Virus replication and evolution drive the kinetics and specificity of SIV-specific cytotoxic T lymphocytes
Summary: SIV (simian immunodeficiency virus) infection of cynomolgus macaques provides an excellent model for investigating the basis of protective immunity against HIV (human immunodeficiency virus). We explored the protective role of cytotoxic T lymphocytes (CTL) against the pathogenic molecular c...
Ausführliche Beschreibung
Gespeichert in:
| Autor*in: |
Geretti, Anna Maria [verfasserIn] Osterhaus, Albert D. M. E. [verfasserIn] |
|---|
| Format: |
E-Artikel |
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| Erschienen: |
Copenhagen: Munksgaard International Publishers ; 2001 |
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| Umfang: |
Online-Ressource |
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| Reproduktion: |
2002 ; Blackwell Publishing Journal Backfiles 1879-2005 |
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| Übergeordnetes Werk: |
In: Immunological reviews - Oxford : Wiley-Blackwell, 1969, 183(2001), 1, Seite 0 |
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volume:183 ; year:2001 ; number:1 ; pages:0 |
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| DOI / URN: |
10.1034/j.1600-065x.2001.1830109.x |
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| 520 | |a Summary: SIV (simian immunodeficiency virus) infection of cynomolgus macaques provides an excellent model for investigating the basis of protective immunity against HIV (human immunodeficiency virus). We explored the protective role of cytotoxic T lymphocytes (CTL) against the pathogenic molecular clone SIVmac-J5. Vaccine-induced CTL precursors (CTLp) against Env, Gag or Nef did not protect macaques against intravenous challenge. However, detection of Rev-specific CTLp in infected macaques was associated with effective virus containment. Furthermore, CTL against an immunodominant Gag/p26 epitope (amino acids 242–250) resulted in the emergence of a mutant virus that uniformly replaced wild-type virus in the spleen and partially escaped recognition. During primary infection, CTLp detection in blood coincided with decreasing viremia. After 12 months, two outcomes emerged. In one group of macaques, persistent viremia was associated with high viral load in lymphoid organs and declining CD4+ T-cell counts. CTLp were maintained in asymptomatic macaques, but declined in the symptomatic phase of infection. In a second group, loss of detectable viremia was associated with low-level virus reservoirs in lymphoid organs, asymptomatic status and maintained CD4+ T-cell counts. CTLp peaked in the first 4 months of infection and subsequently declined in this group. These studies provide insights into the complex interplay between virus replication and host immunity. | ||
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10.1034/j.1600-065x.2001.1830109.x doi (DE-627)NLEJ242662609 DE-627 ger DE-627 rakwb Geretti, Anna Maria verfasserin aut Virus replication and evolution drive the kinetics and specificity of SIV-specific cytotoxic T lymphocytes Copenhagen Munksgaard International Publishers 2001 Online-Ressource nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Summary: SIV (simian immunodeficiency virus) infection of cynomolgus macaques provides an excellent model for investigating the basis of protective immunity against HIV (human immunodeficiency virus). We explored the protective role of cytotoxic T lymphocytes (CTL) against the pathogenic molecular clone SIVmac-J5. Vaccine-induced CTL precursors (CTLp) against Env, Gag or Nef did not protect macaques against intravenous challenge. However, detection of Rev-specific CTLp in infected macaques was associated with effective virus containment. Furthermore, CTL against an immunodominant Gag/p26 epitope (amino acids 242–250) resulted in the emergence of a mutant virus that uniformly replaced wild-type virus in the spleen and partially escaped recognition. During primary infection, CTLp detection in blood coincided with decreasing viremia. After 12 months, two outcomes emerged. In one group of macaques, persistent viremia was associated with high viral load in lymphoid organs and declining CD4+ T-cell counts. CTLp were maintained in asymptomatic macaques, but declined in the symptomatic phase of infection. In a second group, loss of detectable viremia was associated with low-level virus reservoirs in lymphoid organs, asymptomatic status and maintained CD4+ T-cell counts. CTLp peaked in the first 4 months of infection and subsequently declined in this group. These studies provide insights into the complex interplay between virus replication and host immunity. 2002 Blackwell Publishing Journal Backfiles 1879-2005 |2002|||||||||| Osterhaus, Albert D. M. E. verfasserin aut In Immunological reviews Oxford : Wiley-Blackwell, 1969 183(2001), 1, Seite 0 Online-Ressource (DE-627)NLEJ243927398 (DE-600)2038276-5 1600-065X volume:183 year:2001 number:1 pages:0 http://dx.doi.org/10.1034/j.1600-065x.2001.1830109.x text/html Verlag Deutschlandweit zugänglich Volltext GBV_USEFLAG_U ZDB-1-DJB GBV_NL_ARTICLE AR 183 2001 1 0 |
