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Dysfunctional B-cell responses during HIV-1 infection: implication for influenza vaccination and highly active antiretroviral therapy

Identifieur interne : 000C41 ( PascalFrancis/Curation ); précédent : 000C40; suivant : 000C42

Dysfunctional B-cell responses during HIV-1 infection: implication for influenza vaccination and highly active antiretroviral therapy

Auteurs : Alberto Cagigi [Suède] ; Anna Nilsson [Suède] ; Simone Pensieroso [Suède] ; Francesca Chiodi [Suède]

Source :

RBID : Pascal:10-0325970

Descripteurs français

English descriptors

Abstract

Although HIV-1 infection does not directly target B cells, B-cell numbers are reduced and their function is impaired during HIV infection. Antibody titres against antigens previously encountered through vaccination or natural infection are low in patients with HIV Intrinsic B-cell defects might be involved in the impairment of humoral immunity during early HIV infection. Abnormal T-cell activation and the altered expression of molecules involved in the B-cell homing process cause dysfunctional interaction between T and B cells in the germinal centres of lymphoid tissues, which might impair B-cell responses during HIV infection. Class-switch recombination is also impaired in individuals with HIV. Protective immune responses against T-cell-dependent antigens, including influenza antigens, rely on the production of neutralising antibodies. Impaired B-cell responses during HIV infection could therefore hamper the effectiveness of vaccinations against seasonal influenza or the new pandemic influenza A H1N1 vaccines in individuals with HIV. By maintaining B-cell responses, highly active antiretroviral therapy might improve the efficacy of influenza vaccines in individuals with HIV.
pA  
A01 01  1    @0 1473-3099
A03   1    @0 Lancet. Infect. dis. : (print)
A05       @2 10
A06       @2 7
A08 01  1  ENG  @1 Dysfunctional B-cell responses during HIV-1 infection: implication for influenza vaccination and highly active antiretroviral therapy
A11 01  1    @1 CAGIGI (Alberto)
A11 02  1    @1 NILSSON (Anna)
A11 03  1    @1 PENSIEROSO (Simone)
A11 04  1    @1 CHIODI (Francesca)
A14 01      @1 Department of Laboratory Medicine, Karolinska Institutet @2 Stockholm @3 SWE @Z 1 aut.
A14 02      @1 Department of Microbiology, Tumour and Cell Biology, Karolinska Institutet @2 Stockholm @3 SWE @Z 2 aut. @Z 3 aut. @Z 4 aut.
A14 03      @1 Paediatric Infectious Diseases Unit, Department of Women and Child Health, Karolinska Institutet @2 Stockholm @3 SWE @Z 2 aut.
A20       @1 499-503
A21       @1 2010
A23 01      @0 ENG
A43 01      @1 INIST @2 27478 @5 354000180746180060
A44       @0 0000 @1 © 2010 INIST-CNRS. All rights reserved.
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C01 01    ENG  @0 Although HIV-1 infection does not directly target B cells, B-cell numbers are reduced and their function is impaired during HIV infection. Antibody titres against antigens previously encountered through vaccination or natural infection are low in patients with HIV Intrinsic B-cell defects might be involved in the impairment of humoral immunity during early HIV infection. Abnormal T-cell activation and the altered expression of molecules involved in the B-cell homing process cause dysfunctional interaction between T and B cells in the germinal centres of lymphoid tissues, which might impair B-cell responses during HIV infection. Class-switch recombination is also impaired in individuals with HIV. Protective immune responses against T-cell-dependent antigens, including influenza antigens, rely on the production of neutralising antibodies. Impaired B-cell responses during HIV infection could therefore hamper the effectiveness of vaccinations against seasonal influenza or the new pandemic influenza A H1N1 vaccines in individuals with HIV. By maintaining B-cell responses, highly active antiretroviral therapy might improve the efficacy of influenza vaccines in individuals with HIV.
C02 01  X    @0 002B05C02D
C02 02  X    @0 002B05C02C
C02 03  X    @0 002B06D01
C03 01  X  FRE  @0 SIDA @5 01
C03 01  X  ENG  @0 AIDS @5 01
C03 01  X  SPA  @0 SIDA @5 01
C03 02  X  FRE  @0 Grippe @5 02
C03 02  X  ENG  @0 Influenza @5 02
C03 02  X  SPA  @0 Gripe @5 02
C03 03  X  FRE  @0 Immunoprophylaxie @5 04
C03 03  X  ENG  @0 Immunoprophylaxis @5 04
C03 03  X  SPA  @0 Inmunoprofilaxia @5 04
C03 04  X  FRE  @0 Chimiothérapie @5 05
C03 04  X  ENG  @0 Chemotherapy @5 05
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C03 05  X  SPA  @0 Célula β @5 07
C03 06  X  FRE  @0 Vaccination @5 08
C03 06  X  ENG  @0 Vaccination @5 08
C03 06  X  SPA  @0 Vacunación @5 08
C03 07  X  FRE  @0 Virus HIV1 @2 NW @5 10
C03 07  X  ENG  @0 HIV-1 virus @2 NW @5 10
C03 07  X  SPA  @0 HIV-1 virus @2 NW @5 10
C03 08  X  FRE  @0 Antiviral @5 30
C03 08  X  ENG  @0 Antiviral @5 30
C03 08  X  SPA  @0 Antiviral @5 30
C03 09  X  FRE  @0 Protocole HAART @4 INC @5 86
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C07 01  X  ENG  @0 Viral disease
C07 01  X  SPA  @0 Virosis
C07 02  X  FRE  @0 Infection
C07 02  X  ENG  @0 Infection
C07 02  X  SPA  @0 Infección
C07 03  X  FRE  @0 Traitement
C07 03  X  ENG  @0 Treatment
C07 03  X  SPA  @0 Tratamiento
C07 04  X  FRE  @0 Virus immunodéficience humaine @2 NW
C07 04  X  ENG  @0 Human immunodeficiency virus @2 NW
C07 04  X  SPA  @0 Human immunodeficiency virus @2 NW
C07 05  X  FRE  @0 Lentivirus @2 NW
C07 05  X  ENG  @0 Lentivirus @2 NW
C07 05  X  SPA  @0 Lentivirus @2 NW
C07 06  X  FRE  @0 Retroviridae @2 NW
C07 06  X  ENG  @0 Retroviridae @2 NW
C07 06  X  SPA  @0 Retroviridae @2 NW
C07 07  X  FRE  @0 Virus @2 NW
C07 07  X  ENG  @0 Virus @2 NW
C07 07  X  SPA  @0 Virus @2 NW
C07 08  X  FRE  @0 Immunodéficit @5 37
C07 08  X  ENG  @0 Immune deficiency @5 37
C07 08  X  SPA  @0 Inmunodeficiencia @5 37
C07 09  X  FRE  @0 Immunopathologie @5 39
C07 09  X  ENG  @0 Immunopathology @5 39
C07 09  X  SPA  @0 Inmunopatología @5 39
C07 10  X  FRE  @0 Prévention @5 40
C07 10  X  ENG  @0 Prevention @5 40
C07 10  X  SPA  @0 Prevención @5 40
N21       @1 207
N44 01      @1 OTO
N82       @1 OTO

