3 research outputs found

    COVID-19 related complete blood count changes among asymptomatic pregnant women

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    Objective: To evaluate complete blood count (CBC) changes that suggest coronavirus disease-2019 (COVID-19) among asymptomatic pregnant women attending routine antenatal care Methods: A cross-sectional study included 187 healthy pregnant women who were attending the antenatal care clinic of a tertiary University hospital between March and June 2020. After a thorough history and examinations, a venous blood sample was taken from each participant for complete and differential blood counts. Those who showed CBC findings suggestive of COVID-19 were further scheduled for a nasopharyngeal swab for detection of SARS-CoV-2 specific antigens through polymerase chain reaction (PCR). Results: We found 5.3% (n=10) of the study population showed CBC changes that are suggestive of COVID-19. When they were scheduled for nasopharyngeal swab for a PCR confirmatory test, 30% (n=3) of them were PCR positive (which represented 1.6% of the entire study population). The most frequently encountered COVID-19-suggestive change in peripheral blood leukocyte differential counts was leucopenia (100%), followed by decreased eosinophil count (50%), then neutropenia and lymphocytopenia (30%). Conclusions: Certain differential leucocyte count changes (leucopenia, neutropenia, lymphocytopenia and decreased eosinophil count) among asymptomatic pregnant women might be related to COVID-19 infection and may indicate a need for further testing

    Whole-genome sequencing reveals host factors underlying critical COVID-19

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    Critical COVID-19 is caused by immune-mediated inflammatory lung injury. Host genetic variation influences the development of illness requiring critical care1 or hospitalization2,3,4 after infection with SARS-CoV-2. The GenOMICC (Genetics of Mortality in Critical Care) study enables the comparison of genomes from individuals who are critically ill with those of population controls to find underlying disease mechanisms. Here we use whole-genome sequencing in 7,491 critically ill individuals compared with 48,400 controls to discover and replicate 23 independent variants that significantly predispose to critical COVID-19. We identify 16 new independent associations, including variants within genes that are involved in interferon signalling (IL10RB and PLSCR1), leucocyte differentiation (BCL11A) and blood-type antigen secretor status (FUT2). Using transcriptome-wide association and colocalization to infer the effect of gene expression on disease severity, we find evidence that implicates multiple genes—including reduced expression of a membrane flippase (ATP11A), and increased expression of a mucin (MUC1)—in critical disease. Mendelian randomization provides evidence in support of causal roles for myeloid cell adhesion molecules (SELE, ICAM5 and CD209) and the coagulation factor F8, all of which are potentially druggable targets. Our results are broadly consistent with a multi-component model of COVID-19 pathophysiology, in which at least two distinct mechanisms can predispose to life-threatening disease: failure to control viral replication; or an enhanced tendency towards pulmonary inflammation and intravascular coagulation. We show that comparison between cases of critical illness and population controls is highly efficient for the detection of therapeutically relevant mechanisms of disease

    Whole-genome sequencing reveals host factors underlying critical COVID-19