<HashMap><database>biostudies-literature</database><scores/><additional><omics_type>Unknown</omics_type><volume>327</volume><submitter>Castillo G</submitter><pubmed_abstract>Human coronavirus NL63 (HCoV-NL63) is spread globally, causing upper and lower respiratory tract infections mainly in young children. HCoV-NL63 shares a host receptor (ACE2) with severe acute respiratory syndrome coronavirus (SARS-CoV) and SARS-CoV-2 but, unlike them, HCoV-NL63 primarily develops into self-limiting mild to moderate respiratory disease. Although with different efficiency, both HCoV-NL63 and SARS-like CoVs infect ciliated respiratory cells using ACE2 as receptor for binding and cell entry. Working with SARS-like CoVs require access to BSL-3 facilities, while HCoV-NL63 research can be performed at BSL-2 laboratories. Thus, HCoV-NL63 could be used as a safer surrogate for comparative studies on receptor dynamics, infectivity and virus replication, disease mechanism, and potent</pubmed_abstract><journal>Virus research</journal><pagination>199078</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC9944649</full_dataset_link><repository>biostudies-literature</repository><pubmed_title>Molecular mechanisms of human coronavirus NL63 infection and replication.</pubmed_title><pmcid>PMC9944649</pmcid><pubmed_authors>Breuer M</pubmed_authors><pubmed_authors>Singh P</pubmed_authors><pubmed_authors>Nelli RK</pubmed_authors><pubmed_authors>Gimenez-Lirola LG</pubmed_authors><pubmed_authors>Mora-Diaz JC</pubmed_authors><pubmed_authors>Castillo G</pubmed_authors></additional><is_claimable>false</is_claimable><name>Molecular mechanisms of human coronavirus NL63 infection and replication.</name><description>Human coronavirus NL63 (HCoV-NL63) is spread globally, causing upper and lower respiratory tract infections mainly in young children. HCoV-NL63 shares a host receptor (ACE2) with severe acute respiratory syndrome coronavirus (SARS-CoV) and SARS-CoV-2 but, unlike them, HCoV-NL63 primarily develops into self-limiting mild to moderate respiratory disease. Although with different efficiency, both HCoV-NL63 and SARS-like CoVs infect ciliated respiratory cells using ACE2 as receptor for binding and cell entry. Working with SARS-like CoVs require access to BSL-3 facilities, while HCoV-NL63 research can be performed at BSL-2 laboratories. Thus, HCoV-NL63 could be used as a safer surrogate for comparative studies on receptor dynamics, infectivity and virus replication, disease mechanism, and potent</description><dates><release>2023-01-01T00:00:00Z</release><publication>2023 Apr</publication><modification>2025-04-04T14:17:06.237Z</modification><creation>2025-02-19T02:23:52.358Z</creation></dates><accession>S-EPMC9944649</accession><cross_references><pubmed>36813239</pubmed><doi>10.1016/j.virusres.2023.199078</doi></cross_references></HashMap>