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10.1034/j.1600-065x.2001.1830109.x doi (DE-627)NLEJ242662609 DE-627 ger DE-627 rakwb Geretti, Anna Maria verfasserin aut Virus replication and evolution drive the kinetics and specificity of SIV-specific cytotoxic T lymphocytes Copenhagen Munksgaard International Publishers 2001 Online-Ressource nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Summary: SIV (simian immunodeficiency virus) infection of cynomolgus macaques provides an excellent model for investigating the basis of protective immunity against HIV (human immunodeficiency virus). We explored the protective role of cytotoxic T lymphocytes (CTL) against the pathogenic molecular clone SIVmac-J5. Vaccine-induced CTL precursors (CTLp) against Env, Gag or Nef did not protect macaques against intravenous challenge. However, detection of Rev-specific CTLp in infected macaques was associated with effective virus containment. Furthermore, CTL against an immunodominant Gag/p26 epitope (amino acids 242–250) resulted in the emergence of a mutant virus that uniformly replaced wild-type virus in the spleen and partially escaped recognition. During primary infection, CTLp detection in blood coincided with decreasing viremia. After 12 months, two outcomes emerged. In one group of macaques, persistent viremia was associated with high viral load in lymphoid organs and declining CD4+ T-cell counts. CTLp were maintained in asymptomatic macaques, but declined in the symptomatic phase of infection. In a second group, loss of detectable viremia was associated with low-level virus reservoirs in lymphoid organs, asymptomatic status and maintained CD4+ T-cell counts. CTLp peaked in the first 4 months of infection and subsequently declined in this group. These studies provide insights into the complex interplay between virus replication and host immunity. 2002 Blackwell Publishing Journal Backfiles 1879-2005 |2002|||||||||| Osterhaus, Albert D. M. E. verfasserin aut In Immunological reviews Oxford : Wiley-Blackwell, 1969 183(2001), 1, Seite 0 Online-Ressource (DE-627)NLEJ243927398 (DE-600)2038276-5 1600-065X volume:183 year:2001 number:1 pages:0 http://dx.doi.org/10.1034/j.1600-065x.2001.1830109.x text/html Verlag Deutschlandweit zugänglich Volltext GBV_USEFLAG_U ZDB-1-DJB GBV_NL_ARTICLE AR 183 2001 1 0 |
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10.1034/j.1600-065x.2001.1830109.x doi (DE-627)NLEJ242662609 DE-627 ger DE-627 rakwb Geretti, Anna Maria verfasserin aut Virus replication and evolution drive the kinetics and specificity of SIV-specific cytotoxic T lymphocytes Copenhagen Munksgaard International Publishers 2001 Online-Ressource nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Summary: SIV (simian immunodeficiency virus) infection of cynomolgus macaques provides an excellent model for investigating the basis of protective immunity against HIV (human immunodeficiency virus). We explored the protective role of cytotoxic T lymphocytes (CTL) against the pathogenic molecular clone SIVmac-J5. Vaccine-induced CTL precursors (CTLp) against Env, Gag or Nef did not protect macaques against intravenous challenge. However, detection of Rev-specific CTLp in infected macaques was associated with effective virus containment. Furthermore, CTL against an immunodominant Gag/p26 epitope (amino acids 242–250) resulted in the emergence of a mutant virus that uniformly replaced wild-type virus in the spleen and partially escaped recognition. During primary infection, CTLp detection in blood coincided with decreasing viremia. After 12 months, two outcomes emerged. In one group of macaques, persistent viremia was associated with high viral load in lymphoid organs and declining CD4+ T-cell counts. CTLp were maintained in asymptomatic macaques, but declined in the symptomatic phase of infection. In a second group, loss of detectable viremia was associated with low-level virus reservoirs in lymphoid organs, asymptomatic status and maintained CD4+ T-cell counts. CTLp peaked in the first 4 months of infection and subsequently declined in this group. These studies provide insights into the complex interplay between virus replication and host immunity. 2002 Blackwell Publishing Journal Backfiles 1879-2005 |2002|||||||||| Osterhaus, Albert D. M. E. verfasserin aut In Immunological reviews Oxford : Wiley-Blackwell, 1969 183(2001), 1, Seite 0 Online-Ressource (DE-627)NLEJ243927398 (DE-600)2038276-5 1600-065X volume:183 year:2001 number:1 pages:0 http://dx.doi.org/10.1034/j.1600-065x.2001.1830109.x text/html Verlag Deutschlandweit zugänglich Volltext GBV_USEFLAG_U ZDB-1-DJB GBV_NL_ARTICLE AR 183 2001 1 0 |
