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We have previously reported that the HIV protein Tat which circulates in all HIV\u2010positive individuals whatever their immune status caused an increased rate of colocalization between <jats:italic>IGH<\/jats:italic> and <jats:italic>MYC<\/jats:italic> in B\u2010cells nuclei. We here present in vitro evidence that Tat activates the expression of the <jats:italic>AICDA<\/jats:italic> gene that encodes the activation\u2010induced cytidine deaminase whose physiological function is to create double\u2010strand breaks for immunoglobulin gene maturation. In the presence of Tat, DNA damage was observed concomitantly in both <jats:italic>MYC<\/jats:italic> and <jats:italic>IGH<\/jats:italic>, followed by DNA repair by nonhomologous end joining. <jats:italic>AICDA<\/jats:italic> was further found overexpressed in vivo in peripheral blood B\u2010cells from HIV\u2010infected individuals. Thus, the capacity of Tat to spontaneously penetrate B\u2010cells could be sufficient to favor the occurrence of <jats:italic>MYC\u2010IGH<\/jats:italic> oncogenic rearrangements during erroneous repair, a plausible cause for the increased incidence of Burkitt lymphoma in the HIV\u2010infected population.<\/jats:p>","DOI":"10.1002\/jcp.28219","type":"journal-article","created":{"date-parts":[[2019,1,31]],"date-time":"2019-01-31T10:06:44Z","timestamp":1548929204000},"page":"15678-15685","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":29,"title":["HIV\u20101 Tat protein induces aberrant activation of <i>AICDA<\/i> in human B\u2010lymphocytes from peripheral blood"],"prefix":"10.1002","volume":"234","author":[{"given":"Fatimata Bintou","family":"Sall","sequence":"first","affiliation":[{"name":"Department of UMR8126, Institut Gustave Roussy Villejuif France"},{"name":"LIA 1066 French\u2013Russian Joint Cancer Research Laboratory 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