Abstract
Coronavirus disease 2019 (COVID-19) is now being investigated for its distinctive patterns in the course of disease development which can be indicated with miscellaneous immune responses in infected individuals. Besides this series of investigations on the pathophysiology of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), significant fundamental immunological and physiological processes are indispensable to address clinical markers of COVID-19 disease and essential to identify or design effective therapeutics. Recent developments in the literature suggest that deficiency of type I interferon (IFN) in serum samples can be used to represent a severe progression of COVID-19 disease and can be used as the basis to develop combined immunotherapeutic strategies. Precise control over inflammatory response is a significant aspect of targeting viral infections. This account presents a brief review of the pathophysiological characteristics of the SARS-CoV-2 virus and the understanding of the immune status of infected patients. We further discuss the immune system’s interaction with the SARS-CoV-2 virus and their subsequent involvement of dysfunctional immune responses during the progression of the disease. Finally, we highlight some of the implications of the different approaches applicable in developing promising therapeutic interventions that redirect immunoregulation and viral infection.
Highlights
angiotensin-converting enzyme 22 (ACE2) upregulation triggered by RAS inhibition leads to the more effective entry of SARS-CoV-2 viruses; there is a severe threat for the users of RAS inhibitors of becoming more vulnerable to SARS-CoV-2 infection [56]
We present the significance of understanding the severe symptoms in SARSCoV-2 infected patients and the need for potential anti-inflammatory measures, which is of great interest since hyper inflammation enhances the risk and severity of the disease
Based on recent developments in the literature, we believe that deficiency of type-I IFN is a sign of severe SARS-CoV-2 infected patients
Summary
An excess inflammatory immune response in individuals infected by SARS-CoV-2 viruses is known to ensure the foremost cause of severe disease development, organ failure, and mortality [11,12]. It is interrelated with elevated levels of cytokines, mainly circulating ones [12], deep lymphopenia [13], and involved with extensive mononuclear cell infiltration in different organs, including lungs [14], spleen [15], heart [16], lymph nodes [17] and kidney [18], as observed in a post-mortem examination. In this account, we discuss potential inflammatory responses that have been identified so far in individuals with COVID-19 disease. We briefly highlight emerging pharmaceutical interventions, therapeutic modulations for pulmonary phase, inflammatory immunopathogenesis, immune-boosting strategies, the significance of tracking immune status, and specific aspects of macrophages and monocytes in the pathophysiology of SARS-CoV-2 infection
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