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The cellular transcription factor NF-\u03baB is considered a master mediator of HIV-1 escape from latency induced by LRAs. Nevertheless, a systemic activation of NF-\u03baB in HIV-1-infected patients resulting from the combined administration of different LRAs could represent a potential risk, especially in the case of a prolonged treatment. We demonstrate here that conventional treatments with bryostatin-1 and hexamethylenebisacetamide (HMBA) or ionomycin synergistically reactivate HIV-1 from latency, even under conditions where NF-\u03baB activation is repressed. Our study provides a molecular proof of concept for the use of anti-inflammatory drugs, like aspirin, capable of inhibiting NF-\u03baB in patients under combination antiretroviral therapy during the shock-and-kill approach, to avoid potential autoimmune and inflammatory disorders that can be elicited by combinations of LRAs.<\/jats:p>","DOI":"10.1128\/jvi.00495-19","type":"journal-article","created":{"date-parts":[[2019,6,25]],"date-time":"2019-06-25T12:26:42Z","timestamp":1561465602000},"update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":29,"title":["Alternate NF-\u03baB-Independent Signaling Reactivation of Latent HIV-1 Provirus"],"prefix":"10.1128","volume":"93","author":[{"given":"Chiara","family":"Acchioni","sequence":"first","affiliation":[{"name":"Department of Infectious Diseases, Istituto Superiore di Sanit\u00e0, Rome, Italy"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Anna 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