HIV-1 envelope, integrins and co-receptor use in mucosal transmission of HIV
Abstract It is well established that HIV-1 infection typically involves an interaction between the viral envelope protein gp120/41 and the CD4 molecule followed by a second interaction with a chemokine receptor, usually CCR5 or CXCR4. In the early stages of an HIV-1 infection CCR5 using viruses (R5...
Ausführliche Beschreibung
Gespeichert in:
| Autor*in: |
Cicala, Claudia [verfasserIn] |
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| Format: |
E-Artikel |
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| Sprache: |
Englisch |
| Erschienen: |
2011 |
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| Schlagwörter: |
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| Anmerkung: |
© Cicala et al; licensee BioMed Central Ltd. 2010 |
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| Übergeordnetes Werk: |
Enthalten in: Journal of translational medicine - London : BioMed Central, 2003, 9(2011), Suppl 1 vom: 27. Jan. |
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| Übergeordnetes Werk: |
volume:9 ; year:2011 ; number:Suppl 1 ; day:27 ; month:01 |
| Links: |
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| DOI / URN: |
10.1186/1479-5876-9-S1-S2 |
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| Katalog-ID: |
SPR028940717 |
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| 100 | 1 | |a Cicala, Claudia |e verfasserin |4 aut | |
| 245 | 1 | 0 | |a HIV-1 envelope, integrins and co-receptor use in mucosal transmission of HIV |
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| 520 | |a Abstract It is well established that HIV-1 infection typically involves an interaction between the viral envelope protein gp120/41 and the CD4 molecule followed by a second interaction with a chemokine receptor, usually CCR5 or CXCR4. In the early stages of an HIV-1 infection CCR5 using viruses (R5 viruses) predominate. In some viral subtypes there is a propensity to switch to CXCR4 usage (X4 viruses). The receptor switch occurs in ~ 40% of the infected individuals and is associated with faster disease progression. This holds for subtypes B and D, but occurs less frequently in subtypes A and C. There are several hypotheses to explain the preferential transmission of R5 viruses and the mechanisms that lead to switching of co-receptor usage; however, there is no definitive explanation for either. One important consideration regarding transmission is that signaling by R5 gp120 may facilitate transmission of R5 viruses by inducing a permissive environment for HIV replication. In the case of sexual transmission, infection by HIV requires the virus to breach the mucosal barrier to gain access to the immune cell targets that it infects; however, the immediate events that follow HIV exposure at genital mucosal sites are not well understood. Upon transmission, the HIV quasispecies that is replicating in an infected donor contracts through a “genetic bottleneck”, and often infection results from a single infectious event. Many details surrounding this initial infection remain unresolved. In mucosal tissues, $ CD4^{+} $ T cells express high levels of CCR5, and a subset of these $ CD4^{+} $/$ CCR5^{high} $ cells express the integrin $ α_{4} %$ β_{7} $, the gut homing receptor. $ CD4^{+} $/$ CCR5^{high} $/ $ α4β7^{high} $ T cells are highly susceptible to infection by HIV-1 and are ideal targets for an efficient productive infection at the point of transmission. In this context we have demonstrated that the HIV-1 envelope protein gp120 binds to $ α_{4} %$ β_{7} $ on $ CD4^{+} $ T cells. On $ CD4^{+} $/$ CCR5^{high} $/ $ α4β7^{high} $ T cells, $ α_{4} %$ β_{7} $ is closely associated with CD4 and CCR5. Furthermore, $ α_{4} %$ β_{7} $ is ~3 times the size of CD4 on the cell surface, that makes it a prominent receptor for an efficient virus capture. gp120-$ α_{4} %$ β_{7} $ interactions mediate the activation of the adhesion-associated integrin LFA-1. LFA-1 facilitates the formation of virological synapses and cell-to-cell spread of HIV-1. gp120 binding to $ α_{4} %$ β_{7} $ is mediated by a tripeptide located in the V1/V2 domain of gp120. Of note, the V1/V2 domain of gp120 has been linked to variations in transmission fitness among viral isolates raising the intriguing possibility that gp120-$ α_{4} %$ β_{7} $ interactions may be linked to transmission fitness. Although many details remain unresolved, we hypothesize that gp120-$ α_{4} %$ β_{7} $ interactions play an important role in the very early events following sexual transmission of HIV and may have important implication in the design of vaccine strategies for the prevention of acquisition of HIV infection | ||
