<?xml version="1.0" encoding="UTF-8"?>
<STUDY_SET xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance">
  <STUDY center_name="GEO" alias="GSE163363" accession="SRP298208">
    <IDENTIFIERS>
      <PRIMARY_ID>SRP298208</PRIMARY_ID>
      <EXTERNAL_ID namespace="BioProject" label="primary">PRJNA685825</EXTERNAL_ID>
      <EXTERNAL_ID namespace="GEO">GSE163363</EXTERNAL_ID>
    </IDENTIFIERS>
    <DESCRIPTOR>
      <STUDY_TITLE>Chromatin accessibility regions in GC B cells during acute and chronic viral infection</STUDY_TITLE>
      <STUDY_TYPE existing_study_type="Other"/>
      <STUDY_ABSTRACT>To study how chronic viral infection disrupts B cell differentiation pathways and identify key intrinsic regulators in an endogenous polyclonal response, we used the comparative LCMV model. Wild-type mice were infected with either the acute (WE) versus chronic (Docile) strains of LCMV, GC B cells (CD19+IgDloCD95+CD38loCD138-) isolated 14 days post-infection, an ATAC-seq (Assay for Transposase-Accessible Chromatin using sequencing) was undertaken. Overall design: 8 samples. Each group has at least 4 biological replicates.</STUDY_ABSTRACT>
      <CENTER_PROJECT_NAME>GSE163363</CENTER_PROJECT_NAME>
    </DESCRIPTOR>
    <STUDY_LINKS>
      <STUDY_LINK>
        <XREF_LINK>
          <DB>pubmed</DB>
          <ID>34845392</ID>
        </XREF_LINK>
      </STUDY_LINK>
    </STUDY_LINKS>
    <STUDY_ATTRIBUTES>
      <STUDY_ATTRIBUTE>
        <TAG>parent_bioproject</TAG>
        <VALUE>PRJNA685814</VALUE>
      </STUDY_ATTRIBUTE>
    </STUDY_ATTRIBUTES>
  </STUDY>
</STUDY_SET>
