<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Weiskopf D</submitter><funding>NIAID NIH HHS</funding><pagination>11383-94</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC4178794</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>88(19)</volume><pubmed_abstract>&lt;h4>Unlabelled&lt;/h4>Dengue virus (DENV) is the causative agent of dengue fever (DF). This disease can be caused by any of four DENV serotypes (DENV1 to -4) which share 67 to 75% sequence homology with one another. The effect of subsequent infections with different serotypes on the T cell repertoire is not fully understood. We utilized mice transgenic for human leukocyte antigens (HLA) lacking the alpha/beta interferon (IFN-α/β) receptor to study responses to heterologous DENV infection. First, we defined the primary T cell response to DENV3 in the context of a wide range of HLA molecules. The primary DENV3 immune response recognized epitopes derived from all 10 DENV proteins, with a significant fraction of the response specific for structural proteins. This is in contrast to primary DENV2 i</pubmed_abstract><journal>Journal of virology</journal><pubmed_title>Immunodominance changes as a function of the infecting dengue virus serotype and primary versus secondary infection.</pubmed_title><pmcid>PMC4178794</pmcid><funding_grant_id>HHSN272200900042C</funding_grant_id><funding_grant_id>U54AI057517</funding_grant_id><pubmed_authors>Weiskopf D</pubmed_authors><pubmed_authors>Peters B</pubmed_authors><pubmed_authors>Sette A</pubmed_authors><pubmed_authors>Angelo MA</pubmed_authors><pubmed_authors>Sidney J</pubmed_authors><pubmed_authors>Shresta S</pubmed_authors></additional><is_claimable>false</is_claimable><name>Immunodominance changes as a function of the infecting dengue virus serotype and primary versus secondary infection.</name><description>&lt;h4>Unlabelled&lt;/h4>Dengue virus (DENV) is the causative agent of dengue fever (DF). This disease can be caused by any of four DENV serotypes (DENV1 to -4) which share 67 to 75% sequence homology with one another. The effect of subsequent infections with different serotypes on the T cell repertoire is not fully understood. We utilized mice transgenic for human leukocyte antigens (HLA) lacking the alpha/beta interferon (IFN-α/β) receptor to study responses to heterologous DENV infection. First, we defined the primary T cell response to DENV3 in the context of a wide range of HLA molecules. The primary DENV3 immune response recognized epitopes derived from all 10 DENV proteins, with a significant fraction of the response specific for structural proteins. This is in contrast to primary DENV2 i</description><dates><release>2014-01-01T00:00:00Z</release><publication>2014 Oct</publication><modification>2025-04-22T20:42:01.229Z</modification><creation>2019-03-27T01:36:41Z</creation></dates><accession>S-EPMC4178794</accession><cross_references><pubmed>25056881</pubmed><doi>10.1128/jvi.01108-14</doi><doi>10.1128/JVI.01108-14</doi></cross_references></HashMap>