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| 700 | 1 | |a Arthos, James |4 aut | |
| 700 | 1 | |a Fauci, Anthony S |4 aut | |
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10.1186/1479-5876-9-S1-S2 doi (DE-627)SPR028940717 (SPR)1479-5876-9-S1-S2-e DE-627 ger DE-627 rakwb eng Cicala, Claudia verfasserin aut HIV-1 envelope, integrins and co-receptor use in mucosal transmission of HIV 2011 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Cicala et al; licensee BioMed Central Ltd. 2010 Abstract It is well established that HIV-1 infection typically involves an interaction between the viral envelope protein gp120/41 and the CD4 molecule followed by a second interaction with a chemokine receptor, usually CCR5 or CXCR4. In the early stages of an HIV-1 infection CCR5 using viruses (R5 viruses) predominate. In some viral subtypes there is a propensity to switch to CXCR4 usage (X4 viruses). The receptor switch occurs in ~ 40% of the infected individuals and is associated with faster disease progression. This holds for subtypes B and D, but occurs less frequently in subtypes A and C. There are several hypotheses to explain the preferential transmission of R5 viruses and the mechanisms that lead to switching of co-receptor usage; however, there is no definitive explanation for either. One important consideration regarding transmission is that signaling by R5 gp120 may facilitate transmission of R5 viruses by inducing a permissive environment for HIV replication. In the case of sexual transmission, infection by HIV requires the virus to breach the mucosal barrier to gain access to the immune cell targets that it infects; however, the immediate events that follow HIV exposure at genital mucosal sites are not well understood. Upon transmission, the HIV quasispecies that is replicating in an infected donor contracts through a “genetic bottleneck”, and often infection results from a single infectious event. Many details surrounding this initial infection remain unresolved. In mucosal tissues, $ CD4^{+} $ T cells express high levels of CCR5, and a subset of these $ CD4^{+} $/$ CCR5^{high} $ cells express the integrin $ α_{4} %$ β_{7} $, the gut homing receptor. $ CD4^{+} $/$ CCR5^{high} $/ $ α4β7^{high} $ T cells are highly susceptible to infection by HIV-1 and are ideal targets for an efficient productive infection at the point of transmission. In this context we have demonstrated that the HIV-1 envelope protein gp120 binds to $ α_{4} %$ β_{7} $ on $ CD4^{+} $ T cells. On $ CD4^{+} $/$ CCR5^{high} $/ $ α4β7^{high} $ T cells, $ α_{4} %$ β_{7} $ is closely associated with CD4 and CCR5. Furthermore, $ α_{4} %$ β_{7} $ is ~3 times the size of CD4 on the cell surface, that makes it a prominent receptor for an efficient virus capture. gp120-$ α_{4} %$ β_{7} $ interactions mediate the activation of the adhesion-associated integrin LFA-1. LFA-1 facilitates the formation of virological synapses and cell-to-cell spread of HIV-1. gp120 binding to $ α_{4} %$ β_{7} $ is mediated by a tripeptide located in the V1/V2 domain of gp120. Of note, the V1/V2 domain of gp120 has been linked to variations in transmission fitness among viral isolates raising the intriguing possibility that gp120-$ α_{4} %$ β_{7} $ interactions may be linked to transmission fitness. Although many details remain unresolved, we hypothesize that gp120-$ α_{4} %$ β_{7} $ interactions play an important role in the very early events following sexual transmission of HIV and may have important implication in the design of vaccine strategies for the prevention of acquisition of HIV infection Variable Loop (dpeaa)DE-He213 Productive Infection (dpeaa)DE-He213 Immunological Synapse (dpeaa)DE-He213 Genital Mucosa (dpeaa)DE-He213 Virological Synapse (dpeaa)DE-He213 Arthos, James aut Fauci, Anthony S aut Enthalten in Journal of translational medicine London : BioMed Central, 2003 9(2011), Suppl 1 vom: 27. Jan. (DE-627)369084136 (DE-600)2118570-0 1479-5876 nnns volume:9 year:2011 number:Suppl 1 day:27 month:01 https://dx.doi.org/10.1186/1479-5876-9-S1-S2 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2009 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2055 GBV_ILN_2111 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 9 2011 Suppl 1 27 01 |
