In the midst of resurging COVID-19 cases, the second NIH/FDA virtual COVID-19 and Cytokines symposium was held on 1 December 2020, focusing on longitudinal studies of COVID-19 immunity, including long-term consequences, potential associations with autoimmunity and the multisystem inflammatory syndrome in children (MIS-C).
A central and ongoing quest in COVID-19 research is to establish why and how SARS-CoV-2 elicits heterogeneity in disease severity and immunopathology among infected individuals. Hence, much effort has been exerted to understand the cellular basis of SARS-CoV-2-induced immune responses, with the aim of identifying new biomarkers and prognostic tools and developing new therapeutic options. Cytokines emerged early as critical parameters in COVID-19 disease progression, and understanding the qualitative, quantitative and temporal differences in cytokine expression is considered critical for the conquest of COVID-19.
As the late-2020 fall surge brought the third phase of the COVID-19 pandemic, with record numbers of new cases and deaths, the NIH/FDA Immunology, COVID-19, and Cytokine Interest Groups hosted the second NIH/FDA virtual COVID-19 and Cytokines symposium, bringing together experts in these areas to present the most up-to-date data and to provide a forum for discussion, which focused on recent immunological characterization of the disease and its consequences, including MIS-C.
Opening with a summary of the current challenges and achievements in fighting SARS-CoV-2, Anthony Fauci (NIAID/NIH) and Janet Woodcock (CDER/FDA) presented a road map for extending these efforts, as our understanding of the disease and tools for managing COVID-19 are evolving1. Fauci reflected on parallels with the human immunodeficiency virus (HIV) epidemic in the 1980s, which revealed gaps in our knowledge but also led to many outstanding basic and clinical discoveries. Similarly, COVID-19 is an enormous public health problem that challenges scientists and clinicians to rapidly advance our understanding of the immune system and its impact on human disease. Fauci further emphasized the importance of delineating the role of cytokines in COVID-19 pathogenesis and resolution and the effects of antiviral and immunomodulatory treatment strategies, as well as vaccines, on immune responses. In turn, Woodcock pointed out that therapeutic interventions serve as a learning tool and can provide new insights into the pathogenesis of the disease. However, the lack of markers defining different stages of the disease has impeded our understanding of the proper timing for treatment regimens, with some therapies resulting in negative effects when given too late or too early in the disease course. The work presented in this symposium outlined efforts to address these issues.
In the midst of resurging COVID-19 cases, the second NIH/FDA virtual COVID-19 and Cytokines symposium was held on 1 December 2020, focusing on longitudinal studies of COVID-19 immunity, including long-term consequences, potential associations with autoimmunity and the multisystem inflammatory syndrome in children (MIS-C).
A central and ongoing quest in COVID-19 research is to establish why and how SARS-CoV-2 elicits heterogeneity in disease severity and immunopathology among infected individuals. Hence, much effort has been exerted to understand the cellular basis of SARS-CoV-2-induced immune responses, with the aim of identifying new biomarkers and prognostic tools and developing new therapeutic options. Cytokines emerged early as critical parameters in COVID-19 disease progression, and understanding the qualitative, quantitative and temporal differences in cytokine expression is considered critical for the conquest of COVID-19.
As the late-2020 fall surge brought the third phase of the COVID-19 pandemic, with record numbers of new cases and deaths, the NIH/FDA Immunology, COVID-19, and Cytokine Interest Groups hosted the second NIH/FDA virtual COVID-19 and Cytokines symposium, bringing together experts in these areas to present the most up-to-date data and to provide a forum for discussion, which focused on recent immunological characterization of the disease and its consequences, including MIS-C.
Opening with a summary of the current challenges and achievements in fighting SARS-CoV-2, Anthony Fauci (NIAID/NIH) and Janet Woodcock (CDER/FDA) presented a road map for extending these efforts, as our understanding of the disease and tools for managing COVID-19 are evolving1. Fauci reflected on parallels with the human immunodeficiency virus (HIV) epidemic in the 1980s, which revealed gaps in our knowledge but also led to many outstanding basic and clinical discoveries. Similarly, COVID-19 is an enormous public health problem that challenges scientists and clinicians to rapidly advance our understanding of the immune system and its impact on human disease. Fauci further emphasized the importance of delineating the role of cytokines in COVID-19 pathogenesis and resolution and the effects of antiviral and immunomodulatory treatment strategies, as well as vaccines, on immune responses. In turn, Woodcock pointed out that therapeutic interventions serve as a learning tool and can provide new insights into the pathogenesis of the disease. However, the lack of markers defining different stages of the disease has impeded our understanding of the proper timing for treatment regimens, with some therapies resulting in negative effects when given too late or too early in the disease course. The work presented in this symposium outlined efforts to address these issues.
Concluding remarks
It has become abundantly clear that cytokines play a commanding role in the pathogenesis of COVID-19. Cytokine expression is not only a prognostic biomarker for the disease outcome and severity of COVID-19, but SARS-CoV-2-induced cytokine expression is also understood to be a potent agitator of the host immune system, leading to destructive autoinflammation, organ failure and death. As such, the second NIH/FDA symposium on Cytokines in COVID-19 was timely, showcasing cutting-edge research conducted by the immunology community to understand the cytokine-driven pathology of COVID-19. Harnessing knowledge of the virus as well as of autoimmune processes, the speakers highlighted emerging areas of research that may yield new therapeutic targets to reduce the clinical impact of the disease and minimize sequelae.
The virtual nature of the symposium permitted speakers and audiences from around the world to participate in real time, with over 800 viewers logging in on the day of the event and many more subsequently making use of the archived videos. Such worldwide interest illustrated the cutting-edge nature of the talks but also accentuated the need for rapid dissemination of COVID-19-related data to the scientific community. Nonetheless, it was also clear that many questions remain, including the expression patterns and timing of cytokines that are relevant to the disease course and how differences in genetics and environment may contribute. Furthermore, the many nuances to measuring cytokines, including methods for and timing of the collection, treatment, storage and assay of samples, may need to be addressed before specific cytokines can be used reproducibly as disease biomarkers to monitor and predict disease progression and recovery. SARS-CoV-2 presents a set of unique challenges that require navigation through uncharted territories and collaboration on the part of the scientific community. We expect that increasing efforts to interrogate the role of cytokines in COVID-19 will provides us with new tools to map and understand the molecular landscape of this viral disease.
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