VIRAL PERSISTENCE: HIV's Strategies of Immune System Evasion
Abstract In contrast to most animal viruses, infection with the human and simian immunodeficiency viruses results in prolonged, continuous viral replication in the infected host. Remarkably, viral persistence is not thwarted by the presence of apparently vigorous, virus-specific immune responses. Se...
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E-Artikel |
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2002 |
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20 |
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Annual Reviews Electronic Back Volume Collection 1932-2005ff |
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in: Annual review of medicine - Palo Alto, Calif. : Annual Reviews, 1950, 53(2002), Seite 499-518 |
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volume:53 ; year:2002 ; pages:499-518 ; extent:20 |
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| 520 | |a Abstract In contrast to most animal viruses, infection with the human and simian immunodeficiency viruses results in prolonged, continuous viral replication in the infected host. Remarkably, viral persistence is not thwarted by the presence of apparently vigorous, virus-specific immune responses. Several factors are thought to contribute to persistent viral replication, most notably the destruction of virus-specific T helper cells, the emergence of antigenic escape variants, and the expression of an envelope complex that structurally minimizes antibody access to conserved epitopes. Not as well understood, though potentially important, is the ability of at least one viral encoded protein (Nef) to prevent presentation of viral antigens in the context of major histocompatibility complex. The future success of antiviral therapies and vaccination strategies may depend largely on understanding how and to what degree each of these factors (and presumably others) contributes to immune evasion. | ||
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(DE-627)NLEJ164129685 DE-627 ger DE-627 rakwb VIRAL PERSISTENCE: HIV's Strategies of Immune System Evasion 2002 20 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Abstract In contrast to most animal viruses, infection with the human and simian immunodeficiency viruses results in prolonged, continuous viral replication in the infected host. Remarkably, viral persistence is not thwarted by the presence of apparently vigorous, virus-specific immune responses. Several factors are thought to contribute to persistent viral replication, most notably the destruction of virus-specific T helper cells, the emergence of antigenic escape variants, and the expression of an envelope complex that structurally minimizes antibody access to conserved epitopes. Not as well understood, though potentially important, is the ability of at least one viral encoded protein (Nef) to prevent presentation of viral antigens in the context of major histocompatibility complex. The future success of antiviral therapies and vaccination strategies may depend largely on understanding how and to what degree each of these factors (and presumably others) contributes to immune evasion. Annual Reviews Electronic Back Volume Collection 1932-2005ff Johnson, Welkin E. oth Desrosiers, Ronald C. oth in Annual review of medicine Palo Alto, Calif. : Annual Reviews, 1950 53(2002), Seite 499-518 Online-Ressource (DE-627)NLEJ164018786 (DE-600)1481484-5 1545-326X nnns volume:53 year:2002 pages:499-518 extent:20 http://dx.doi.org/10.1146/annurev.med.53.082901.104053 text/html Deutschlandweit zugänglich GBV_USEFLAG_U ZDB-1-ANR GBV_NL_ARTICLE AR 53 2002 499-518 20 |
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(DE-627)NLEJ164129685 DE-627 ger DE-627 rakwb VIRAL PERSISTENCE: HIV's Strategies of Immune System Evasion 2002 20 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Abstract In contrast to most animal viruses, infection with the human and simian immunodeficiency viruses results in prolonged, continuous viral replication in the infected host. Remarkably, viral persistence is not thwarted by the presence of apparently vigorous, virus-specific immune responses. Several factors are thought to contribute to persistent viral replication, most notably the destruction of virus-specific T helper cells, the emergence of antigenic escape variants, and the expression of an envelope complex that structurally minimizes antibody access to conserved epitopes. Not as well understood, though potentially important, is the ability of at least one viral encoded protein (Nef) to prevent presentation of viral antigens in the context of major histocompatibility complex. The future success of antiviral therapies and vaccination strategies may depend largely on understanding how and to what degree each of these factors (and presumably others) contributes to immune evasion. Annual Reviews Electronic Back Volume Collection 1932-2005ff Johnson, Welkin E. oth Desrosiers, Ronald C. oth in Annual review of medicine Palo Alto, Calif. : Annual Reviews, 1950 53(2002), Seite 499-518 Online-Ressource (DE-627)NLEJ164018786 (DE-600)1481484-5 1545-326X nnns volume:53 year:2002 pages:499-518 extent:20 http://dx.doi.org/10.1146/annurev.med.53.082901.104053 text/html Deutschlandweit zugänglich GBV_USEFLAG_U ZDB-1-ANR GBV_NL_ARTICLE AR 53 2002 499-518 20 |
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(DE-627)NLEJ164129685 DE-627 ger DE-627 rakwb VIRAL PERSISTENCE: HIV's Strategies of Immune System Evasion 2002 20 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Abstract In contrast to most animal viruses, infection with the human and simian immunodeficiency viruses results in prolonged, continuous viral replication in the infected host. Remarkably, viral persistence is not thwarted by the presence of apparently vigorous, virus-specific immune responses. Several factors are thought to contribute to persistent viral replication, most notably the destruction of virus-specific T helper cells, the emergence of antigenic escape variants, and the expression of an envelope complex that structurally minimizes antibody access to conserved epitopes. Not as well understood, though potentially important, is the ability of at least one viral encoded protein (Nef) to prevent presentation of viral antigens in the context of major histocompatibility complex. The future success of antiviral therapies and vaccination strategies may depend largely on understanding how and to what degree each of these factors (and presumably others) contributes to immune evasion. Annual Reviews Electronic Back Volume Collection 1932-2005ff Johnson, Welkin E. oth Desrosiers, Ronald C. oth in Annual review of medicine Palo Alto, Calif. : Annual Reviews, 1950 53(2002), Seite 499-518 Online-Ressource (DE-627)NLEJ164018786 (DE-600)1481484-5 1545-326X nnns volume:53 year:2002 pages:499-518 extent:20 http://dx.doi.org/10.1146/annurev.med.53.082901.104053 text/html Deutschlandweit zugänglich GBV_USEFLAG_U ZDB-1-ANR GBV_NL_ARTICLE AR 53 2002 499-518 20 |
