{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,16]],"date-time":"2026-09-16T05:03:59Z","timestamp":1789535039801,"version":"build-2803163510"},"reference-count":86,"publisher":"Frontiers Media SA","license":[{"start":{"date-parts":[[2026,9,16]],"date-time":"2026-09-16T00:00:00Z","timestamp":1789516800000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":["frontiersin.org"],"crossmark-restriction":true},"short-container-title":["Front. Cell. Infect. Microbiol."],"abstract":"<jats:p>\n                    Most human immunodeficiency virus type 1 (HIV-1) transmission occurs at mucosal surfaces, which are colonized by the host microbiota. However, interactions between HIV and bacteria or bacterial products derived from the human microbiome are poorly characterized, and their biological consequences are largely unexplored. Here, we evaluated the effects of sialic acid-binding lectins expressed by bacterial species ubiquitous in the human microbiota on HIV-1 infectivity using viruses produced in 293T cells and human primary cells. We demonstrated that these bacterial lectins enhanced HIV-1 infectivity in a sialoglycan-dependent manner. Specifically, Siglec-like binding region lectins (SLBR-N, SLBR-H, and SLBR-B) from\n                    <jats:italic>Streptococcus gordonii<\/jats:italic>\n                    and staphylococcal superantigen-like lectins (SSL3, SSL4, and SSL11) from\n                    <jats:italic>Staphylococcus aureus<\/jats:italic>\n                    increased HIV-1 infectivity to varying extents, depending on lectin type and virus strain. Among these lectins, SLBR-N exhibited the greatest potency, corresponding with its superior ability to bind virions and promote virus\u2013cell attachment. This enhancing activity was observed for direct infection of TZM-bl reporter cells and primary CD4\n                    <jats:sup>+<\/jats:sup>\n                    T cells, as well as trans-infection in the presence or absence of the mannose-binding host lectin DC-SIGN. Importantly, these findings were corroborated\n                    <jats:italic>in vivo<\/jats:italic>\n                    using humanized mice, in which pre-exposure to SLBR-N promoted rectal HIV-1 transmission and increased viral burdens in plasma and splenic cells. Collectively, the data show sialoglycan-binding bacterial lectins as microbial factors that can enhance HIV-1 transmission at mucosal surfaces, highlighting a potential direct role for the microbiota in modulating HIV-1 acquisition risk.\n                  <\/jats:p>","DOI":"10.3389\/fcimb.2026.1879791","type":"journal-article","created":{"date-parts":[[2026,9,16]],"date-time":"2026-09-16T04:28:45Z","timestamp":1789532925000},"update-policy":"https:\/\/doi.org\/10.3389\/crossmark-policy","source":"Crossref","is-referenced-by-count":0,"title":["HIV-1 interactions with sialic acid-binding bacterial lectins promote virus infectivity in vitro and mucosal transmission in humanized mice"],"prefix":"10.3389","volume":"16","author":[{"given":"Clauvis Kunkeng","family":"Yengo","sequence":"first","affiliation":[{"name":"Division of Infectious Diseases, Department of Medicine, Icahn School of Medicine at Mount Sinai","place":["New York, NY, United States"]},{"name":"Research and Development Service, James J. Peters VA Medical Center","place":["Bronx, NY, United States"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Xiaomei","family":"Liu","sequence":"additional","affiliation":[{"name":"Division of Infectious Diseases, Department of Medicine, Icahn School of Medicine at Mount Sinai","place":["New York, NY, United States"]},{"name":"Research and Development Service, James J. Peters VA Medical Center","place":["Bronx, NY, United States"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ries J.","family":"Langley","sequence":"additional","affiliation":[{"name":"Molecular Medicine and Pathology, University of Auckland","place":["Auckland, New Zealand"]},{"name":"Maurice Wilkins Centre for Molecular Biodiscovery, University of Auckland","place":["Auckland, New Zealand"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Frida","family":"Avila","sequence":"additional","affiliation":[{"name":"Department of Medicine, Boston University Chobanian & Avedisian School of Medicine","place":["Boston, MA, United States"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Manish","family":"Sagar","sequence":"additional","affiliation":[{"name":"Department of Medicine, Boston University Chobanian & Avedisian School of Medicine","place":["Boston, MA, United States"]},{"name":"Department of Virology, Immunology and Microbiology, Boston University Chobanian & Avedisian School of Medicine","place":["Boston, MA, United States"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Christina","family":"Ochsenbauer","sequence":"additional","affiliation":[{"name":"Department of Medicine, Heersink School of Medicine, University of Alabama at Birmingham","place":["Birmingham, AL, United States"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Barbara A.","family":"Bensing","sequence":"additional","affiliation":[{"name":"Department of Medicine, San Francisco Veterans Affairs Medical Center and University of California, San Francisco","place":["San Francisco, CA, United States"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Catarina E.","family":"Hioe","sequence":"additional","affiliation":[{"name":"Division of Infectious Diseases, Department of Medicine, Icahn School of Medicine at Mount Sinai","place":["New York, NY, United States"]},{"name":"Research and Development Service, James J. 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