| spelling |
10.1186/1479-5876-9-S1-S2 doi (DE-627)SPR028940717 (SPR)1479-5876-9-S1-S2-e DE-627 ger DE-627 rakwb eng Cicala, Claudia verfasserin aut HIV-1 envelope, integrins and co-receptor use in mucosal transmission of HIV 2011 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Cicala et al; licensee BioMed Central Ltd. 2010 Abstract It is well established that HIV-1 infection typically involves an interaction between the viral envelope protein gp120/41 and the CD4 molecule followed by a second interaction with a chemokine receptor, usually CCR5 or CXCR4. In the early stages of an HIV-1 infection CCR5 using viruses (R5 viruses) predominate. In some viral subtypes there is a propensity to switch to CXCR4 usage (X4 viruses). The receptor switch occurs in ~ 40% of the infected individuals and is associated with faster disease progression. This holds for subtypes B and D, but occurs less frequently in subtypes A and C. There are several hypotheses to explain the preferential transmission of R5 viruses and the mechanisms that lead to switching of co-receptor usage; however, there is no definitive explanation for either. One important consideration regarding transmission is that signaling by R5 gp120 may facilitate transmission of R5 viruses by inducing a permissive environment for HIV replication. In the case of sexual transmission, infection by HIV requires the virus to breach the mucosal barrier to gain access to the immune cell targets that it infects; however, the immediate events that follow HIV exposure at genital mucosal sites are not well understood. Upon transmission, the HIV quasispecies that is replicating in an infected donor contracts through a “genetic bottleneck”, and often infection results from a single infectious event. Many details surrounding this initial infection remain unresolved. In mucosal tissues, $ CD4^{+} $ T cells express high levels of CCR5, and a subset of these $ CD4^{+} $/$ CCR5^{high} $ cells express the integrin $ α_{4} %$ β_{7} $, the gut homing receptor. $ CD4^{+} $/$ CCR5^{high} $/ $ α4β7^{high} $ T cells are highly susceptible to infection by HIV-1 and are ideal targets for an efficient productive infection at the point of transmission. In this context we have demonstrated that the HIV-1 envelope protein gp120 binds to $ α_{4} %$ β_{7} $ on $ CD4^{+} $ T cells. On $ CD4^{+} $/$ CCR5^{high} $/ $ α4β7^{high} $ T cells, $ α_{4} %$ β_{7} $ is closely associated with CD4 and CCR5. Furthermore, $ α_{4} %$ β_{7} $ is ~3 times the size of CD4 on the cell surface, that makes it a prominent receptor for an efficient virus capture. gp120-$ α_{4} %$ β_{7} $ interactions mediate the activation of the adhesion-associated integrin LFA-1. LFA-1 facilitates the formation of virological synapses and cell-to-cell spread of HIV-1. gp120 binding to $ α_{4} %$ β_{7} $ is mediated by a tripeptide located in the V1/V2 domain of gp120. Of note, the V1/V2 domain of gp120 has been linked to variations in transmission fitness among viral isolates raising the intriguing possibility that gp120-$ α_{4} %$ β_{7} $ interactions may be linked to transmission fitness. Although many details remain unresolved, we hypothesize that gp120-$ α_{4} %$ β_{7} $ interactions play an important role in the very early events following sexual transmission of HIV and may have important implication in the design of vaccine strategies for the prevention of acquisition of HIV infection Variable Loop (dpeaa)DE-He213 Productive Infection (dpeaa)DE-He213 Immunological Synapse (dpeaa)DE-He213 Genital Mucosa (dpeaa)DE-He213 Virological Synapse (dpeaa)DE-He213 Arthos, James aut Fauci, Anthony S aut Enthalten in Journal of translational medicine London : BioMed Central, 2003 9(2011), Suppl 1 vom: 27. Jan. (DE-627)369084136 (DE-600)2118570-0 1479-5876 nnns volume:9 year:2011 number:Suppl 1 day:27 month:01 https://dx.doi.org/10.1186/1479-5876-9-S1-S2 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2009 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2055 GBV_ILN_2111 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 9 2011 Suppl 1 27 01 |
| allfields_unstemmed |
