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Factors Secreted by Human T Lymphotropic Virus Type I (HTLV-I)–infected Cells Can Enhance or Inhibit Replication of HIV-1 in HTLV-I–uninfected Cells: Implications for In Vivo Coinfection with HTLV-I and HIV-1
It remains controversial whether human T lymphotropic virus type I (HTLV-I) coinfection leads to more rapid progression of human immunodeficiency virus (HIV) disease in dually infected individuals. To investigate whether HTLV-I infection of certain cells can modulate HIV-1 infection of surrounding c...
Autores principales: | , , |
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Formato: | Texto |
Lenguaje: | English |
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The Rockefeller University Press
1998
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2212300/ https://www.ncbi.nlm.nih.gov/pubmed/9584147 |
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author | Moriuchi, Hiroyuki Moriuchi, Masako Fauci, Anthony S. |
author_facet | Moriuchi, Hiroyuki Moriuchi, Masako Fauci, Anthony S. |
author_sort | Moriuchi, Hiroyuki |
collection | PubMed |
description | It remains controversial whether human T lymphotropic virus type I (HTLV-I) coinfection leads to more rapid progression of human immunodeficiency virus (HIV) disease in dually infected individuals. To investigate whether HTLV-I infection of certain cells can modulate HIV-1 infection of surrounding cells, primary CD4(+) T cells were treated with cell-free supernatants from HTLV-I–infected MT-2 cell cultures. The primary CD4(+) T cells became resistant to macrophage (M)-tropic HIV-1 but highly susceptible to T cell (T)-tropic HIV-1. The CC chemokines RANTES (regulated on activation, normal T cell expressed and secreted), macrophage inflammatory protein (MIP)-1α, and MIP-1β in the MT-2 cell supernatants were identified as the major suppressive factors for M-tropic HIV-1 as well as the enhancers of T-tropic HIV-1 infection, whereas soluble Tax protein increased susceptibility to both M- and T-tropic HIV-1. The effect of Tax or CC chemokines on T-tropic HIV-1 was mediated, at least in part, by increasing HIV Env-mediated fusogenicity. Our data suggest that the net effect of HTLV-I coinfection in HIV-infected individuals favors the transition from M- to T-tropic HIV phenotype, which is generally indicative of progressive HIV disease. |
format | Text |
id | pubmed-2212300 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 1998 |
publisher | The Rockefeller University Press |
record_format | MEDLINE/PubMed |
spelling | pubmed-22123002008-04-16 Factors Secreted by Human T Lymphotropic Virus Type I (HTLV-I)–infected Cells Can Enhance or Inhibit Replication of HIV-1 in HTLV-I–uninfected Cells: Implications for In Vivo Coinfection with HTLV-I and HIV-1 Moriuchi, Hiroyuki Moriuchi, Masako Fauci, Anthony S. J Exp Med Article It remains controversial whether human T lymphotropic virus type I (HTLV-I) coinfection leads to more rapid progression of human immunodeficiency virus (HIV) disease in dually infected individuals. To investigate whether HTLV-I infection of certain cells can modulate HIV-1 infection of surrounding cells, primary CD4(+) T cells were treated with cell-free supernatants from HTLV-I–infected MT-2 cell cultures. The primary CD4(+) T cells became resistant to macrophage (M)-tropic HIV-1 but highly susceptible to T cell (T)-tropic HIV-1. The CC chemokines RANTES (regulated on activation, normal T cell expressed and secreted), macrophage inflammatory protein (MIP)-1α, and MIP-1β in the MT-2 cell supernatants were identified as the major suppressive factors for M-tropic HIV-1 as well as the enhancers of T-tropic HIV-1 infection, whereas soluble Tax protein increased susceptibility to both M- and T-tropic HIV-1. The effect of Tax or CC chemokines on T-tropic HIV-1 was mediated, at least in part, by increasing HIV Env-mediated fusogenicity. Our data suggest that the net effect of HTLV-I coinfection in HIV-infected individuals favors the transition from M- to T-tropic HIV phenotype, which is generally indicative of progressive HIV disease. The Rockefeller University Press 1998-05-18 /pmc/articles/PMC2212300/ /pubmed/9584147 Text en This article is distributed under the terms of an Attribution–Noncommercial–Share Alike–No Mirror Sites license for the first six months after the publication date (see http://www.rupress.org/terms). After six months it is available under a Creative Commons License (Attribution–Noncommercial–Share Alike 4.0 Unported license, as described at http://creativecommons.org/licenses/by-nc-sa/4.0/). |
spellingShingle | Article Moriuchi, Hiroyuki Moriuchi, Masako Fauci, Anthony S. Factors Secreted by Human T Lymphotropic Virus Type I (HTLV-I)–infected Cells Can Enhance or Inhibit Replication of HIV-1 in HTLV-I–uninfected Cells: Implications for In Vivo Coinfection with HTLV-I and HIV-1 |
title | Factors Secreted by Human T Lymphotropic Virus Type I (HTLV-I)–infected Cells Can Enhance or Inhibit Replication of HIV-1 in HTLV-I–uninfected Cells: Implications for In Vivo Coinfection with HTLV-I and HIV-1 |
title_full | Factors Secreted by Human T Lymphotropic Virus Type I (HTLV-I)–infected Cells Can Enhance or Inhibit Replication of HIV-1 in HTLV-I–uninfected Cells: Implications for In Vivo Coinfection with HTLV-I and HIV-1 |
title_fullStr | Factors Secreted by Human T Lymphotropic Virus Type I (HTLV-I)–infected Cells Can Enhance or Inhibit Replication of HIV-1 in HTLV-I–uninfected Cells: Implications for In Vivo Coinfection with HTLV-I and HIV-1 |
title_full_unstemmed | Factors Secreted by Human T Lymphotropic Virus Type I (HTLV-I)–infected Cells Can Enhance or Inhibit Replication of HIV-1 in HTLV-I–uninfected Cells: Implications for In Vivo Coinfection with HTLV-I and HIV-1 |
title_short | Factors Secreted by Human T Lymphotropic Virus Type I (HTLV-I)–infected Cells Can Enhance or Inhibit Replication of HIV-1 in HTLV-I–uninfected Cells: Implications for In Vivo Coinfection with HTLV-I and HIV-1 |
title_sort | factors secreted by human t lymphotropic virus type i (htlv-i)–infected cells can enhance or inhibit replication of hiv-1 in htlv-i–uninfected cells: implications for in vivo coinfection with htlv-i and hiv-1 |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2212300/ https://www.ncbi.nlm.nih.gov/pubmed/9584147 |
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