{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"institution":[{"name":"bioRxiv"}],"indexed":{"date-parts":[[2026,5,9]],"date-time":"2026-05-09T15:10:20Z","timestamp":1778339420304,"version":"3.51.4"},"posted":{"date-parts":[[2026,5,6]]},"group-title":"Microbiology","reference-count":83,"publisher":"openRxiv","license":[{"start":{"date-parts":[[2026,5,6]],"date-time":"2026-05-06T00:00:00Z","timestamp":1778025600000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/publicdomain\/zero\/1.0\/"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"accepted":{"date-parts":[[2026,5,6]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                <jats:p>\n                  Most 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-cell attachment. This enhancing activity was observed for direct infection of TZM-bl reporter cells and primary CD4+ 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 in vivo 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>\n                <jats:sec>\n                  <jats:title>Author Summary<\/jats:title>\n                  <jats:p>\n                    HIV is commonly transmitted from one person to another across mucosal surfaces, such as those lining the genital and rectal tracts, which are densely populated by bacteria that make up the human microbiota. Yet, surprisingly little is known about how these bacteria and the molecules they produce influence HIV infection. In this study, we investigated a group of bacterial proteins known as sialic acid-binding lectins that are expressed by common members of the human microbiome: Siglec-like binding region lectins from\n                    <jats:italic>Streptococcus gordonii<\/jats:italic>\n                    and superantigen-like lectins from\n                    <jats:italic>Staphylococcus aureus<\/jats:italic>\n                    . Using multiple HIV strains and several types of target cells, we demonstrate that lectin binding to HIV can increase virus attachment to target cells and thereby enhance infection, although the magnitude of this effect varies among lectins and virus strains. Lectin binding also facilitates HIV spread from cell to cell and promotes mucosal HIV infection in a humanized mouse model, resulting in a higher viral burden in the blood and tissues. These findings identify bacterial lectins as important factors that can influence HIV infection and implicate a potential role for the human microbiota in determining susceptibility to HIV infection.\n                  <\/jats:p>\n                <\/jats:sec>","DOI":"10.64898\/2026.05.05.722898","type":"posted-content","created":{"date-parts":[[2026,5,7]],"date-time":"2026-05-07T07:50:14Z","timestamp":1778140214000},"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":"10.64898","author":[{"given":"Clauvis Kunkeng","family":"Yengo","sequence":"first","affiliation":[{"name":"Division of Infectious Diseases, Department of Medicine, Icahn School of Medicine at Mount Sinai, New York, NY, USA"},{"name":"James J. Peters VA Medical Center, Bronx, NY, USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Xiaomei","family":"Liu","sequence":"additional","affiliation":[{"name":"Division of Infectious Diseases, Department of Medicine, Icahn School of Medicine at Mount Sinai, New York, NY, USA"},{"name":"James J. Peters VA Medical Center, Bronx, NY, USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Ries J.","family":"Langley","sequence":"additional","affiliation":[{"name":"Molecular Medicine and Pathology, University of Auckland, Auckland, New Zealand"},{"name":"Maurice Wilkins Centre for Molecular Biodiscovery, University of Auckland, Auckland, New Zealand"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Frida","family":"Avila","sequence":"additional","affiliation":[{"name":"Department of Medicine, Boston University Chobanian & Avedisian School of Medicine, Boston, MA, USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Manish","family":"Sagar","sequence":"additional","affiliation":[{"name":"Department of Medicine, Boston University Chobanian & Avedisian School of Medicine, Boston, MA, USA"},{"name":"Department of Virology, Immunology and Microbiology, Boston University Chobanian & Avedisian School of Medicine, Boston, USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Christina","family":"Ochsenbauer","sequence":"additional","affiliation":[{"name":"Department of Medicine, Heersink School of Medicine, University of Alabama at Birmingham, Birmingham, AL, United States"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Barbara A.","family":"Bensing","sequence":"additional","affiliation":[{"name":"Department of Medicine, San Francisco Veterans Affairs Medical Center and University of California, San Francisco, CA, USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-9245-9788","authenticated-orcid":false,"given":"Catarina E.","family":"Hioe","sequence":"additional","affiliation":[{"name":"Division of Infectious Diseases, Department of Medicine, Icahn School of Medicine at Mount Sinai, New York, NY, USA"},{"name":"James J. 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