10.1186/1479-5876-9-S1-S2 doi (DE-627)SPR028940717 (SPR)1479-5876-9-S1-S2-e DE-627 ger DE-627 rakwb eng Cicala, Claudia verfasserin aut HIV-1 envelope, integrins and co-receptor use in mucosal transmission of HIV 2011 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Cicala et al; licensee BioMed Central Ltd. 2010 Abstract It is well established that HIV-1 infection typically involves an interaction between the viral envelope protein gp120/41 and the CD4 molecule followed by a second interaction with a chemokine receptor, usually CCR5 or CXCR4. In the early stages of an HIV-1 infection CCR5 using viruses (R5 viruses) predominate. In some viral subtypes there is a propensity to switch to CXCR4 usage (X4 viruses). The receptor switch occurs in ~ 40% of the infected individuals and is associated with faster disease progression. This holds for subtypes B and D, but occurs less frequently in subtypes A and C. There are several hypotheses to explain the preferential transmission of R5 viruses and the mechanisms that lead to switching of co-receptor usage; however, there is no definitive explanation for either. One important consideration regarding transmission is that signaling by R5 gp120 may facilitate transmission of R5 viruses by inducing a permissive environment for HIV replication. In the case of sexual transmission, infection by HIV requires the virus to breach the mucosal barrier to gain access to the immune cell targets that it infects; however, the immediate events that follow HIV exposure at genital mucosal sites are not well understood. Upon transmission, the HIV quasispecies that is replicating in an infected donor contracts through a “genetic bottleneck”, and often infection results from a single infectious event. Many details surrounding this initial infection remain unresolved. In mucosal tissues, $ CD4^{+} $ T cells express high levels of CCR5, and a subset of these $ CD4^{+} $/$ CCR5^{high} $ cells express the integrin $ α_{4} %$ β_{7} $, the gut homing receptor. $ CD4^{+} $/$ CCR5^{high} $/ $ α4β7^{high} $ T cells are highly susceptible to infection by HIV-1 and are ideal targets for an efficient productive infection at the point of transmission. In this context we have demonstrated that the HIV-1 envelope protein gp120 binds to $ α_{4} %$ β_{7} $ on $ CD4^{+} $ T cells. On $ CD4^{+} $/$ CCR5^{high} $/ $ α4β7^{high} $ T cells, $ α_{4} %$ β_{7} $ is closely associated with CD4 and CCR5. Furthermore, $ α_{4} %$ β_{7} $ is ~3 times the size of CD4 on the cell surface, that makes it a prominent receptor for an efficient virus capture. gp120-$ α_{4} %$ β_{7} $ interactions mediate the activation of the adhesion-associated integrin LFA-1. LFA-1 facilitates the formation of virological synapses and cell-to-cell spread of HIV-1. gp120 binding to $ α_{4} %$ β_{7} $ is mediated by a tripeptide located in the V1/V2 domain of gp120. Of note, the V1/V2 domain of gp120 has been linked to variations in transmission fitness among viral isolates raising the intriguing possibility that gp120-$ α_{4} %$ β_{7} $ interactions may be linked to transmission fitness. Although many details remain unresolved, we hypothesize that gp120-$ α_{4} %$ β_{7} $ interactions play an important role in the very early events following sexual transmission of HIV and may have important implication in the design of vaccine strategies for the prevention of acquisition of HIV infection Variable Loop (dpeaa)DE-He213 Productive Infection (dpeaa)DE-He213 Immunological Synapse (dpeaa)DE-He213 Genital Mucosa (dpeaa)DE-He213 Virological Synapse (dpeaa)DE-He213 Arthos, James aut Fauci, Anthony S aut Enthalten in Journal of translational medicine London : BioMed Central, 2003 9(2011), Suppl 1 vom: 27. Jan. (DE-627)369084136 (DE-600)2118570-0 1479-5876 nnns volume:9 year:2011 number:Suppl 1 day:27 month:01 https://dx.doi.org/10.1186/1479-5876-9-S1-S2 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2009 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2055 GBV_ILN_2111 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 9 2011 Suppl 1 27 01 |
