<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Sugrue E</submitter><funding>Medical Research Council</funding><funding>Wellcome Trust</funding><pagination>e1010973</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC9718408</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>18(11)</volume><pubmed_abstract>HIV-1 transmission via sexual exposure is an inefficient process. When transmission does occur, newly infected individuals are colonized by the descendants of either a single virion or a very small number of establishing virions. These transmitted founder (TF) viruses are more interferon (IFN)-resistant than chronic control (CC) viruses present 6 months after transmission. To identify the specific molecular defences that make CC viruses more susceptible to the IFN-induced 'antiviral state', we established a single pair of fluorescent TF and CC viruses and used arrayed interferon-stimulated gene (ISG) expression screening to identify candidate antiviral effectors. However, we observed a relatively uniform ISG resistance of transmitted HIV-1, and this directed us to investigate possible unde</pubmed_abstract><journal>PLoS pathogens</journal><pubmed_title>The apparent interferon resistance of transmitted HIV-1 is possibly a consequence of enhanced replicative fitness.</pubmed_title><pmcid>PMC9718408</pmcid><funding_grant_id>MR/V01157X/1</funding_grant_id><funding_grant_id>201366/Z/16/Z</funding_grant_id><funding_grant_id>MC_UU_12014/10</funding_grant_id><funding_grant_id>MC_UU_12018/12</funding_grant_id><funding_grant_id>MC_UU_12014/12</funding_grant_id><funding_grant_id>MR/P022642/1</funding_grant_id><pubmed_authors>da Silva Filipe A</pubmed_authors><pubmed_authors>Wickenhagen A</pubmed_authors><pubmed_authors>Wilson SJ</pubmed_authors><pubmed_authors>Tong L</pubmed_authors><pubmed_authors>Mollentze N</pubmed_authors><pubmed_authors>Sugrue E</pubmed_authors><pubmed_authors>Aziz MA</pubmed_authors><pubmed_authors>Robertson DL</pubmed_authors><pubmed_authors>Hughes J</pubmed_authors><pubmed_authors>Rihn SJ</pubmed_authors><pubmed_authors>Sreenu VB</pubmed_authors><pubmed_authors>Truxa S</pubmed_authors></additional><is_claimable>false</is_claimable><name>The apparent interferon resistance of transmitted HIV-1 is possibly a consequence of enhanced replicative fitness.</name><description>HIV-1 transmission via sexual exposure is an inefficient process. When transmission does occur, newly infected individuals are colonized by the descendants of either a single virion or a very small number of establishing virions. These transmitted founder (TF) viruses are more interferon (IFN)-resistant than chronic control (CC) viruses present 6 months after transmission. To identify the specific molecular defences that make CC viruses more susceptible to the IFN-induced 'antiviral state', we established a single pair of fluorescent TF and CC viruses and used arrayed interferon-stimulated gene (ISG) expression screening to identify candidate antiviral effectors. However, we observed a relatively uniform ISG resistance of transmitted HIV-1, and this directed us to investigate possible unde</description><dates><release>2022-01-01T00:00:00Z</release><publication>2022 Nov</publication><modification>2026-05-28T06:50:03.657Z</modification><creation>2025-02-19T04:20:28.536Z</creation></dates><accession>S-EPMC9718408</accession><cross_references><pubmed>36399512</pubmed><doi>10.1371/journal.ppat.1010973</doi></cross_references></HashMap>