{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,2]],"date-time":"2026-10-02T10:30:58Z","timestamp":1790937058005,"version":"4.1.0"},"reference-count":42,"publisher":"American Society for Microbiology","issue":"17","license":[{"start":{"date-parts":[[2010,9,1]],"date-time":"2010-09-01T00:00:00Z","timestamp":1283299200000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.asm.org\/non-commercial-tdm-license"}],"content-domain":{"domain":["journals.asm.org"],"crossmark-restriction":true},"short-container-title":["J Virol"],"published-print":{"date-parts":[[2010,9]]},"abstract":"<jats:title>ABSTRACT<\/jats:title><jats:p><jats:italic>Mycobacterium<\/jats:italic><jats:italic>tuberculosis<\/jats:italic>is a leading killer of HIV-infected individuals worldwide, particularly in sub-Saharan Africa, where it is responsible for up to 50% of HIV-related deaths. Infection by HIV predisposes individuals to<jats:italic>M. tuberculosis<\/jats:italic>infection, and coinfection accelerates the progression of both diseases. In contrast to most other opportunistic infections associated with HIV, an increased risk of<jats:italic>M. tuberculosis<\/jats:italic>infection occurs during early-stage HIV disease, long before CD4 T cell counts fall below critical levels. We hypothesized that<jats:italic>M. tuberculosis<\/jats:italic>infection contributes to HIV pathogenesis by interfering with dendritic cell (DC)-mediated immune control. DCs carry pathogens like<jats:italic>M. tuberculosis<\/jats:italic>and HIV from sites of infection into lymphoid tissues, where they process and present antigenic peptides to CD4 T cells. Paradoxically, DCs can also deliver infectious HIV to T cells without first becoming infected, a process known as<jats:italic>trans<\/jats:italic>-infection. Lipopolysaccharide (LPS)-activated DCs sequester HIV in pocketlike membrane invaginations that remain open to the cell surface, and individual virions are delivered from the pocket into T cells at the site of contact during<jats:italic>trans<\/jats:italic>-infection. Here we report that<jats:italic>M. tuberculosis<\/jats:italic>exposure increases HIV<jats:italic>trans<\/jats:italic>-infection and induces viral sequestration within surface-accessible compartments identical to those seen in LPS-stimulated DCs. At the same time,<jats:italic>M. tuberculosis<\/jats:italic>dramatically decreases the degradative processing and major histocompatibility complex class II (MHC-II) presentation of HIV antigens to CD4 T cells. Our data suggest that<jats:italic>M. tuberculosis<\/jats:italic>infection promotes a shift in the dynamic balance between antigen processing and intact virion presentation, favoring DC-mediated amplification of HIV infections.<\/jats:p>","DOI":"10.1128\/jvi.02303-09","type":"journal-article","created":{"date-parts":[[2010,7,1]],"date-time":"2010-07-01T02:14:51Z","timestamp":1277950491000},"page":"8549-8560","update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":19,"title":["<i>Mycobacterium tuberculosis<\/i>Promotes HIV<i>trans<\/i>-Infection and Suppresses Major Histocompatibility Complex Class II Antigen Processing by Dendritic Cells"],"prefix":"10.1128","volume":"84","author":[{"given":"Morgan A.","family":"Reuter","sequence":"first","affiliation":[{"name":"Department of Molecular Biology and Microbiology"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Nicole D.","family":"Pecora","sequence":"additional","affiliation":[{"name":"Department of Pathology"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Clifford V.","family":"Harding","sequence":"additional","affiliation":[{"name":"Department of Pathology"},{"name":"Case\/UH Center for AIDS Research, Case Western Reserve University School of Medicine"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"David H.","family":"Canaday","sequence":"additional","affiliation":[{"name":"Division of Infectious Diseases"},{"name":"Case\/UH Center for AIDS Research, Case Western Reserve University School of Medicine"},{"name":"Geriatric Research, Education and Clinical Center, Louis Stokes VAMC, Cleveland, Ohio 44106"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"David","family":"McDonald","sequence":"additional","affiliation":[{"name":"Department of Molecular Biology and Microbiology"},{"name":"Case\/UH Center for AIDS Research, Case Western Reserve University School of Medicine"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"235","reference":[{"key":"e_1_3_2_2_2","doi-asserted-by":"publisher","DOI":"10.1111\/j.1462-5822.2007.01097.x"},{"key":"e_1_3_2_3_2","doi-asserted-by":"publisher","DOI":"10.1128\/JVI.78.20.10848-10855.2004"},{"key":"e_1_3_2_4_2","doi-asserted-by":"publisher","DOI":"10.1084\/jem.20051782"},{"key":"e_1_3_2_5_2","doi-asserted-by":"publisher","DOI":"10.1038\/32588"},{"key":"e_1_3_2_6_2","doi-asserted-by":"publisher","DOI":"10.1128\/jvi.71.10.7478-7487.1997"},{"key":"e_1_3_2_7_2","doi-asserted-by":"publisher","DOI":"10.1038\/nature01004"},{"key":"e_1_3_2_8_2","doi-asserted-by":"publisher","DOI":"10.1128\/JVI.01661-06"},{"key":"e_1_3_2_9_2","doi-asserted-by":"publisher","DOI":"10.1016\/j.jim.2003.07.004"},{"key":"e_1_3_2_10_2","doi-asserted-by":"publisher","DOI":"10.1084\/jem.181.1.257"},{"key":"e_1_3_2_11_2","doi-asserted-by":"publisher","DOI":"10.1242\/jcs.113.19.3365"},{"key":"e_1_3_2_12_2","doi-asserted-by":"publisher","DOI":"10.1007\/s15010-009-8450-7"},{"key":"e_1_3_2_13_2","doi-asserted-by":"publisher","DOI":"10.1111\/j.1600-0854.2005.00293.x"},{"key":"e_1_3_2_14_2","doi-asserted-by":"publisher","DOI":"10.1016\/S0092-8674(00)00038-6"},{"key":"e_1_3_2_15_2","doi-asserted-by":"publisher","DOI":"10.1016\/S0092-8674(00)80694-7"},{"key":"e_1_3_2_16_2","doi-asserted-by":"publisher","DOI":"10.1084\/jem.20021229"},{"key":"e_1_3_2_17_2","doi-asserted-by":"crossref","first-page":"635","DOI":"10.4049\/jimmunol.159.2.635","volume":"159","year":"1997","unstructured":"Henderson, R. 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