<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Fechtner S</submitter><funding>BLRD VA</funding><funding>NIAID NIH HHS</funding><funding>National Institutes of Health</funding><funding>NIAMS NIH HHS</funding><funding>U.S. Department of Veterans Affairs</funding><funding>NIH HHS</funding><funding>NIGMS NIH HHS</funding><pagination>597-603</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC8957485</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>74(4)</volume><pubmed_abstract>&lt;h4>Objective&lt;/h4>Patients with established rheumatoid arthritis (RA) demonstrate altered immune responses to Epstein-Barr virus (EBV), but the presence and roles of EBV have not been fully explored during the pre-clinical disease period. This study was undertaken to determine if EBV infection, as evidenced by an altered anti-EBV antibody response, either plays an important role in driving the development of RA or is a result of expanded RA-related autoimmunity.&lt;h4>Methods&lt;/h4>A total of 83 subjects with RA according to the 1987 American College of Rheumatology (ACR) criteria and 83 age-, sex-, and race-matched control subjects without RA were included in our study. We collected sera from RA subjects and matched controls during the pre-RA and post-RA diagnosis periods and tested the sera f</pubmed_abstract><journal>Arthritis &amp; rheumatology (Hoboken, N.J.)</journal><pubmed_title>Antibody Responses to Epstein-Barr Virus in the Preclinical Period of Rheumatoid Arthritis Suggest the Presence of Increased Viral Reactivation Cycles.</pubmed_title><pmcid>PMC8957485</pmcid><funding_grant_id>U54 GM104938</funding_grant_id><funding_grant_id>UM1 AI144292</funding_grant_id><funding_grant_id>U01‐AI‐101981</funding_grant_id><funding_grant_id>I01BX001834</funding_grant_id><funding_grant_id>R01‐AI‐24727</funding_grant_id><funding_grant_id>P30‐A‐073750</funding_grant_id><funding_grant_id>I01 BX001834</funding_grant_id><funding_grant_id>UM1‐AI‐144292</funding_grant_id><funding_grant_id>T32 AI074491</funding_grant_id><funding_grant_id>P30 AR073750</funding_grant_id><funding_grant_id>U01 AI101981</funding_grant_id><funding_grant_id>R01 AI024717</funding_grant_id><funding_grant_id>R01-AI-24727</funding_grant_id><funding_grant_id>T32‐AI‐074491</funding_grant_id><pubmed_authors>Holers VM</pubmed_authors><pubmed_authors>Carlson NE</pubmed_authors><pubmed_authors>James JA</pubmed_authors><pubmed_authors>Deane KD</pubmed_authors><pubmed_authors>Johnson RL</pubmed_authors><pubmed_authors>Robinson WH</pubmed_authors><pubmed_authors>Norris JA</pubmed_authors><pubmed_authors>Berens H</pubmed_authors><pubmed_authors>Guthridge CJ</pubmed_authors><pubmed_authors>Edison JD</pubmed_authors><pubmed_authors>Demoruelle MK</pubmed_authors><pubmed_authors>Harley JB</pubmed_authors><pubmed_authors>Fechtner S</pubmed_authors><pubmed_authors>Bemis E</pubmed_authors></additional><is_claimable>false</is_claimable><name>Antibody Responses to Epstein-Barr Virus in the Preclinical Period of Rheumatoid Arthritis Suggest the Presence of Increased Viral Reactivation Cycles.</name><description>&lt;h4>Objective&lt;/h4>Patients with established rheumatoid arthritis (RA) demonstrate altered immune responses to Epstein-Barr virus (EBV), but the presence and roles of EBV have not been fully explored during the pre-clinical disease period. This study was undertaken to determine if EBV infection, as evidenced by an altered anti-EBV antibody response, either plays an important role in driving the development of RA or is a result of expanded RA-related autoimmunity.&lt;h4>Methods&lt;/h4>A total of 83 subjects with RA according to the 1987 American College of Rheumatology (ACR) criteria and 83 age-, sex-, and race-matched control subjects without RA were included in our study. We collected sera from RA subjects and matched controls during the pre-RA and post-RA diagnosis periods and tested the sera f</description><dates><release>2022-01-01T00:00:00Z</release><publication>2022 Apr</publication><modification>2025-04-19T23:47:58.212Z</modification><creation>2025-04-19T23:47:58.212Z</creation></dates><accession>S-EPMC8957485</accession><cross_references><pubmed>34605217</pubmed><doi>10.1002/art.41994</doi></cross_references></HashMap>