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10.1034/j.1600-065x.2001.1830109.x doi (DE-627)NLEJ242662609 DE-627 ger DE-627 rakwb Geretti, Anna Maria verfasserin aut Virus replication and evolution drive the kinetics and specificity of SIV-specific cytotoxic T lymphocytes Copenhagen Munksgaard International Publishers 2001 Online-Ressource nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Summary: SIV (simian immunodeficiency virus) infection of cynomolgus macaques provides an excellent model for investigating the basis of protective immunity against HIV (human immunodeficiency virus). We explored the protective role of cytotoxic T lymphocytes (CTL) against the pathogenic molecular clone SIVmac-J5. Vaccine-induced CTL precursors (CTLp) against Env, Gag or Nef did not protect macaques against intravenous challenge. However, detection of Rev-specific CTLp in infected macaques was associated with effective virus containment. Furthermore, CTL against an immunodominant Gag/p26 epitope (amino acids 242–250) resulted in the emergence of a mutant virus that uniformly replaced wild-type virus in the spleen and partially escaped recognition. During primary infection, CTLp detection in blood coincided with decreasing viremia. After 12 months, two outcomes emerged. In one group of macaques, persistent viremia was associated with high viral load in lymphoid organs and declining CD4+ T-cell counts. CTLp were maintained in asymptomatic macaques, but declined in the symptomatic phase of infection. In a second group, loss of detectable viremia was associated with low-level virus reservoirs in lymphoid organs, asymptomatic status and maintained CD4+ T-cell counts. CTLp peaked in the first 4 months of infection and subsequently declined in this group. These studies provide insights into the complex interplay between virus replication and host immunity. 2002 Blackwell Publishing Journal Backfiles 1879-2005 |2002|||||||||| Osterhaus, Albert D. M. E. verfasserin aut In Immunological reviews Oxford : Wiley-Blackwell, 1969 183(2001), 1, Seite 0 Online-Ressource (DE-627)NLEJ243927398 (DE-600)2038276-5 1600-065X volume:183 year:2001 number:1 pages:0 http://dx.doi.org/10.1034/j.1600-065x.2001.1830109.x text/html Verlag Deutschlandweit zugänglich Volltext GBV_USEFLAG_U ZDB-1-DJB GBV_NL_ARTICLE AR 183 2001 1 0 |
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10.1034/j.1600-065x.2001.1830109.x doi (DE-627)NLEJ242662609 DE-627 ger DE-627 rakwb Geretti, Anna Maria verfasserin aut Virus replication and evolution drive the kinetics and specificity of SIV-specific cytotoxic T lymphocytes Copenhagen Munksgaard International Publishers 2001 Online-Ressource nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Summary: SIV (simian immunodeficiency virus) infection of cynomolgus macaques provides an excellent model for investigating the basis of protective immunity against HIV (human immunodeficiency virus). We explored the protective role of cytotoxic T lymphocytes (CTL) against the pathogenic molecular clone SIVmac-J5. Vaccine-induced CTL precursors (CTLp) against Env, Gag or Nef did not protect macaques against intravenous challenge. However, detection of Rev-specific CTLp in infected macaques was associated with effective virus containment. Furthermore, CTL against an immunodominant Gag/p26 epitope (amino acids 242–250) resulted in the emergence of a mutant virus that uniformly replaced wild-type virus in the spleen and partially escaped recognition. During primary infection, CTLp detection in blood coincided with decreasing viremia. After 12 months, two outcomes emerged. In one group of macaques, persistent viremia was associated with high viral load in lymphoid organs and declining CD4+ T-cell counts. CTLp were maintained in asymptomatic macaques, but declined in the symptomatic phase of infection. In a second group, loss of detectable viremia was associated with low-level virus reservoirs in lymphoid organs, asymptomatic status and maintained CD4+ T-cell counts. CTLp peaked in the first 4 months of infection and subsequently declined in this group. These studies provide insights into the complex interplay between virus replication and host immunity. 2002 Blackwell Publishing Journal Backfiles 1879-2005 |2002|||||||||| Osterhaus, Albert D. M. E. verfasserin aut In Immunological reviews Oxford : Wiley-Blackwell, 1969 183(2001), 1, Seite 0 Online-Ressource (DE-627)NLEJ243927398 (DE-600)2038276-5 1600-065X volume:183 year:2001 number:1 pages:0 http://dx.doi.org/10.1034/j.1600-065x.2001.1830109.x text/html Verlag Deutschlandweit zugänglich Volltext GBV_USEFLAG_U ZDB-1-DJB GBV_NL_ARTICLE AR 183 2001 1 0 |