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10.1186/1479-5876-9-S1-S2 doi (DE-627)SPR028940717 (SPR)1479-5876-9-S1-S2-e DE-627 ger DE-627 rakwb eng Cicala, Claudia verfasserin aut HIV-1 envelope, integrins and co-receptor use in mucosal transmission of HIV 2011 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Cicala et al; licensee BioMed Central Ltd. 2010 Abstract It is well established that HIV-1 infection typically involves an interaction between the viral envelope protein gp120/41 and the CD4 molecule followed by a second interaction with a chemokine receptor, usually CCR5 or CXCR4. In the early stages of an HIV-1 infection CCR5 using viruses (R5 viruses) predominate. In some viral subtypes there is a propensity to switch to CXCR4 usage (X4 viruses). The receptor switch occurs in ~ 40% of the infected individuals and is associated with faster disease progression. This holds for subtypes B and D, but occurs less frequently in subtypes A and C. There are several hypotheses to explain the preferential transmission of R5 viruses and the mechanisms that lead to switching of co-receptor usage; however, there is no definitive explanation for either. One important consideration regarding transmission is that signaling by R5 gp120 may facilitate transmission of R5 viruses by inducing a permissive environment for HIV replication. In the case of sexual transmission, infection by HIV requires the virus to breach the mucosal barrier to gain access to the immune cell targets that it infects; however, the immediate events that follow HIV exposure at genital mucosal sites are not well understood. Upon transmission, the HIV quasispecies that is replicating in an infected donor contracts through a “genetic bottleneck”, and often infection results from a single infectious event. Many details surrounding this initial infection remain unresolved. In mucosal tissues, $ CD4^{+} $ T cells express high levels of CCR5, and a subset of these $ CD4^{+} $/$ CCR5^{high} $ cells express the integrin $ α_{4} %$ β_{7} $, the gut homing receptor. $ CD4^{+} $/$ CCR5^{high} $/ $ α4β7^{high} $ T cells are highly susceptible to infection by HIV-1 and are ideal targets for an efficient productive infection at the point of transmission. In this context we have demonstrated that the HIV-1 envelope protein gp120 binds to $ α_{4} %$ β_{7} $ on $ CD4^{+} $ T cells. On $ CD4^{+} $/$ CCR5^{high} $/ $ α4β7^{high} $ T cells, $ α_{4} %$ β_{7} $ is closely associated with CD4 and CCR5. Furthermore, $ α_{4} %$ β_{7} $ is ~3 times the size of CD4 on the cell surface, that makes it a prominent receptor for an efficient virus capture. gp120-$ α_{4} %$ β_{7} $ interactions mediate the activation of the adhesion-associated integrin LFA-1. LFA-1 facilitates the formation of virological synapses and cell-to-cell spread of HIV-1. gp120 binding to $ α_{4} %$ β_{7} $ is mediated by a tripeptide located in the V1/V2 domain of gp120. Of note, the V1/V2 domain of gp120 has been linked to variations in transmission fitness among viral isolates raising the intriguing possibility that gp120-$ α_{4} %$ β_{7} $ interactions may be linked to transmission fitness. Although many details remain unresolved, we hypothesize that gp120-$ α_{4} %$ β_{7} $ interactions play an important role in the very early events following sexual transmission of HIV and may have important implication in the design of vaccine strategies for the prevention of acquisition of HIV infection Variable Loop (dpeaa)DE-He213 Productive Infection (dpeaa)DE-He213 Immunological Synapse (dpeaa)DE-He213 Genital Mucosa (dpeaa)DE-He213 Virological Synapse (dpeaa)DE-He213 Arthos, James aut Fauci, Anthony S aut Enthalten in Journal of translational medicine London : BioMed Central, 2003 9(2011), Suppl 1 vom: 27. Jan. (DE-627)369084136 (DE-600)2118570-0 1479-5876 nnns volume:9 year:2011 number:Suppl 1 day:27 month:01 https://dx.doi.org/10.1186/1479-5876-9-S1-S2 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2009 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2055 GBV_ILN_2111 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 9 2011 Suppl 1 27 01 |
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10.1186/1479-5876-9-S1-S2 doi (DE-627)SPR028940717 (SPR)1479-5876-9-S1-S2-e DE-627 ger DE-627 rakwb eng Cicala, Claudia verfasserin aut HIV-1 envelope, integrins and co-receptor use in mucosal transmission of HIV 2011 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Cicala et al; licensee BioMed Central Ltd. 2010 Abstract It is well established that HIV-1 infection typically involves an interaction between the viral envelope protein gp120/41 and the CD4 molecule followed by a second interaction with a chemokine receptor, usually CCR5 or CXCR4. In the early stages of an HIV-1 infection CCR5 using viruses (R5 viruses) predominate. In some viral subtypes there is a propensity to switch to CXCR4 usage (X4 viruses). The receptor switch occurs in ~ 40% of the infected individuals and is associated with faster disease progression. This holds for subtypes B and D, but occurs less