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Cintia Gisela Cevallos

Cintia Gisela Cevallos
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Cintia Gisela Cevallos

SARS CoV2 viral load and replication in postmortem pulmonary and extrapulmonary tissues

University of Buenos Aires INBIRS, Argentina

My name is Cintia Cevallos from Argentina and I will proceed to describe briefly my academic and professional training.
2010: I started an internship as an undergraduate student to obtain a bachelor's degree at the School of Chemistry, Biochemistry and Pharmacy, University of San Luis, Argentina. Research topic: Effects of exposure to cadmium in drinking water on parameters related to oxidative stress in the small intestine of rats. Supervisor: Dr. Larregle Ethel Viviana.
2012: I got a BSc. in Molecular Biology from the School of Chemistry, Biochemistry and Pharmacy, University of San Luis, Argentina.
2013: I started my doctoral studies when the National Research Council from Argentina (CONICET) awarded me with a fellowship. Research project: Study of the evolution of the Human Immunodeficiency Virus (HIV) in Men who have sex with men in Argentina (2000-2013) at the Institute for Biomedical Research on Retroviruses and AIDS (INBIRS, School of Medicine, University of Buenos Aires). Supervisor: Dr. Maria Mercedes Avila and co-supervisor: Dr. Jorge Quarleri.
2019: I got a PhD. in Medical Science from the School of Medical Sciences, University of Buenos Aires, Argentina. In this year I also worked as a Forensic expert for the Scientific Police Department of Buenos Aires city in the forensic genetics area.
2020: I started my post-doctoral studies when the National Research Council from Argentina (CONICET) awarded me with a fellowship. Research project: Cellular cross-talk and modulation of the hepatic profibrotic profile in the context of HIV-HCV coinfection. Supervisor: Dr. Jorge Quarleri.
Furthermore, since the COVID-19 outbreak, I also started to participate in the diagnosis area of INBIRS Institute processing a large number of samples (nasopharyngeal swabs) for SARS-CoV-2 detection, working under ISO9001 requirements.
2021: In the context of the SARS-CoV-2 pandemic as a postdoctoral student I joined to work on a research project focused on evaluating the direct mechanisms of pathogenesis cells associated with the coronavirus SARS-CoV-2.

Abstract
Background. The novel coronavirus disease 2019 (COVID-19), caused by SARS-CoV-2 is severe and involves multiple organs in approximately 5%-10% of patients, leading to multi-organ dysfunction and failure.
Methods. Necropsy tissues (lungs, heart, liver, kidney, small-intestine) were obtained through minimally invasive autopsy from 15 cadaveric donors whose postmortem swabs tested positive for SARS-CoV-2 (median age:69 years; females:8; hospitalized:7; vaccinated:7). Until use tissues were stored in RNAlater® at -70°C. SARS-CoV-2 RNA detection and viral load –VL– (as RNA copies/mL, for ORF1ab and N gene) were determined (RT-qPCR-DisCoVery); SARS-CoV-2 infectivity was measured using VeroE6 cell culture and VL (in 7-day/cell culture supernatants).

Results. SARS-CoV-2 RNA was detected in lung (8/15), heart (6/15), liver and kidney (4/15), and small-intestine (4/9). The highest VL level (median values in copies/mL for ORF1ab/N gene) was measured in lung samples (1.5x104/1.9x104; range: 1.01x102 to 1.14x108) but without significant differences against extrapulmonary tissues (liver:5.6x102/1.6x102, heart:5.5x102/4.4 x102, kidney:1.3x103/9.1x102, and small intestine:9.4x103/1.6x102). Median VL measured in tissues from non-hospitalized vs. hospitalized cases was slightly lower (5.5x101 vs. 3.0x103 copies/mL; p=0.1). Infectious SARS-CoV-2 was demonstrated in different tissues (lung:8/15, heart:11/15, liver:4/15; kidney:3/15; small-intestine:2/9) but the VL (as RNA copies/mL) was significantly higher (p<0.05) in the lung (1.4x106) and heart (1.9x106) samples than other tissues. Conclusions. The postmortem presence of infectious SARS-CoV-2 is demonstrated in pulmonary and extrapulmonary tissues even among vaccine-recipient decedents. Autopsies of COVID-19 cases are associated with a consistent biological risk. These findings support initiatives that make transplants safe by reducing the potential for transmission of SARS-CoV-2

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