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PubMed; 2021.
Preprint in English | PubMed | ID: ppcovidwho-296897


The Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) virus has infected over 115 million people and caused over 2.5 million deaths worldwide. Yet, the molecular mechanisms underlying the clinical manifestations of COVID-19, as well as what distinguishes them from common seasonal influenza virus and other lung injury states such as Acute Respiratory Distress Syndrome (ARDS), remains poorly understood. To address these challenges, we combined transcriptional profiling of 646 clinical nasopharyngeal swabs and 39 patient autopsy tissues, matched with spatial protein and expression profiling (GeoMx) across 357 tissue sections. These results define both body-wide and tissue-specific (heart, liver, lung, kidney, and lymph nodes) damage wrought by the SARS-CoV-2 infection, evident as a function of varying viral load (high vs. low) during the course of infection and specific, transcriptional dysregulation in splicing isoforms, T cell receptor expression, and cellular expression states. In particular, cardiac and lung tissues revealed the largest degree of splicing isoform switching and cell expression state loss. Overall, these findings reveal a systemic disruption of cellular and transcriptional pathways from COVID-19 across all tissues, which can inform subsequent studies to combat the mortality of COVID-19, as well to better understand the molecular dynamics of lethal SARS-CoV-2 infection and other viruses.

American Journal of Transplantation ; 21(SUPPL 4):314, 2021.
Article in English | EMBASE | ID: covidwho-1494449


Purpose: SARS-CoV-2 antibody prevalence in kidney transplant recipients is beginning to be reported, although little is known about the humoral immune response in the immediate post-transplant period when immunosuppressive therapy burden is highest and graft recipients are least likely to mount a robust immune response. Methods: Patients transplanted from May 28, 2020 until October 1, 2020 (n=78) were followed prospectively. SARS-CoV-2 antibody testing was performed at the time of transplant. Semi-quantitative IgM and IgG data was collected on a subset of patients and followed both before and after transplant. Results: At the time of kidney transplantation, SARS-CoV-2 antibody prevalence was 22%. Patient demographics are shown in Table 1. Of the patients with a positive antibody (n=17), 10 either had symptoms consistent with COVID-19 infection or had documented SARS-CoV-2 PCR positive testing prior to transplant. A total of 13 patients had follow-up antibody testing between 30 and 60 days post transplantation and 12 (92%) had persistent antibodies at the time of follow up. Figures 1A and B demonstrate box and whisker plots of the median and the 25th and 75th percentile values (bottom and top of each box, respectively), levels of IgM and IgG from the pre- and post-transplant period. Both SARS-CoV-2 IgM and IgG antibody levels declined in the post transplantation period but remained above the threshold for positivity (an index value of 1) despite induction therapy with ATG and the initiation of maintenance immunosuppression with CNI and MMF. To date, none of the 78 patients transplanted has manifested new or recurrent SARS-CoV-2 infection. Conclusions: SARS-CoV-2 antibodies remain positive despite the high dose immunosuppression in the early post transplant period. Our data provide a framework for future prospective studies on the kinetics and isotype of SARSCoV- 2 antibody response and as an essential reference to gauge immune response following vaccination.