune system, we can evaluate the development and persistence of inflammation in the lungs and reduce the risk of CoV-induced lung inflammation with a new group of genetic variants. Here, we aim to discuss some recent changes in host cell factors that may be used by CoV to promote the proliferation cycle. We also discuss different host cell signaling pathways that can be considered in the host-pathogen interactions at the molecular level. The pandemic of coronavirus disease 2019 (COVID-19), caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), has created new challenges for the cultural, economic, and health infrastructures. Therefore, it is important that healthcare systems and physicians recognize a global integrated framework for monitoring the progression of COVID-19 to develop targeted therapies that can potentially save human lives. Coronaviruses (CoVs) are single-stranded, positivesense RNA viruses that are widely distributed in humans and other mammals, causing respiratory, gastrointestinal and neurological disorders (1) . Under electron microscopy, CoVs appear to be almost spherical or relatively polymorphic, with distinct "clublike" predictions formed by the spike protein (S) (2, 3) . There is a symmetric nucleocapsid inside the virion, which is a helical positive-sense RNA virus genome with an extremely large size (about 26-32 kb) (4 (6) . More than half of patients with COVID-19 experience shortness of breath. The median time from the onset of disease to shortness of breath is about eight days (7) . Patients with COVID-19 may progress to acute respiratory distress syndrome (ARDS), followed by septic shock, refractory metabolic acidosis, and coagulation dysfunction if the infection is not controlled (6) . STAT proteins are required for cellular differentiation of immune responses to viral infections; these proteins are also involved in cytokine signals (21) . Cytokines, such as TNF-α, IL-6, and IL-1, can contribute to inflammation (20) . Moreover, the Janus kinase/signal transducers and activators of transcription (JAK-STAT) signaling pathway is involved in inflammatory and autoimmune diseases (22) . Also, SOCS-1 and SOCS3 play regulatory roles in both Th1 and Th2 responses. The cytokine signaling pathway is regulated by various systems and mechanisms, including suppressors of cytokine signaling (SOCS) proteins, which suppress signaling to JAK or cytokine receptors. SOCS1 and SOCS3 are also inhibitors of JAK signaling pathway through activating their kinase inhibitory region (23). Coronavirus pathogenesis Electron microscopy in diagnostics of SARS case Rapid diagnosis by electron microscopy of avian coronavirus infection The molecular biology of coronaviruses Accessory proteins of SARS-CoV and other coronaviruses National Health Commission of the People's Republic of China. Guidelines for the diagnosis and treatment of Corona Virus Disease-2019 infection by the National Health Commission b4204a79db5b8912d4440/files/7260301a393845fc87fcf6dd5296 5ecb.pdf Clinical features of patients infected with 2019 novel coronavirus in Wuhan, China Dysregulation of Immune Response in Patients With Coronavirus 2019 (COVID-19) in Wuhan, China Risk Factors Associated With Acute Respiratory Distress Syndrome and Death in Patients With Coronavirus Disease ACE2) as a SARS-CoV-2 receptor: molecular mechanisms and potential therapeutic target Angiotensin-Converting Enzyme 2 (ACE2) Is a Key Modulator of the Renin Angiotensin System in Health and Disease Angiotensin I-converting enzyme: genotype and disease associations Coronavirus infections and immune responses Pathogen recognition and innate immunity Chitin induces accumulation in tissue of innate immune cells associated with allergy A universal role for MyD88 in TLR/IL-1R-mediated signaling Toll-like receptors control activation of adaptive immune responses Pathways in opposition A conserved PLPLRT/SD motif of STING mediates the recruitment and activation of TBK1 TANK-Binding Kinase 1-Dependent Responses in Health and STAT signaling in inflammation Signaling as a Target for Inflammatory and Autoimmune Diseases: Current and Future Prospects