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(DE-627)NLEJ164129685 DE-627 ger DE-627 rakwb VIRAL PERSISTENCE: HIV's Strategies of Immune System Evasion 2002 20 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Abstract In contrast to most animal viruses, infection with the human and simian immunodeficiency viruses results in prolonged, continuous viral replication in the infected host. Remarkably, viral persistence is not thwarted by the presence of apparently vigorous, virus-specific immune responses. Several factors are thought to contribute to persistent viral replication, most notably the destruction of virus-specific T helper cells, the emergence of antigenic escape variants, and the expression of an envelope complex that structurally minimizes antibody access to conserved epitopes. Not as well understood, though potentially important, is the ability of at least one viral encoded protein (Nef) to prevent presentation of viral antigens in the context of major histocompatibility complex. The future success of antiviral therapies and vaccination strategies may depend largely on understanding how and to what degree each of these factors (and presumably others) contributes to immune evasion. Annual Reviews Electronic Back Volume Collection 1932-2005ff Johnson, Welkin E. oth Desrosiers, Ronald C. oth in Annual review of medicine Palo Alto, Calif. : Annual Reviews, 1950 53(2002), Seite 499-518 Online-Ressource (DE-627)NLEJ164018786 (DE-600)1481484-5 1545-326X nnns volume:53 year:2002 pages:499-518 extent:20 http://dx.doi.org/10.1146/annurev.med.53.082901.104053 text/html Deutschlandweit zugänglich GBV_USEFLAG_U ZDB-1-ANR GBV_NL_ARTICLE AR 53 2002 499-518 20 |
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(DE-627)NLEJ164129685 DE-627 ger DE-627 rakwb VIRAL PERSISTENCE: HIV's Strategies of Immune System Evasion 2002 20 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Abstract In contrast to most animal viruses, infection with the human and simian immunodeficiency viruses results in prolonged, continuous viral replication in the infected host. Remarkably, viral persistence is not thwarted by the presence of apparently vigorous, virus-specific immune responses. Several factors are thought to contribute to persistent viral replication, most notably the destruction of virus-specific T helper cells, the emergence of antigenic escape variants, and the expression of an envelope complex that structurally minimizes antibody access to conserved epitopes. Not as well understood, though potentially important, is the ability of at least one viral encoded protein (Nef) to prevent presentation of viral antigens in the context of major histocompatibility complex. The future success of antiviral therapies and vaccination strategies may depend largely on understanding how and to what degree each of these factors (and presumably others) contributes to immune evasion. Annual Reviews Electronic Back Volume Collection 1932-2005ff Johnson, Welkin E. oth Desrosiers, Ronald C. oth in Annual review of medicine Palo Alto, Calif. : Annual Reviews, 1950 53(2002), Seite 499-518 Online-Ressource (DE-627)NLEJ164018786 (DE-600)1481484-5 1545-326X nnns volume:53 year:2002 pages:499-518 extent:20 http://dx.doi.org/10.1146/annurev.med.53.082901.104053 text/html Deutschlandweit zugänglich GBV_USEFLAG_U ZDB-1-ANR GBV_NL_ARTICLE AR 53 2002 499-518 20 |
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Abstract In contrast to most animal viruses, infection with the human and simian immunodeficiency viruses results in prolonged, continuous viral replication in the infected host. Remarkably, viral persistence is not thwarted by the presence of apparently vigorous, virus-specific immune responses. Several factors are thought to contribute to persistent viral replication, most notably the destruction of virus-specific T helper cells, the emergence of antigenic escape variants, and the expression of an envelope complex that structurally minimizes antibody access to conserved epitopes. Not as well understood, though potentially important, is the ability of at least one viral encoded protein (Nef) to prevent presentation of viral antigens in the context of major histocompatibility complex. The future success of antiviral therapies and vaccination strategies may depend largely on understanding how and to what degree each of these factors (and presumably others) contributes to immune evasion. |
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Abstract In contrast to most animal viruses, infection with the human and simian immunodeficiency viruses results in prolonged, continuous viral replication in the infected host. Remarkably, viral persistence is not thwarted by the presence of apparently vigorous, virus-specific immune responses. Several factors are thought to contribute to persistent viral replication, most notably the destruction of virus-specific T helper cells, the emergence of antigenic escape variants, and the expression of an envelope complex that structurally minimizes antibody access to conserved epitopes. Not as well understood, though potentially important, is the ability of at least one viral encoded protein (Nef) to prevent presentation of viral antigens in the context of major histocompatibility complex. The future success of antiviral therapies and vaccination strategies may depend largely on understanding how and to what degree each of these factors (and presumably others) contributes to immune evasion. |
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Abstract In contrast to most animal viruses, infection with the human and simian immunodeficiency viruses results in prolonged, continuous viral replication in the infected host. Remarkably, viral persistence is not thwarted by the presence of apparently vigorous, virus-specific immune responses. Several factors are thought to contribute to persistent viral replication, most notably the destruction of virus-specific T helper cells, the emergence of antigenic escape variants, and the expression of an envelope complex that structurally minimizes antibody access to conserved epitopes. Not as well understood, though potentially important, is the ability of at least one viral encoded protein (Nef) to prevent presentation of viral antigens in the context of major histocompatibility complex. The future success of antiviral therapies and vaccination strategies may depend largely on understanding how and to what degree each of these factors (and presumably others) contributes to immune evasion. |
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