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In the year plus since the first cases of COVID-19 were announced, the SARS-CoV-2 virus has spread globally, causing a significant halt to normal life for much of the world. Nature Immunology presents the Series “Coping with COVID,” in which commissioned articles from authors across the globe describe how COVID-19 has impacted their countries and the ensuing responses to this public health crisis. Throughout the coming year, additional content will be included in this collection. Also included will be archival primary research published by Nature Immunology on immune responses to SARS-CoV-2 infection.
To cope with the new situation during the pandemic, the Turkish people have united in the fight against SARS-CoV-2 with their healthcare workers, scientists and government. We are waiting for the global pandemic to end soon.
Early preparedness, contact tracing, isolation and testing, coupled with timely border closure, physical distancing and community adherence, have been key measures in controlling COVID-19 in Vietnam.
New Zealand has avoided the major health impacts of the SARS-CoV-2 pandemic due to a strict country-wide lockdown, the end-goal of which was elimination rather than mitigation and suppression. The New Zealand government’s use of scientific expertise, spanning public health, infectious diseases, genomics, modeling and immunology, has been one of the keys to the success of its SARS-CoV-2 elimination and control strategy.
From the onset of the SARS-CoV-2 pandemic and following the creation of the ‘Coronavirus Unit’, Argentinean scientists and technologists have contributed by leading basic and translational research initiatives, including developing diagnostic and serological kits, designing new therapeutic approaches, establishing epidemiological platforms, executing clinical trials and implementing social measures to protect the most vulnerable groups of the population.
Taiwan has leveraged its experience in containing the 2003 SARS outbreak by responding to the COVID-19 crisis with rapid measures, early deployment, prudent actions and transparency. Collectively, these actions have created the ‘Taiwan model’ for combating COVID-19.
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).
Like other countries in the region, the United Arab Emirates (UAE) was deeply affected by the pandemic. However, its foresight and proactive policies helped to create opportunities out of the challenges and spurred the development of trilateral collaborations involving government, academia and industry.
Could we have predicted that the second deadliest pandemic encountered since the influenza pandemic of 1918 would result in the highest mortality and adverse health outcomes among minority and underserved populations in the United States? Given the abundant evidence documenting the disproportionately high burden of preventable disease, disability, and injury among these underserved groups, our answer should echo a resounding ‘yes’.
The contribution of T cells to the SARS-CoV-2 response remains an important and unresolved question. Moss and colleagues examine T cell and antibody kinetics in a large cohort of patients with COVID-19 and find robust and durable T cell responses.
Severe COVID-19 is characterized by hyperinflammation, and there is a need for accurate predictive biomarkers of progression. Lehuen et al. demonstrate that patients with severe COVID-19 show a dramatic loss of MAIT cells, and those that do remain are in a highly activated state.
Andreakos and colleagues provide a longitudinal study comparing patients with COVID-19 to patients infected with influenza. They report a dysregulated interferon response whereby IFN-λ and type I IFN production were diminished and delayed in patients with COVID-19, exhibiting a response that is ‘untuned’ with other inflammatory cytokines.
Geisbert and colleagues report that African green monkeys infected with the SARS-CoV-2 virus develop disease symptoms that closely resemble those seen in infected humans, making this animal model a useful surrogate to investigate immune responses to coronavirus infection.
Mantovani and colleagues report elevated circulating concentrations of the long pentraxin PTX3 in patients with severe COVID-19. Within this cohort, early detection of high PTX3 concentrations emerged as a strong predictor of decreased survival.
COVID-19 is often characterized by a hyperinflammatory syndrome. Wang and colleagues show that low levels of IgG fucosylation enhance interactions with activating Fcγ receptors, boosting the inflammatory cytokines associated with severe COVID-19.
Farber and colleagues report distinct antibody responses to SARS-CoV-2 in pediatric cohorts, including those who developed multisystem inflammatory syndrome (MIS-C), and adult COVID-19 cohorts.
Sanz and colleagues examine B cell subsets in a cohort of patients with COVID-19. Severely ill patients have higher frequencies of activated extrafollicular T-bet+ B cells that form antibody-secreting cells, the majority of which express germline sequences and are reminiscent of antibody responses observed in patients with systemic lupus erythematosus during flares.
SARS-CoV-2-specific CD4+ and CD8+ T cell epitopes are found in both convalescent patients and virus-naive volunteers and are indicative of heterologous recognition shared with seasonal cold viruses.
Questions have arisen as to whether patients with severe COVID-19 disease can generate a T cell response against SARS-CoV-2. Tao Dong and colleagues report that convalescent patients with COVID-19 harbor functional memory CD4+ and CD8+ T cells that recognize multiple epitopes that span the viral proteome. CD4+ T cells predominated the memory response in patients with severe disease, whereas higher proportions of CD8+ T cells were found in patients with mild disease.
“The role of cytokines in COVID-19” online symposium was presented on 18 June 2020 by the NIH/FDA Immunology and Cytokine Interest Groups and was purposed to discuss our rapidly changing understanding of COVID-19-related cytokine responses in different stages of infection, including the etiologies, downstream consequences and possible mitigation strategies. The recording is available at https://nci.rev.vbrick.com/sharevideo/03106730-66cc-47ba-870b-f6e6274a998a.
Diamond and colleagues generate a K18-hACE2 model of SARS-CoV-2 infection that shares many features of severe COVID-19 infection and can be used to define the basis of lung disease and test immune and antiviral-based countermeasures.
Accurate serology testing is urgently needed to help diagnose SARS-CoV-2 infection. Here Valkenburg and colleagues use a luciferase immunoprecipitation system to assess the antibody responses to 15 different SARS-CoV-2 antigens in patients with COVID-19 and find ORF8 and ORF3b antibodies, taken together as a cluster of points, identified 96.5% of COVID-19 samples at early and late time points of disease with 99.5% specificity
Severe COVID-19 is characterized—among other things—by a hyperinflammatory state. Wang and colleagues describe the single-cell transcriptional landscape of moderate, severe and convalescent cases of patients with COVID-19.
The innate sensors of SARS-CoV-2 are still being determined. Kanneganti and colleagues find that SARS-CoV-2 envelope protein is sensed by TLR2 and this drives pathogenic inflammatory cytokine production.
RIG-I is a cytosolic nucleic acid sensor triggering type I IFN production. Takaoka and colleagues find that RIG-I recognizes SARS-CoV-2 RNA in a noncanonical manner and fails to activate type I IFN, but it directly restricts viral replication.