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Langerhans Cell Function HIV-1 Susceptibility by Affecting Herpes

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Langerhans Cell Function HIV-1 Susceptibility by Affecting Herpes Herpes Simplex Virus Type 2 Enhances HIV-1 Susceptibility by Affecting Langerhans Cell Function This information is current as Marein A. W. P. de Jong, Lot de Witte, Maureen E. Taylor of September 27, 2021. and Teunis B. H. Geijtenbeek J Immunol 2010; 185:1633-1641; Prepublished online 30 June 2010; doi: 10.4049/jimmunol.0904137 http://www.jimmunol.org/content/185/3/1633 Downloaded from References This article cites 45 articles, 14 of which you can access for free at: http://www.jimmunol.org/content/185/3/1633.full#ref-list-1 http://www.jimmunol.org/ Why The JI? Submit online. • Rapid Reviews! 30 days* from submission to initial decision • No Triage! Every submission reviewed by practicing scientists • Fast Publication! 4 weeks from acceptance to publication by guest on September 27, 2021 *average Subscription Information about subscribing to The Journal of Immunology is online at: http://jimmunol.org/subscription Permissions Submit copyright permission requests at: http://www.aai.org/About/Publications/JI/copyright.html Email Alerts Receive free email-alerts when new articles cite this article. Sign up at: http://jimmunol.org/alerts The Journal of Immunology is published twice each month by The American Association of Immunologists, Inc., 1451 Rockville Pike, Suite 650, Rockville, MD 20852 Copyright © 2010 by The American Association of Immunologists, Inc. All rights reserved. Print ISSN: 0022-1767 Online ISSN: 1550-6606. The Journal of Immunology Herpes Simplex Virus Type 2 Enhances HIV-1 Susceptibility by Affecting Langerhans Cell Function Marein A. W. P. de Jong,*,†, ‡ Lot de Witte,x Maureen E. Taylor,{ and Teunis B. H. Geijtenbeek*,† Genital herpes is the most prevalent viral sexually transmitted infection worldwide and is mainly caused by HSV type 2 (HSV-2). HSV-2 infection enhances HIV-1 susceptibility, even in the absence of clinical symptoms. In this study, we investigated the effect of HSV-2 on HIV-1 transmission by mucosal Langerhans cells (LCs). LCs are important in heterosexual transmission because they form a barrier against HIV-1 infection; LCs efficiently capture and degrade HIV-1 through the C-type lectin langerin, thereby preventing HIV-1 transmission. Notably, our data showed that HSV-2 enhanced HIV-1 infection of LCs and subsequent HIV-1 transmission to T cells. HSV-2 interfered with HIV-1 capture by langerin, which allowed efficient HIV-1 infection of LCs. HSV-2 inhibited the antiviral function of langerin at two levels; HSV-2 decreased langerin expression and competed with HIV-1 for langerin binding. HSV-2 replication was not required, because both UV-inactivated HSV-2 and TLR-3 agonist polyinosinic:poly- Downloaded from cytidylic acid similarly increased HIV-1 transmission by LCs. Therefore, we identified a mechanism by which HSV-2 enhances HIV-1 susceptibility, even in the absence of clinical symptoms. Our data demonstrated that viral coinfections, such as HSV-2, breach the protective function of LCs by abrogating langerin function, which increases HIV-1 susceptibility. These data reinforce the importance of preventing sexually transmitted infections, such as HSV-2, to reduce the transmission of HIV-1. The Journal of Immunology, 2010, 185: 1633–1641. http://www.jimmunol.org/ ore than 30 million people worldwide are infected by Notably, HSV-2 can enhance HIV-1 susceptibility in the absence HIV-1, the causative agent of AIDS, and heterosexual of apparent lesions (5). HSV-2 also induces inflammation, thereby M transmission of HIV-1 is the primary route of infection including T cell influx, even in the absence of clinically apparent (1). Numerous studies demonstrated that sexually transmitted lesions. Furthermore, HIV-1–susceptible inflammatory cells can infections (STIs) enhance susceptibility to HIV-1 acquisition and persist for a long period of time after HSV-2 infection has been transmission, even in the absence of clinical symptoms (1–5). The cleared and the lesions have healed (10). most common viral STI acquired during sexual contact in the HSV-2 infection occurs via direct contact with infected lesions or developing world is genital herpes (6), which is primarily caused body fluids and enters the body at mucosal tissues or through small by guest on September 27, 2021 by HSV type 2 (HSV-2), although HSV type 1 infection can also lesions. Epithelial cells and keratinocytes are the primary target cells lead to genital herpes (7). Pre-existing HSV-2 infection is a risk for HSV-2, but it also infects neuronal and immune cells (11). Once factor for acquiring HIV-1 infection through sexual contact (1–4). infected, thevirus causes life-long infection of the host by establishing Although it remains unclear how HSV-2 enhances HIV-1 suscep- latency in the neurons of the sensitive ganglia. Reactivation occurs tibility, several mechanisms have been proposed. The formation of periodically, at