{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,3,9]],"date-time":"2026-03-09T01:08:10Z","timestamp":1773018490632,"version":"3.50.1"},"reference-count":63,"publisher":"Wiley","issue":"1","license":[{"start":{"date-parts":[[2026,2,25]],"date-time":"2026-02-25T00:00:00Z","timestamp":1771977600000},"content-version":"vor","delay-in-days":55,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"},{"start":{"date-parts":[[2026,1,1]],"date-time":"2026-01-01T00:00:00Z","timestamp":1767225600000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/doi.wiley.com\/10.1002\/tdm_license_1.1"}],"funder":[{"DOI":"10.13039\/501100003074","name":"Agencia Nacional de Promoci\u00f3n Cient\u00edfica y Tecnol\u00f3gica","doi-asserted-by":"publisher","award":["PICTO-2021-00005-COVID Secuelas"],"award-info":[{"award-number":["PICTO-2021-00005-COVID Secuelas"]}],"id":[{"id":"10.13039\/501100003074","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100008056","name":"Fundaci\u00f3n Florencio Fiorini","doi-asserted-by":"publisher","award":["2024"],"award-info":[{"award-number":["2024"]}],"id":[{"id":"10.13039\/100008056","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Journal of Immunology Research"],"published-print":{"date-parts":[[2026,1]]},"abstract":"<jats:sec>\n                    <jats:title>Introduction<\/jats:title>\n                    <jats:p>Coronavirus disease 2019 (COVID\u201019) may have both short\u2010 and long\u2010term impacts on the progression of human immunodeficiency virus (HIV)\u20101 after acute SARS\u2010CoV\u20102 infection in people living with HIV (PLWH), even those on combined antiretroviral therapy (cART). This study aimed to investigate whether SARS\u2010CoV\u20102 could influence HIV reactivation in latently infected lymphoid cells.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>HIV\u2010infected lymphoid (J\u2010Lat) cells, characterized by proviral latency under unstimulated conditions, were used for latency reversal assays with phorbol 12\u2010myristate 13\u2010acetate (PMA), free SARS\u2010CoV\u20102 particles, or conditioned media (CM) from macrophages. Monocytes isolated from donor blood were differentiated into macrophages (monocyte\u2010derived macrophages [MDMs]) and polarized to M1 or M2 phenotypes before stimulation or with two SARS\u2010CoV\u20102 variants (wild\u2010type and BA.5) infection. Additionally, the effects of redox imbalance on latency reversal in both J\u2010Lat and myeloid (U1) latency models were measured. SARS\u2010CoV\u20102 RNA was quantified by RT\u2010qPCR targeting ORF1ab and N genes, and latency reversal and reactive oxygen species (ROS) levels were assessed by flow cytometry. TNF\u03b1 involvement was confirmed through neutralization assays, while cytokines and polarization markers were analyzed via ELISA and fluorescent antibodies.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>Jurkat and J\u2010Lat cells had low ACE2 expression and were not permissive to SARS\u2010CoV\u20102 infection. SARS\u2010CoV\u20102 exposure alone did not induce HIV latency reversal in J\u2010Lat cells. However, CM from M1\u2010polarized, resiquimod (R\u2010848)\u2010treated, and SARS\u2010CoV\u20102\u2010infected macrophages significantly reactivated latent HIV. TNF\u03b1 was identified as the primary driver of latency reversal, with no significant changes in ROS levels. Prolonged SARS\u2010CoV\u20102 exposure shifted macrophage polarization toward an anti\u2010inflammatory M2 phenotype, characterized by IL\u201010 release, which reduced latency reactivation.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>This study demonstrates that SARS\u2010CoV\u20102 can indirectly reverse HIV latency in lymphoid cells by promoting the release of pro\u2010inflammatory cytokines from infected macrophages. These findings suggest potential therapeutic strategies for preventing HIV reactivation during SARS\u2010CoV\u20102 coinfection, emphasizing the modulation of cytokine signaling to control inflammation while minimizing immune dysregulation.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1155\/jimr\/9986845","type":"journal-article","created":{"date-parts":[[2026,3,9]],"date-time":"2026-03-09T00:13:05Z","timestamp":1773015185000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["SARS\u2010CoV\u20102\u2010Induced Macrophage Polarization Reverses HIV\u20101 Latency in J\u2010Lat Cells Through TNF\u03b1 Signaling"],"prefix":"10.1155","volume":"2026","author":[{"ORCID":"https:\/\/orcid.org\/0009-0006-2844-2873","authenticated-orcid":false,"given":"Patricio","family":"Jarmoluk","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Franco Agust\u00edn","family":"Sviercz","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Cintia","family":"Cevallos","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"ORCID":"https:\/\/orcid.org\/0009-0001-7461-5687","authenticated-orcid":false,"given":"Rosa Nicole","family":"Freiberger","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Cynthia Alicia","family":"L\u00f3pez","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-2077-8509","authenticated-orcid":false,"given":"M. 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