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To KK, Chan WM, Ip JD, et al. Unique SARS-CoV-2 clusters causing a large COVID-19 outbreak in Hong Kong. Clin Infect Dis. 2020 Aug 5:ciaa1119. PubMed: https://pubmed.gov/32756996. Full-text: https://doi.org/10.1093/cid/ciaa1119
With a total of 617 locally acquired laboratory-confirmed cases reported between July 5 and 21, Hong Kong has experienced the largest local COVID-19 outbreak since the beginning of the pandemic. This phylogenetic study by Kwok-Yung Yuen, Kelvin Kai-Wang To and colleagues shows that this outbreak was related to imported cases and not to silent carriers from previous waves. Two unique SARS-CoV-2 clusters were identified.
Klompas M, Baker MA, Rhee C. Airborne Transmission of SARS-CoV-2: Theoretical Considerations and Available Evidence. JAMA. 2020 Aug 4;324(5):441-442. PubMed: https://pubmed.gov/32749495 . Full-text: https://doi.org/10.1001/jama.2020.12458
Brief review. It is impossible to conclude that aerosol-based transmission never occurs, write Michael Klompas and colleagues, but the balance of currently available evidence suggests that long-range aerosol-based transmission is not the dominant mode of SARS-CoV-2 transmission.
Joonaki E, Hassanpouryouzband A, Heldt Cl, et al. Surface Chemistry Can Unlock Drivers of Surface Stability of SARS-CoV-2 in Variety of Environmental Conditions. Chem, August 06, 2020. Full-text: https://doi.org/10.1016/j.chempr.2020.08.001
Nice overview of existing knowledge concerning viral spread, molecular structure of SARS-CoV-2, and the stability of the virus surface. Edris Joonaki and colleagues discuss potential drivers of the SARS-CoV-2 surface adsorption and stability in various environmental conditions.
Rodriguez, L, Pekkarinen, PT, Lakshmikanth, T, et al. Systems-level immunomonitoring from acute to recovery phase of severe COVID-19. Cell Rep Med 2020, published 5 August. Full-text: https://www.cell.com/cell-reports-medicine/fulltext/S2666-3791(20)30099-9
To treat hyperinflammation in severe COVID-19 we need to better understand which cells are involved, how they interact and which protein mediators they use to orchestrate their responses. To this end, Petter Brodin and colleagues followed 37 adult patients diagnosed with COVID-19 from the acute to the recovery phases of the disease and performed longitudinal systems-level blood immunomonitoring. They describe an IFNγ – eosinophil axis activated prior to lung hyperinflammation and changes in cell-cell coregulation during different stages of the disease.
Schulte-Schrepping J, Reusch N, Paclik D, et al. Severe COVID-19 is marked by a dysregulated myeloid cell compartment. Cell August 05, 2020. Full-text: https://doi.org/10.1016/j.cell.2020.08.001
This German study revealed profound alterations in the myeloid cell compartment associated with severe COVID-19. By combining single-cell RNA-sequencing and single-cell proteomics of whole blood and peripheral blood mononuclear cells, Joachim Schultze and colleagues determined changes in immune cell composition and activation in mild versus severe COVID-19 cases (n = 109) over time. HLA-DRhiCD11chi inflammatory monocytes with an interferon-stimulated gene signature were elevated in mild COVID-19. Severe COVID-19 was marked by occurrence of neutrophil precursors, as evidence of emergency myelopoiesis, dysfunctional mature neutrophils, and HLA-DRlo monocytes.
Silvin A, Chapuis N, Dunsmore G, et al. Elevated calprotectin and abnormal myeloid cell subsets discriminate severe from mild COVID-19. Published: August 05, 2020. Full-text: https://doi.org/10.1016/j.cell.2020.08.002
Performing high dimensional flow cytometry and single cell RNA sequencing of COVID-19 patients, Eric Solary, Michaela Fontenay, Florent Ginhoux and colleagues found that severe COVID-19 was associated with a burst of circulating calprotectin that preceded cytokine release syndrome, low levels of non-classical monocytes in the peripheral blood, and an emergency myelopoiesis that releases immature and dysplastic myeloid cells with an immune suppressive phenotype. This work provides further rationale for the testing of several clinical strategies, including blocking emergency myelopoiesis.
Pujadas E, Chaudry F, McBride R, et al. SARS-CoV-2 viral load predicts COVID-19 mortality. Lancet Respir Med August 06, 2020. Full-text: https://doi.org/10.1016/S2213-2600(20)30354-4
In this large cohort (n=1145) of hospitalized, symptomatic patients from New York, viral loads were measured. In a Cox proportional hazards model adjusting for several confounders, Carlos Cordon-Cardo and colleagues found a significant independent association between viral load and mortality (hazard ratio 1.07, 95% CI 1.03–1.11, p = 0.0014), with a 7% increase in hazard for each log transformed copy / mL.
Hodge C, Marra F, Marzolini C, et al. Drug interactions: a review of the unseen danger of experimental COVID-19 therapies. J Antimicrob Chemother. 2020 Aug 4:dkaa340. PubMed: https://pubmed.gov/32750131 . Full-text: https://doi.org/10.1093/jac/dkaa340
Experimental COVID-19 therapies carry significant risk for drug-drug interactions (DDIs), especially the HIV protease inhibitor lopinavir/ritonavir, chloroquine, hydroxychloroquine and ruxolitinib. In contrast, anakinra, baricitinib, favipiravir, interferon-b, nitazoxanide, ribavirin, remdesivir, sarilumab and tocilizumab have lower propensity for drug interactions. In March 2020, this group from Liverpool (famous for their HIV interaction website) published a DDI resource for experimental COVID therapies (www.covid19-druginteractions.org). Here Saye Khoo and colleagues summarize the methodology and processes undertaken to establish this resource.
Moorlag SJ, van Deuren RX, van Werkhoven CH, et al. Safety and COVID-19 symptoms in individuals recently vaccinated with BCG: a retrospective cohort study. Cell Rep Med August 05, 2020. Full-text: https://www.sciencedirect.com/science/article/pii/S2666379120300938
Mihai Netea and colleagues retrospectively assessed COVID-19 related symptoms in three cohorts of healthy volunteers who either received BCG in the last five years (n = 266) or not (n = 164). BCG vaccination was not associated with increased incidence of symptoms and might be associated with a decrease in the incidence of sickness during the COVID-19 pandemic, and lower incidence of extreme fatigue. However, caution is warranted in interpreting these findings: limitations include the retrospective nature of the study in two relatively small groups of volunteers, and the potential for selection bias.
Parker-Pope T. The Many Symptoms of Covid-19. The New York Times 2020, published 5 August. Full-text: https://www.nytimes.com/2020/08/05/well/live/coronavirus-covid-symptoms.html
“From a sniffle or cough that feels like allergies to severe body aches and crippling fatigue, the symptoms of coronavirus can be unpredictable from head to toe.” Plain English for all of us.