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Authors:Stanczak, Sanin, Apostolova et al. 

Journal/ Pre-Print:MedXriv 

Tags: Clinical, Immunology/Immunity, Inflammation 

Research Highlights 

  1. Professional rather than household exposure as determinant for transmission. 

  1. Serum conversion correlates with innate inflammatory cytokine signature. 

  1. IL-33 correlates with antibody titres and is expressed in BALF cell subsets.  

Summary 

This study investigated common immunological features associated with serum conversion in SARS-CoV2 patients. For this purpose, the authors looked at blood samples of 155 individuals and characterised lymphoid and myeloid cells several weeks post-infection. In their cohort, serum converted individuals maintained high titre of anti-Spike/-RBD IgG antibodies over a ~2-month period. The authors found that most SARS-CoV2 transmission occurs in professional rather than household settings. Lastly, although most immunological characteristics did not correlate with serum conversion, the authors found that serum converted individuals show a higher inflammatory signature when circulating immune cells are re-activated ex vivo. In this setting, IL-33 showed the strongest correlation with activated (CD69+) CD4+ T cells. Using publicly available scRNAseq data of cells from BALF, the authors found a subset cluster producing increased levels of IL-33. Though many results are not necessarily surprising, the implication of IL-33 in COVID19 with the associated pulmonary tissue damage may be a valuable insight for further investigation. 

Impact for SARS-CoV2/COVID19 research efforts 

Understand the immune response to SARS-CoV2/COVID19  

Using their cohort, the authors dissect the immune phenotype in recovered vs. non-infected individuals and look at potential long-term effects on the state of the immune system. This may help to understand the recovery process and the determinants involved in successful serum conversion. 
 

Study Type  

  • In vivo study 

  • Clinical Cohort study 

Strengths and limitations of the paper 

Novelty: IL-33 implication in COVID-19 pathology 

Standing in the field:Thus far IL33 has not been identified as a major player in SARS-CoV2  
pathology, as most papers looking at serum cytokines did not detect any increases systemically of IL33. However, IL-33 is usually found to be released locally in damaged tissues, including the lung. However, its role ipotentially skewing the immune response during SARS-CoV2 infection remains unclear at the present.  

Appropriate statistics:Yes, appropriate statistics were used 

Viral model used:Blood from SARS-CoV2 infected patients and non-infected controls  
(tested by PCR weeks before blood donation) were used in this study 

Translatability:Low translatability. At present this study presents very much  
descriptive information without providing much mechanistical insights. 

Main limitations: The paper looks at individuals at one time point after they recovered from their infection. It would have been nice to get a more longitudinal perspective. This would have given more insights into persistence of antibody responses. 
 
The paper does not include many hospitalised, hence correlation with disease severity is difficult. 

Using serum-conversion as a classifier, rather than a positive PCR test, is potentially misleading as other studies show the emergence of SARS-CoV2-specific T cells upon infection without strong IgG responses. 

Although out of scope of this paper, it would have been great to gain more mechanistical insight to the role of IL-33 during this viral infection.