times when the immune system is suboptimal, result- pustules and ulcers by genital herpes can facilitate HIV-1 entry ing in the formation of vesicles that break into ulcerations at the into mucosal tissues (8). In addition, mucosal inflammation by genital mucosa (8, 12). The genital mucosa is crucial in sexual trans- HSV-2 can cause an influx of activated CD4+ T cells, which mission of HIV-1, and coinfections with HSV-2 might affect the in- facilitates HIV-1 infection and subsequent dissemination (9). tegrity of the genital mucosa and consequently increase HIV-1 susceptibility. Genital tissues contain Langerhans cells (LCs), the main dendritic cell (DC) subset present in stratified epithelia and *Center of Infection and Immunity Amsterdam and †Center for Experimental and mucosal tissues (13). LCs are involved in HIV-1 dissemination; Molecular Medicine, Academic Medical Center, University of Amsterdam; HIV-1 can infect LCs, and infected LCs subsequently migrate to the ‡Department of Molecular Cell Biology and Immunology, VU University Medical Center, Amsterdam; xDepartment of Virology, Erasmus Medical Center, University lymphoid tissues where they transmit the virus efficiently to T cells Medical Center, Rotterdam, The Netherlands; and {Division of Molecular Bioscien- and, thereby, mediate infection of the host (14). However, we recently ces, Department of Life Sciences, Imperial College, London, United Kingdom showed that LCs have an anti–HIV-1 function (15). Under noninflam- Received for publication December 22, 2009. Accepted for publication May 18, matory conditions, LCs prevent HIV-1 transmission by efficient cap- 2010. ture of invading HIV-1 via the C-type lectin langerin, which targets This work was supported by Dutch Scientific Organization Grants 91204025 (to M.d.J.) and 91746367 (to L.d.W.) and Wellcome Trust Grant 075565 (to M.E.T.). the virus for degradation (15). Langerin prevents HIV-1 infection of Address correspondence and reprint requests to Dr. Teunis B.H. Geijtenbeek, Center LCs and, thereby, transmission of the virus to T cells in lymphoid for Experimental and Molecular Medicine, Academic Medical Center, University of tissues. Thus, LCs form a first line of defense against HIV-1infection. Amsterdam, Meibergdreef, 9 1105 AZ, Amsterdam, The Netherlands. E-mail ad- However, inhibition of the antiviral function of langerin or inflamma- dress: [email protected] tory conditions allows infection of LCs by HIV-1, and infected LCs Abbreviations used in this paper: CpG-ODN, CpG-containing oligonucleotides; DC, dendritic cell; eGFP, enhanced GFP; HIV-1–eGFP, HIV-1 virus R5-tropic enhanced efficiently transmit HIV-1 to T cells (15, 16). Therefore, we hypoth- GFP-expressing HIV-1-NL4.3-BaL; HSV-2, HSV type 2; LC, Langerhans cell; MOI, esized that viral STIs, such as HSV-2, increase HIV-1susceptibility by multiplicity of infection; PI, propidium iodide; poly(I:C), polyinosinic:polycytidylic affecting the protective function of LCs. acid; STI, sexually transmitted infection; UV, HSV-2; UV-inactivated HSV type 2. In this article, we show that HSV-2 productively infects LCs Copyright Ó 2010 by The American Association of Immunologists, Inc. 0022-1767/10/$16.00 and that LC activation by HSV-2 increases HIV-1 transmission by www.jimmunol.org/cgi/doi/10.4049/jimmunol.0904137 1634 HSV-2 INFECTION OF LCs ENHANCES HIV-1 TRANSMISSION LCstoT cells.Weidentifiedtwo distincteffects ofHSV-2ontheanti– of LCs. For TNF-a production, cells were incubated with different HIV-1 function of LCs; HSV-2 induced downregulation of langerin concentrations of HSV-2 or UV–HSV-2 for 6, 12, and 24 h or with poly a expression and in addition HSV-2 virions inhibited HIV-1 binding to (I:C). Supernatant was harvested, and TNF- protein production was measured by ELISA (BioSource International, Camarillo, CA). langerin by direct competition with HIV-1. The reduced langerin expression and function, decreased HIV-1 capture by LCs and Fluorescent bead adhesion assay allowed infection of LCs by HIV-1, which increased HIV-1 trans- Streptavidin-coated beads (TransFluorSpheres, Molecular Probes) were coated mission to T cells. Notably, active HSV-2 replication was not re- with HIV-1 gp120, as described previously (21). The adhesion assay (Fig. 3A) quired, because UV-inactivated HSV-2 (UV–HSV-2) similarly was performed as follows (19, 22, 23): 1 3 105 cells were incubated overnight increased HIV-1 transmission by LCs. Furthermore, our data show with TLR agonists or different concentrations of HSV-2 and UV–HSV-2. Cells that TLR-3 agonist polyinosinic:polycytidylic acid [poly(I:C)] also were washed extensively with PBS and stained with CD1a-FITC. Next, cells were washed in Tris buffer (20 mM Tris-HCl [pH 7], 150 mM NaCl, 1 mM increased HIV-1 transmission. Thus, coinfection with HSV-2 is CaCl2,2mMMgCl2 supplemented with 0.5% BSA) before adding HIV-1 a major risk factor that increases HIV-1 susceptibility by affecting gp120 beads for 45 min at 37˚C. Cells were washed and binding was measured the anti–HIV-1 function of LCs.
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