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            <funder>SJ was supported by a fellowship from the University Paris Diderot, Sorbonne Paris Cité. NH was supported by the Fondation Beytout. MP was the recipient of a fellowship from Sidaction and NT by a fellowship from the ANRS (French Agency for Research on HIV and Hepatitis). MMT received a grant from the French Agency of AIDS Research, ANRS (AO 2012–2, 13390). The Infectious Disease Models and Innovative Therapies (IDMIT) center in Fontenay-aux-Roses, France, is funded by the French government’s Investissements d’Avenir program for infrastructures (PIA) under grant ANR-11-INBS-0008 and the PIA grant ANR-10-EQPX-02-01.</funder>
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                  <date type="datePub">2020-12-09</date>
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              <idno type="doi">10.1186/s13148-020-00971-w</idno>
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              <p>The molecular mechanisms underlying HIV-induced inflammation, which persists even during effective long-term treatment, remain incompletely defined. Here, we studied pathogenic and nonpathogenic simian immunodeficiency virus (SIV) infections in macaques and African green monkeys, respectively. We longitudinally analyzed genome-wide DNA methylation changes in CD4 + T cells from lymph node and blood, using arrays. DNA methylation changes after SIV infection were more pronounced in lymph nodes than blood and already detected in primary infection. Differentially methylated genes in pathogenic SIV infection were enriched for Th1-signaling (e.g., RUNX3, STAT4, NFKB1) and metabolic pathways (e.g., PRKCZ). In contrast, nonpathogenic SIVagm infection induced DNA methylation in genes coding for regulatory proteins such as LAG-3, arginase-2, interleukin-21 and interleukin-31. Between 15 and 18% of genes with DNA methylation changes were differentially expressed in CD4 + T cells in vivo. Selected identified sites were validated using bisulfite pyrosequencing in an independent cohort of uninfected, viremic and SIV controller macaques. Altered DNA methylation was confirmed in blood and lymph node CD4 + T cells in viremic macaques but was notably absent from SIV controller macaques. Our study identified key genes differentially methylated already in primary infection and in tissues that could contribute to the persisting metabolic disorders and inflammation in HIV-infected individuals despite effective treatment.</p>
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