frequently in subtypes A and C. There are several hypotheses to explain the preferential transmission of R5 viruses and the mechanisms that lead to switching of co-receptor usage; however, there is no definitive explanation for either. One important consideration regarding transmission is that signaling by R5 gp120 may facilitate transmission of R5 viruses by inducing a permissive environment for HIV replication. In the case of sexual transmission, infection by HIV requires the virus to breach the mucosal barrier to gain access to the immune cell targets that it infects; however, the immediate events that follow HIV exposure at genital mucosal sites are not well understood. Upon transmission, the HIV quasispecies that is replicating in an infected donor contracts through a “genetic bottleneck”, and often infection results from a single infectious event. Many details surrounding this initial infection remain unresolved. In mucosal tissues, $ CD4^{+} $ T cells express high levels of CCR5, and a subset of these $ CD4^{+} $/$ CCR5^{high} $ cells express the integrin $ α_{4} %$ β_{7} $, the gut homing receptor. $ CD4^{+} $/$ CCR5^{high} $/ $ α4β7^{high} $ T cells are highly susceptible to infection by HIV-1 and are ideal targets for an efficient productive infection at the point of transmission. In this context we have demonstrated that the HIV-1 envelope protein gp120 binds to $ α_{4} %$ β_{7} $ on $ CD4^{+} $ T cells. On $ CD4^{+} $/$ CCR5^{high} $/ $ α4β7^{high} $ T cells, $ α_{4} %$ β_{7} $ is closely associated with CD4 and CCR5. Furthermore, $ α_{4} %$ β_{7} $ is ~3 times the size of CD4 on the cell surface, that makes it a prominent receptor for an efficient virus capture. gp120-$ α_{4} %$ β_{7} $ interactions mediate the activation of the adhesion-associated integrin LFA-1. LFA-1 facilitates the formation of virological synapses and cell-to-cell spread of HIV-1. gp120 binding to $ α_{4} %$ β_{7} $ is mediated by a tripeptide located in the V1/V2 domain of gp120. Of note, the V1/V2 domain of gp120 has been linked to variations in transmission fitness among viral isolates raising the intriguing possibility that gp120-$ α_{4} %$ β_{7} $ interactions may be linked to transmission fitness. Although many details remain unresolved, we hypothesize that gp120-$ α_{4} %$ β_{7} $ interactions play an important role in the very early events following sexual transmission of HIV and may have important implication in the design of vaccine strategies for the prevention of acquisition of HIV infection Variable Loop (dpeaa)DE-He213 Productive Infection (dpeaa)DE-He213 Immunological Synapse (dpeaa)DE-He213 Genital Mucosa (dpeaa)DE-He213 Virological Synapse (dpeaa)DE-He213 Arthos, James aut Fauci, Anthony S aut Enthalten in Journal of translational medicine London : BioMed Central, 2003 9(2011), Suppl 1 vom: 27. Jan. (DE-627)369084136 (DE-600)2118570-0 1479-5876 nnns volume:9 year:2011 number:Suppl 1 day:27 month:01 https://dx.doi.org/10.1186/1479-5876-9-S1-S2 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2009 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2055 GBV_ILN_2111 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 9 2011 Suppl 1 27 01 |
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HIV-1 envelope, integrins and co-receptor use in mucosal transmission of HIV Variable Loop (dpeaa)DE-He213 Productive Infection (dpeaa)DE-He213 Immunological Synapse (dpeaa)DE-He213 Genital Mucosa (dpeaa)DE-He213 Virological Synapse (dpeaa)DE-He213 |
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hiv-1 envelope, integrins and co-receptor use in mucosal transmission of hiv |
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HIV-1 envelope, integrins and co-receptor use in mucosal transmission of HIV |
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Abstract It is well established that HIV-1 infection typically involves an interaction between the viral envelope protein gp120/41 and the CD4 molecule followed by a second interaction with a chemokine receptor, usually CCR5 or CXCR4. In the early stages of an HIV-1 infection CCR5 using viruses (R5 viruses) predominate. In some viral subtypes there is a propensity to switch to CXCR4 usage (X4 viruses). The receptor switch occurs in ~ 40% of the infected individuals and is associated with faster disease progression. This holds for subtypes B and D, but occurs less frequently in subtypes A and C. There are several hypotheses to explain the