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Summary: SIV (simian immunodeficiency virus) infection of cynomolgus macaques provides an excellent model for investigating the basis of protective immunity against HIV (human immunodeficiency virus). We explored the protective role of cytotoxic T lymphocytes (CTL) against the pathogenic molecular clone SIVmac-J5. Vaccine-induced CTL precursors (CTLp) against Env, Gag or Nef did not protect macaques against intravenous challenge. However, detection of Rev-specific CTLp in infected macaques was associated with effective virus containment. Furthermore, CTL against an immunodominant Gag/p26 epitope (amino acids 242–250) resulted in the emergence of a mutant virus that uniformly replaced wild-type virus in the spleen and partially escaped recognition. During primary infection, CTLp detection in blood coincided with decreasing viremia. After 12 months, two outcomes emerged. In one group of macaques, persistent viremia was associated with high viral load in lymphoid organs and declining CD4+ T-cell counts. CTLp were maintained in asymptomatic macaques, but declined in the symptomatic phase of infection. In a second group, loss of detectable viremia was associated with low-level virus reservoirs in lymphoid organs, asymptomatic status and maintained CD4+ T-cell counts. CTLp peaked in the first 4 months of infection and subsequently declined in this group. These studies provide insights into the complex interplay between virus replication and host immunity. |
| abstractGer |
Summary: SIV (simian immunodeficiency virus) infection of cynomolgus macaques provides an excellent model for investigating the basis of protective immunity against HIV (human immunodeficiency virus). We explored the protective role of cytotoxic T lymphocytes (CTL) against the pathogenic molecular clone SIVmac-J5. Vaccine-induced CTL precursors (CTLp) against Env, Gag or Nef did not protect macaques against intravenous challenge. However, detection of Rev-specific CTLp in infected macaques was associated with effective virus containment. Furthermore, CTL against an immunodominant Gag/p26 epitope (amino acids 242–250) resulted in the emergence of a mutant virus that uniformly replaced wild-type virus in the spleen and partially escaped recognition. During primary infection, CTLp detection in blood coincided with decreasing viremia. After 12 months, two outcomes emerged. In one group of macaques, persistent viremia was associated with high viral load in lymphoid organs and declining CD4+ T-cell counts. CTLp were maintained in asymptomatic macaques, but declined in the symptomatic phase of infection. In a second group, loss of detectable viremia was associated with low-level virus reservoirs in lymphoid organs, asymptomatic status and maintained CD4+ T-cell counts. CTLp peaked in the first 4 months of infection and subsequently declined in this group. These studies provide insights into the complex interplay between virus replication and host immunity. |
| abstract_unstemmed |
Summary: SIV (simian immunodeficiency virus) infection of cynomolgus macaques provides an excellent model for investigating the basis of protective immunity against HIV (human immunodeficiency virus). We explored the protective role of cytotoxic T lymphocytes (CTL) against the pathogenic molecular clone SIVmac-J5. Vaccine-induced CTL precursors (CTLp) against Env, Gag or Nef did not protect macaques against intravenous challenge. However, detection of Rev-specific CTLp in infected macaques was associated with effective virus containment. Furthermore, CTL against an immunodominant Gag/p26 epitope (amino acids 242–250) resulted in the emergence of a mutant virus that uniformly replaced wild-type virus in the spleen and partially escaped recognition. During primary infection, CTLp detection in blood coincided with decreasing viremia. After 12 months, two outcomes emerged. In one group of macaques, persistent viremia was associated with high viral load in lymphoid organs and declining CD4+ T-cell counts. CTLp were maintained in asymptomatic macaques, but declined in the symptomatic phase of infection. In a second group, loss of detectable viremia was associated with low-level virus reservoirs in lymphoid organs, asymptomatic status and maintained CD4+ T-cell counts. CTLp peaked in the first 4 months of infection and subsequently declined in this group. These studies provide insights into the complex interplay between virus replication and host immunity. |
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