{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,5,16]],"date-time":"2026-05-16T23:58:19Z","timestamp":1778975899695,"version":"3.51.4"},"reference-count":24,"publisher":"American Society for Microbiology","issue":"2","license":[{"start":{"date-parts":[[2007,1,15]],"date-time":"2007-01-15T00:00:00Z","timestamp":1168819200000},"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":[[2007,1,15]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n          <jats:p>Human immunodeficiency virus (HIV) infection is often accompanied by infection with other pathogens that affect the clinical course of HIV disease. Here, we identified another virus, human herpesvirus 7 (HHV-7) that interferes with HIV type 1 (HIV-1) replication in human lymphoid tissue, where critical events of HIV disease occur. Like the closely related HHV-6, HHV-7 suppresses the replication of CCR5-tropic (R5) HIV-1 in coinfected blocks of human lymphoid tissue. Unlike HHV-6, which affects HIV-1 by upregulating RANTES, HHV-7 did not upregulate any CCR5-binding chemokine. Rather, the inhibition of R5 HIV-1 by HHV-7 was associated with a marked downregulation of CD4, the cellular receptor shared by HHV-7 and HIV-1. HHV-7-induced CD4 downregulation was sufficient for HIV-1 inhibition, since comparable downregulation of CD4 with cyclotriazadisulfonamide, a synthetic macrocycle that specifically modulates expression of CD4, resulted in the suppression of HIV infection similar to that seen in HHV-7-infected tissues. In contrast to R5 HIV-1, CXCR4-tropic (X4) HIV-1 was only minimally suppressed by HHV-7 coinfection. This selectivity in suppression of R5 and X4 HIV-1 is explained by a suppression of HHV-7 replication in X4- but not in R5-coinfected tissues. These results suggest that HIV-1 and HHV-7 may interfere in lymphoid tissue in vivo, thus potentially affecting the progression of HIV-1 disease. Knowledge of the mechanisms of interaction of HIV-1 with HHV-7, as well as with other pathogens that modulate HIV-1 replication, may provide new insights into HIV pathogenesis and lead to the development of new anti-HIV therapeutic strategies.<\/jats:p>","DOI":"10.1128\/jvi.01367-06","type":"journal-article","created":{"date-parts":[[2006,12,27]],"date-time":"2006-12-27T23:52:56Z","timestamp":1167263576000},"page":"708-717","update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":52,"title":["Viral Interactions in Human Lymphoid Tissue: Human Herpesvirus 7 Suppresses the Replication of CCR5-Tropic Human Immunodeficiency Virus Type 1 via CD4 Modulation"],"prefix":"10.1128","volume":"81","author":[{"given":"Andrea","family":"Lisco","sequence":"first","affiliation":[{"name":"Laboratory of Molecular and Cellular Biophysics, National Institute of Child Health and Human Development, Bethesda, Maryland 20892"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Jean-Charles","family":"Grivel","sequence":"additional","affiliation":[{"name":"Laboratory of Molecular and Cellular Biophysics, National Institute of Child Health and Human Development, Bethesda, Maryland 20892"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Ange\u0301lique","family":"Biancotto","sequence":"additional","affiliation":[{"name":"Laboratory of Molecular and Cellular Biophysics, National Institute of Child Health and Human Development, Bethesda, Maryland 20892"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Christophe","family":"Vanpouille","sequence":"additional","affiliation":[{"name":"Laboratory of Molecular and Cellular Biophysics, National Institute of Child Health and Human Development, Bethesda, Maryland 20892"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Francesco","family":"Origgi","sequence":"additional","affiliation":[{"name":"Unit of Human Virology, DIBIT San Raffaele Scientific Institute, Milano, Italy"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Mauro S.","family":"Malnati","sequence":"additional","affiliation":[{"name":"Unit of Human Virology, DIBIT San Raffaele Scientific Institute, Milano, Italy"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Dominique","family":"Schols","sequence":"additional","affiliation":[{"name":"Rega Institute for Medical Research, Katholieke Universiteit Leuven, Leuven, Belgium"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Paolo","family":"Lusso","sequence":"additional","affiliation":[{"name":"Unit of Human Virology, DIBIT San Raffaele Scientific Institute, Milano, Italy"},{"name":"Department of Medical Sciences, University of Cagliari Medical School, Cagliari, Italy"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Leonid B.","family":"Margolis","sequence":"additional","affiliation":[{"name":"Laboratory of Molecular and Cellular Biophysics, National Institute of Child Health and Human Development, Bethesda, Maryland 20892"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"235","reference":[{"key":"e_1_3_1_2_2","first-page":"549","volume":"8","year":"1994","unstructured":"Ablashi, D. V., Z. N. Berneman, B. Kramarsky, Y. Asano, S. Choudhury, and G. R. Pearson. 1994. Human herpesvirus-7 (HHV-7). In Vivo8:549-554.","journal-title":"In Vivo"},{"key":"e_1_3_1_3_2","doi-asserted-by":"publisher","DOI":"10.1002\/(SICI)1099-1654(199910\/12)9:4<245::AID-RMV253>3.0.CO;2-I"},{"key":"e_1_3_1_4_2","doi-asserted-by":"publisher","DOI":"10.1002\/jmv.20345"},{"key":"e_1_3_1_5_2","first-page":"1222","volume":"9","year":"2002","unstructured":"Broccolo, F., S. Bossolasco, A. M. Careddu, G. Tambussi, A. Lazzarin, and P. Cinque. 2002. Detection of DNA of lymphotropic herpesviruses in plasma of human immunodeficiency virus-infected patients: frequency and clinical significance. Clin. Diagn. Lab. Immunol.9:1222-1228.","journal-title":"Clin. Diagn. Lab. 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