preferential transmission of R5 viruses and the mechanisms that lead to switching of co-receptor usage; however, there is no definitive explanation for either. One important consideration regarding transmission is that signaling by R5 gp120 may facilitate transmission of R5 viruses by inducing a permissive environment for HIV replication. In the case of sexual transmission, infection by HIV requires the virus to breach the mucosal barrier to gain access to the immune cell targets that it infects; however, the immediate events that follow HIV exposure at genital mucosal sites are not well understood. Upon transmission, the HIV quasispecies that is replicating in an infected donor contracts through a “genetic bottleneck”, and often infection results from a single infectious event. Many details surrounding this initial infection remain unresolved. In mucosal tissues, $ CD4^{+} $ T cells express high levels of CCR5, and a subset of these $ CD4^{+} $/$ CCR5^{high} $ cells express the integrin $ α_{4} %$ β_{7} $, the gut homing receptor. $ CD4^{+} $/$ CCR5^{high} $/ $ α4β7^{high} $ T cells are highly susceptible to infection by HIV-1 and are ideal targets for an efficient productive infection at the point of transmission. In this context we have demonstrated that the HIV-1 envelope protein gp120 binds to $ α_{4} %$ β_{7} $ on $ CD4^{+} $ T cells. On $ CD4^{+} $/$ CCR5^{high} $/ $ α4β7^{high} $ T cells, $ α_{4} %$ β_{7} $ is closely associated with CD4 and CCR5. Furthermore, $ α_{4} %$ β_{7} $ is ~3 times the size of CD4 on the cell surface, that makes it a prominent receptor for an efficient virus capture. gp120-$ α_{4} %$ β_{7} $ interactions mediate the activation of the adhesion-associated integrin LFA-1. LFA-1 facilitates the formation of virological synapses and cell-to-cell spread of HIV-1. gp120 binding to $ α_{4} %$ β_{7} $ is mediated by a tripeptide located in the V1/V2 domain of gp120. Of note, the V1/V2 domain of gp120 has been linked to variations in transmission fitness among viral isolates raising the intriguing possibility that gp120-$ α_{4} %$ β_{7} $ interactions may be linked to transmission fitness. Although many details remain unresolved, we hypothesize that gp120-$ α_{4} %$ β_{7} $ interactions play an important role in the very early events following sexual transmission of HIV and may have important implication in the design of vaccine strategies for the prevention of acquisition of HIV infection © Cicala et al; licensee BioMed Central Ltd. 2010 |
| abstractGer |
Abstract It is well established that HIV-1 infection typically involves an interaction between the viral envelope protein gp120/41 and the CD4 molecule followed by a second interaction with a chemokine receptor, usually CCR5 or CXCR4. In the early stages of an HIV-1 infection CCR5 using viruses (R5 viruses) predominate. In some viral subtypes there is a propensity to switch to CXCR4 usage (X4 viruses). The receptor switch occurs in ~ 40% of the infected individuals and is associated with faster disease progression. This holds for subtypes B and D, but occurs less frequently in subtypes A and C. There are several hypotheses to explain the preferential transmission of R5 viruses and the mechanisms that lead to switching of co-receptor usage; however, there is no definitive explanation for either. One important consideration regarding transmission is that signaling by R5 gp120 may facilitate transmission of R5 viruses by inducing a permissive environment for HIV replication. In the case of sexual transmission, infection by HIV requires the virus to breach the mucosal barrier to gain access to the immune cell targets that it infects; however, the immediate events that follow HIV exposure at genital mucosal sites are not well understood. Upon transmission, the HIV quasispecies that is replicating in an infected donor contracts through a “genetic bottleneck”, and often infection results from a single infectious event. Many details surrounding this initial infection remain unresolved. In mucosal tissues, $ CD4^{+} $ T cells express high levels of CCR5, and a subset of these $ CD4^{+} $/$ CCR5^{high} $ cells express the integrin $ α_{4} %$ β_{7} $, the gut homing receptor. $ CD4^{+} $/$ CCR5^{high} $/ $ α4β7^{high} $ T cells are highly susceptible to infection by HIV-1 and are ideal targets for an efficient productive infection at the point of transmission. In this context we have demonstrated that the HIV-1 envelope