<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Gallo A</submitter><funding>Ministero dell'Università e della Ricerca</funding><funding>Ministero della Salute</funding><pagination>151</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC11796281</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>23(1)</volume><pubmed_abstract>&lt;h4>Background&lt;/h4>Since the breakout of COVID-19, the mutated forms of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) have shown enhanced rates of transmission and adaptation to humans. The variants of concern (VOC), designated Alpha, Beta, Gamma, Delta, and Omicron emerged independent of one another, and in turn rapidly became dominant. The success of each VOC, as well as the virus fitness, were enabled by altered intrinsic functional properties and, reasonably, to virus antigenicity changes, conferring the ability to evade a primed immune response.&lt;h4>Methods&lt;/h4>We analysed the gene expression profiles of monocyte-derived macrophages (MDM) isolated from whole blood of healthy participants exposed to the 5 different SARS-CoV-2 VOC: D614G, Alpha (B.1.1.7), Gamma (P1), Delta</pubmed_abstract><journal>Journal of translational medicine</journal><pubmed_title>Transcriptomic profiles of monocyte-derived macrophages exposed to SARS-CoV-2 VOCs reveal immune-evasion escape driven by delta.</pubmed_title><pmcid>PMC11796281</pmcid><funding_grant_id>Ricerca Corrente</funding_grant_id><funding_grant_id>Next Generation EU, Missione 4 Componente 1, CUP B53D23016490001</funding_grant_id><funding_grant_id>grant BIAS no. 2020-12371760</funding_grant_id><funding_grant_id>COVID-2020-12371817</funding_grant_id><funding_grant_id>NextGeneration EU-MUR -National Recovery and Resilience Plan, Mission 4, Component 2 Investment 1.3- Extended Partnership initiative on Emerging Infectious Diseases INF-ACT (project no. PE00000007, CUP B73C22001230006</funding_grant_id><funding_grant_id>NextGeneration EU-MUR -PNRR Extended Partnership initiative on Emerging Infectious Diseases INF-ACT (project no. PE00000007, CUP F13C22001220007</funding_grant_id><funding_grant_id>Ricerca Corrente 80728</funding_grant_id><funding_grant_id>Ricerca Corrente 5x1000 progetto VISION 08069621</funding_grant_id><pubmed_authors>Sammartino JC</pubmed_authors><pubmed_authors>Giambruno R</pubmed_authors><pubmed_authors>Baldanti F</pubmed_authors><pubmed_authors>Miceli V</pubmed_authors><pubmed_authors>Gallo A</pubmed_authors><pubmed_authors>Bulati M</pubmed_authors><pubmed_authors>Vazzana R</pubmed_authors><pubmed_authors>Conaldi PG</pubmed_authors><pubmed_authors>Cuscino N</pubmed_authors><pubmed_authors>Castelbuono S</pubmed_authors><pubmed_authors>Carcione C</pubmed_authors><pubmed_authors>Lilleri D</pubmed_authors><pubmed_authors>Cassaniti I</pubmed_authors></additional><is_claimable>false</is_claimable><name>Transcriptomic profiles of monocyte-derived macrophages exposed to SARS-CoV-2 VOCs reveal immune-evasion escape driven by delta.</name><description>&lt;h4>Background&lt;/h4>Since the breakout of COVID-19, the mutated forms of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) have shown enhanced rates of transmission and adaptation to humans. The variants of concern (VOC), designated Alpha, Beta, Gamma, Delta, and Omicron emerged independent of one another, and in turn rapidly became dominant. The success of each VOC, as well as the virus fitness, were enabled by altered intrinsic functional properties and, reasonably, to virus antigenicity changes, conferring the ability to evade a primed immune response.&lt;h4>Methods&lt;/h4>We analysed the gene expression profiles of monocyte-derived macrophages (MDM) isolated from whole blood of healthy participants exposed to the 5 different SARS-CoV-2 VOC: D614G, Alpha (B.1.1.7), Gamma (P1), Delta</description><dates><release>2025-01-01T00:00:00Z</release><publication>2025 Feb</publication><modification>2025-04-04T07:26:08.77Z</modification><creation>2025-04-04T07:26:08.77Z</creation></dates><accession>S-EPMC11796281</accession><cross_references><pubmed>39905461</pubmed><doi>10.1186/s12967-025-06158-2</doi></cross_references></HashMap>