![]() A high magnitude of pro-inflammatory cytokines could have detrimental impacts on various organs. Activated monocytes and T cells are the main sources of inflammatory cytokine release in response to the disseminated inflammatory mediators. Cytokine release storm is one of the characteristics of the inflammatory disease during the progress of COVID-19. COVID-19 is accompanied by lymphopenia, atrophy of lymphoid tissues, and the infiltrations of neutrophils and monocytes into the tissues involved. During these steps, immunomodulation is beneficial to harness the detrimental inflammatory responses. These events initiate a cascade of inflammatory events culminating in severe lung infiltration with inflammatory cells. The involvement of these tissues is accompanied by a heavy release of danger-associated molecular patterns (DAMPs). By the spread of the virus, the ACE2 expressing tissues such as gastrointestinal and renal tissues could get infected resulting in the disease stage shift to severe stages. ![]() These therapies might reinforce the host in establishment of infection-limiting responses. Approaches for reinforcing the immune system such as convalescent plasma therapy and IFN-α therapy could be advantageous at initial stages. ![]() There are distinct therapeutic strategies for coping with the infection in incubation period and severe stages. When an HLA haplotype fails to present the immunodominant antigens of SARS-CoV-2, adaptive responses will be absent, allowing the expansion of the thriving virus eventuating in the disease progression severe stage. It has been shown that some HLA haplotypes are capable of presenting the SARS-CoV-2 antigens more potently. As indicated above, host factors such as HLA background, plays a critical role in determination of the fate of the infection. However, efficient and specific T- and B-cell adaptive responses can impede the disease progression to severe forms. While during the incubation period, effective immune responses are required for limiting the infection, immune responses are generally deteriorating in severe stages. īy the immunologic prospect, SARS-CoV-2 infection could be divided into the incubation and severe stages. The virus-associated factors could be explained as various mutations affecting the virulence of SARS-CoV-2. The host factors determining the susceptibility to COVID-19 could be summarized as HLA haplotypes, the status of innate immunity, T helper 1/T helper 2 (Th1/Th2) balance, cytokine signature and the expression level and polymorphisms of ACE2, and others. The causative mechanisms for the observed variations in the presentations and the severity of the disease are generally the host- and virus-associated factors. ![]() One of the interesting issues regarding the COVID-19 is a relative variation in clinical presentations of infected individuals ranging from asymptomatic and mild presentations to acute respiratory distress syndrome (ARDS) and multi-organ damage. Despite extensive researches on the physiopathology of this infection, there are still numerous gaps in our knowledge on the virulence of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). The outbreak of COVID-19 has been turned into a serious pandemic health problem and caused considerable mortality all around the globe. ![]()
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