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Journal of Heart & Lung Transplantation ; 41(4):S54-S54, 2022.
Article in English | Academic Search Complete | ID: covidwho-1783340


In April 2020 COVID-19 lockdown measures were instigated leading to a dramatic drop in non-COVID respiratory virus infections (RVI). This provided a unique situation to assess the impact of RVI on annual FEV1 decline, episodes of temporary drop in lung function suggestive of infection (TDLF) and CLAD in lung transplant recipients (LTR). All lung function tests (LFT) of LTR transplanted between 2009-April 2020 were used from post-transplant baseline onward. LFT were censored after COVID-19 infection. Weekly RVI counts from the virology department defined RVI pressure over time. TDLF was defined as sudden, reversible FEV1 drop compared to previous 4 values (any TDLF ≥10% and ≥200ml, severe TDLF ≥20% and ≥500ml). Annual FEV1 decline was estimated using linear mixed effects models with separate estimates for 2009/20 and 2020/21. Effect modification by TDLF frequency of individual LTR (two subgroups, split at median) and RVI pressure was tested. Rates of CLAD and TDLF were analyzed over time. 479 LTR (12,775 LFT) were included. Annual FEV1 change in 2009/20 was -114ml [95%CI -133;-94], while in 2020/21 this was significantly less: 5ml [-38;48] (p<0.001). RVI pressure significantly affected FEV1 level (an increase in weekly RVI-count of 10 leading to a 7ml [-10;-5] lower FEV1 (p<0.001). FEV1 decline in 2009/20 was faster in frequent TDLF LTR vs. infrequent (-150ml [-181;-120] vs. -90ml [-115;-65] p=0.003 Fig A). 2020/21 showed significant decreases in number of any TDLF (OR 0.53 [0.33;0.85], p=0.008) and severe TDLF (OR 0.34 [0.16;0.71] p=0.005) and numerically lower CLAD (OR 0.53 [0.27;1.02] p=0.060). Effect modification by RVI pressure (Figures B-D) indicated an association between the events and RVI. During the lockdown year 2020/21 the broad decline in RVI coincided with substantially less FEV1 decline, TDLFs and possibly CLAD. All these outcomes were moderated by RVI pressure suggesting an important role for RVI in lung function decline in LTR. [ FROM AUTHOR] Copyright of Journal of Heart & Lung Transplantation is the property of Elsevier B.V. and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full . (Copyright applies to all s.)

PUBMED; 2020.
Preprint in English | PUBMED | ID: ppcovidwho-292827


The recent outbreak of the severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2), which causes coronavirus disease 2019 (COVID-19), has led to a worldwide pandemic. One week after initial symptoms develop, a subset of patients progresses to severe disease, with high mortality and limited treatment options. To design novel interventions aimed at preventing spread of the virus and reducing progression to severe disease, detailed knowledge of the cell types and regulating factors driving cellular entry is urgently needed. Here we assess the expression patterns in genes required for COVID-19 entry into cells and replication, and their regulation by genetic, epigenetic and environmental factors, throughout the respiratory tract using samples collected from the upper (nasal) and lower airways (bronchi). Matched samples from the upper and lower airways show a clear increased expression of these genes in the nose compared to the bronchi and parenchyma. Cellular deconvolution indicates a clear association of these genes with the proportion of secretory epithelial cells. Smoking status was found to increase the majority of COVID-19 related genes including ACE2 and TMPRSS2 but only in the lower airways, which was associated with a significant increase in the predicted proportion of goblet cells in bronchial samples of current smokers. Both acute and second hand smoke were found to increase ACE2 expression in the bronchus. Inhaled corticosteroids decrease ACE2 expression in the lower airways. No significant effect of genetics on ACE2 expression was observed, but a strong association of DNA- methylation with ACE2 and TMPRSS2- mRNA expression was identified in the bronchus.