Binding of HIV-1 virions to $ α_{4} $$ β_{7} $ expressing cells and impact of antagonizing $ α_{4} $$ β_{7} $ on HIV-1 infection of primary $ CD4^{+} $ T cells
Abstract HIV-1 envelope glycoprotein is reported to interact with $ α_{4} $$ β_{7} $, an integrin mediating the homing of lymphocytes to gut-associated lymphoid tissue, but the significance of $ α_{4} $$ β_{7} $ in HIV-1 infection remains controversial. Here, using HIV-1 strain BaL, the gp120 of which was previously shown to be capable of interacting with $ α_{4} $$ β_{7} $, we demonstrated that $ α_{4} $$ β_{7} $ can mediate the binding of whole HIV-1 virions to $ α_{4} $$ β_{7} $-expressing transfectants. We further constructed a cell line stably expressing $ α_{4} $$ β_{7} $ and confirmed the $ α_{4} $$ β_{7} $-mediated HIV-1 binding. In primary lymphocytes with activated $ α_{4} $$ β_{7} $ expression, we also observed significant virus binding which can be inhibited by an anti-$ α_{4} $$ β_{7} $ antibody. Moreover, we investigated the impact of antagonizing $ α_{4} $$ β_{7} $ on HIV-1 infection of primary $ CD4^{+} $ T cells. In $ α_{4} $$ β_{7} $-activated $ CD4^{+} $ T cells, both anti-$ α_{4} $$ β_{7} $ antibodies and introduction of short-hairpin RNAs specifically targeting $ α_{4} $$ β_{7} $ resulted in a decreased HIV-1 infection. Our findings indicate that $ α_{4} $$ β_{7} $ may serve as an attachment factor at least for some HIV-1 strains. The established approach provides a promising means for the investigation of other viral strains to understand the potential roles of $ α_{4} $$ β_{7} $ in HIV-1 infection..
Medienart: |
E-Artikel |
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Erscheinungsjahr: |
2014 |
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Erschienen: |
2014 |
Enthalten in: |
Zur Gesamtaufnahme - volume:29 |
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Enthalten in: |
Virologica Sinica - 29(2014), 6 vom: Dez., Seite 381-392 |
Sprache: |
Englisch |
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Beteiligte Personen: |
Li, Chang [VerfasserIn] |
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Links: |
Volltext [lizenzpflichtig] |
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Themen: |
β |
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Anmerkungen: |
© Wuhan Institute of Virology, CAS and Springer-Verlag Berlin Heidelberg 2014 |
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doi: |
10.1007/s12250-014-3525-8 |
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funding: |
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Förderinstitution / Projekttitel: |
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PPN (Katalog-ID): |
OLC2101992485 |
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100 | 1 | |a Li, Chang |e verfasserin |4 aut | |
245 | 1 | 0 | |a Binding of HIV-1 virions to $ α_{4} $$ β_{7} $ expressing cells and impact of antagonizing $ α_{4} $$ β_{7} $ on HIV-1 infection of primary $ CD4^{+} $ T cells |
264 | 1 | |c 2014 | |
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500 | |a © Wuhan Institute of Virology, CAS and Springer-Verlag Berlin Heidelberg 2014 | ||
520 | |a Abstract HIV-1 envelope glycoprotein is reported to interact with $ α_{4} $$ β_{7} $, an integrin mediating the homing of lymphocytes to gut-associated lymphoid tissue, but the significance of $ α_{4} $$ β_{7} $ in HIV-1 infection remains controversial. Here, using HIV-1 strain BaL, the gp120 of which was previously shown to be capable of interacting with $ α_{4} $$ β_{7} $, we demonstrated that $ α_{4} $$ β_{7} $ can mediate the binding of whole HIV-1 virions to $ α_{4} $$ β_{7} $-expressing transfectants. We further constructed a cell line stably expressing $ α_{4} $$ β_{7} $ and confirmed the $ α_{4} $$ β_{7} $-mediated HIV-1 binding. In primary lymphocytes with activated $ α_{4} $$ β_{7} $ expression, we also observed significant virus binding which can be inhibited by an anti-$ α_{4} $$ β_{7} $ antibody. Moreover, we investigated the impact of antagonizing $ α_{4} $$ β_{7} $ on HIV-1 infection of primary $ CD4^{+} $ T cells. In $ α_{4} $$ β_{7} $-activated $ CD4^{+} $ T cells, both anti-$ α_{4} $$ β_{7} $ antibodies and introduction of short-hairpin RNAs specifically targeting $ α_{4} $$ β_{7} $ resulted in a decreased HIV-1 infection. Our findings indicate that $ α_{4} $$ β_{7} $ may serve as an attachment factor at least for some HIV-1 strains. The established approach provides a promising means for the investigation of other viral strains to understand the potential roles of $ α_{4} $$ β_{7} $ in HIV-1 infection. | ||
650 | 4 | |a HIV-1 | |
650 | 4 | |a integrin α | |
650 | 4 | |a β | |
650 | 4 | |a binding | |
650 | 4 | |a infection | |
650 | 4 | |a RNA interference | |
650 | 4 | |a primary CD4 | |
650 | 4 | |a T cells | |
700 | 1 | |a Jin, Wei |4 aut | |
700 | 1 | |a Du, Tao |4 aut | |
700 | 1 | |a Wu, Biao |4 aut | |
700 | 1 | |a Liu, Yalan |4 aut | |
700 | 1 | |a Shattock, Robin J. |4 aut | |
700 | 1 | |a Hu, Qinxue |4 aut | |
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912 | |a GBV_ILN_2057 | ||
912 | |a GBV_ILN_2059 | ||
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912 | |a GBV_ILN_2064 | ||
912 | |a GBV_ILN_2065 | ||
912 | |a GBV_ILN_2068 | ||
912 | |a GBV_ILN_2070 | ||
912 | |a GBV_ILN_2086 | ||
912 | |a GBV_ILN_2088 | ||
912 | |a GBV_ILN_2093 | ||
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912 | |a GBV_ILN_2107 | ||
912 | |a GBV_ILN_2108 | ||
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912 | |a GBV_ILN_2113 | ||
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912 | |a GBV_ILN_2470 | ||
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912 | |a GBV_ILN_4338 | ||
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951 | |a AR | ||
952 | |d 29 |j 2014 |e 6 |c 12 |h 381-392 |