<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Yamamoto A</submitter><funding>National Institute of Environmental Health Sciences</funding><funding>NIEHS NIH HHS</funding><funding>National Health and Medical Research Council, Australia</funding><pagination>271-279</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC9836833</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>248(3)</volume><pubmed_abstract>Epidemiological evidence links lower air quality with increased incidence and severity of COVID-19; however, mechanistic data have yet to be published. We hypothesized air pollution-induced oxidative stress in the nasal epithelium increased viral replication and inflammation. Nasal epithelial cells (NECs), collected from healthy adults, were grown into a fully differentiated epithelium. NECs were infected with the ancestral strain of SARS-CoV-2. An oxidant combustion by-product found in air pollution, the environmentally persistent free radical (EPFR) DCB230, was used to mimic pollution exposure four hours prior to infection. Some wells were pretreated with antioxidant, astaxanthin, for 24 hours prior to EPFR-DCB230 exposure and/or SARS-CoV-2 infection. Outcomes included viral replication,</pubmed_abstract><journal>Experimental biology and medicine (Maywood, N.J.)</journal><pubmed_title>Environmentally persistent free radicals enhance SARS-CoV-2 replication in respiratory epithelium.</pubmed_title><pmcid>PMC9836833</pmcid><funding_grant_id>1193840</funding_grant_id><funding_grant_id>3P42 ES013648-08A1S1</funding_grant_id><funding_grant_id>P42 ES013648</funding_grant_id><pubmed_authors>Khachatryan L</pubmed_authors><pubmed_authors>Short KR</pubmed_authors><pubmed_authors>Yeo AJ</pubmed_authors><pubmed_authors>Chew KY</pubmed_authors><pubmed_authors>Vu LD</pubmed_authors><pubmed_authors>Begum N</pubmed_authors><pubmed_authors>Cormier SA</pubmed_authors><pubmed_authors>Fantino E</pubmed_authors><pubmed_authors>Yamamoto A</pubmed_authors><pubmed_authors>Sly PD</pubmed_authors></additional><is_claimable>false</is_claimable><name>Environmentally persistent free radicals enhance SARS-CoV-2 replication in respiratory epithelium.</name><description>Epidemiological evidence links lower air quality with increased incidence and severity of COVID-19; however, mechanistic data have yet to be published. We hypothesized air pollution-induced oxidative stress in the nasal epithelium increased viral replication and inflammation. Nasal epithelial cells (NECs), collected from healthy adults, were grown into a fully differentiated epithelium. NECs were infected with the ancestral strain of SARS-CoV-2. An oxidant combustion by-product found in air pollution, the environmentally persistent free radical (EPFR) DCB230, was used to mimic pollution exposure four hours prior to infection. Some wells were pretreated with antioxidant, astaxanthin, for 24 hours prior to EPFR-DCB230 exposure and/or SARS-CoV-2 infection. Outcomes included viral replication,</description><dates><release>2023-01-01T00:00:00Z</release><publication>2023 Feb</publication><modification>2026-03-31T11:19:20.777Z</modification><creation>2025-04-19T22:26:45.896Z</creation></dates><accession>S-EPMC9836833</accession><cross_references><pubmed>36628928</pubmed><doi>10.1177/15353702221142616</doi></cross_references></HashMap>