protein gp120 binds to $ α_{4} %$ β_{7} $ on $ CD4^{+} $ T cells. On $ CD4^{+} $/$ CCR5^{high} $/ $ α4β7^{high} $ T cells, $ α_{4} %$ β_{7} $ is closely associated with CD4 and CCR5. Furthermore, $ α_{4} %$ β_{7} $ is ~3 times the size of CD4 on the cell surface, that makes it a prominent receptor for an efficient virus capture. gp120-$ α_{4} %$ β_{7} $ interactions mediate the activation of the adhesion-associated integrin LFA-1. LFA-1 facilitates the formation of virological synapses and cell-to-cell spread of HIV-1. gp120 binding to $ α_{4} %$ β_{7} $ is mediated by a tripeptide located in the V1/V2 domain of gp120. Of note, the V1/V2 domain of gp120 has been linked to variations in transmission fitness among viral isolates raising the intriguing possibility that gp120-$ α_{4} %$ β_{7} $ interactions may be linked to transmission fitness. Although many details remain unresolved, we hypothesize that gp120-$ α_{4} %$ β_{7} $ interactions play an important role in the very early events following sexual transmission of HIV and may have important implication in the design of vaccine strategies for the prevention of acquisition of HIV infection © Cicala et al; licensee BioMed Central Ltd. 2010 |
| abstract_unstemmed |
Abstract It is well established that HIV-1 infection typically involves an interaction between the viral envelope protein gp120/41 and the CD4 molecule followed by a second interaction with a chemokine receptor, usually CCR5 or CXCR4. In the early stages of an HIV-1 infection CCR5 using viruses (R5 viruses) predominate. In some viral subtypes there is a propensity to switch to CXCR4 usage (X4 viruses). The receptor switch occurs in ~ 40% of the infected individuals and is associated with faster disease progression. This holds for subtypes B and D, but occurs less frequently in subtypes A and C. There are several hypotheses to explain the preferential transmission of R5 viruses and the mechanisms that lead to switching of co-receptor usage; however, there is no definitive explanation for either. One important consideration regarding transmission is that signaling by R5 gp120 may facilitate transmission of R5 viruses by inducing a permissive environment for HIV replication. In the case of sexual transmission, infection by HIV requires the virus to breach the mucosal barrier to gain access to the immune cell targets that it infects; however, the immediate events that follow HIV exposure at genital mucosal sites are not well understood. Upon transmission, the HIV quasispecies that is replicating in an infected donor contracts through a “genetic bottleneck”, and often infection results from a single infectious event. Many details surrounding this initial infection remain unresolved. In mucosal tissues, $ CD4^{+} $ T cells express high levels of CCR5, and a subset of these $ CD4^{+} $/$ CCR5^{high} $ cells express the integrin $ α_{4} %$ β_{7} $, the gut homing receptor. $ CD4^{+} $/$ CCR5^{high} $/ $ α4β7^{high} $ T cells are highly susceptible to infection by HIV-1 and are ideal targets for an efficient productive infection at the point of transmission. In this context we have demonstrated that the HIV-1 envelope protein gp120 binds to $ α_{4} %$ β_{7} $ on $ CD4^{+} $ T cells. On $ CD4^{+} $/$ CCR5^{high} $/ $ α4β7^{high} $ T cells, $ α_{4} %$ β_{7} $ is closely associated with CD4 and CCR5. Furthermore, $ α_{4} %$ β_{7} $ is ~3 times the size of CD4 on the cell surface, that makes it a prominent receptor for an efficient virus capture. gp120-$ α_{4} %$ β_{7} $ interactions mediate the activation of the adhesion-associated integrin LFA-1. LFA-1 facilitates the formation of virological synapses and cell-to-cell spread of HIV-1. gp120 binding to $ α_{4} %$ β_{7} $ is mediated by a tripeptide located in the V1/V2 domain of gp120. Of note, the V1/V2 domain of gp120 has been linked to variations in transmission fitness among viral isolates raising the intriguing possibility that gp120-$ α_{4} %$ β_{7} $ interactions may be linked to transmission fitness. Although many details remain unresolved, we hypothesize that gp120-$ α_{4} %$ β_{7} $ interactions play an important role in the very early events following sexual transmission of HIV and may have important implication in the design of vaccine strategies for the prevention of acquisition of HIV infection © Cicala et al; licensee BioMed Central Ltd. 2010 |
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| score |
7.3984814 |