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Pascal:10-0325970

Le document en format XML

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<div type="abstract" xml:lang="en">Although HIV-1 infection does not directly target B cells, B-cell numbers are reduced and their function is impaired during HIV infection. Antibody titres against antigens previously encountered through vaccination or natural infection are low in patients with HIV Intrinsic B-cell defects might be involved in the impairment of humoral immunity during early HIV infection. Abnormal T-cell activation and the altered expression of molecules involved in the B-cell homing process cause dysfunctional interaction between T and B cells in the germinal centres of lymphoid tissues, which might impair B-cell responses during HIV infection. Class-switch recombination is also impaired in individuals with HIV. Protective immune responses against T-cell-dependent antigens, including influenza antigens, rely on the production of neutralising antibodies. Impaired B-cell responses during HIV infection could therefore hamper the effectiveness of vaccinations against seasonal influenza or the new pandemic influenza A H1N1 vaccines in individuals with HIV. By maintaining B-cell responses, highly active antiretroviral therapy might improve the efficacy of influenza vaccines in individuals with HIV.</div>
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<s0>Virosis</s0>
</fC07>
<fC07 i1="02" i2="X" l="FRE">
<s0>Infection</s0>
</fC07>
<fC07 i1="02" i2="X" l="ENG">
<s0>Infection</s0>
</fC07>
<fC07 i1="02" i2="X" l="SPA">
<s0>Infección</s0>
</fC07>
<fC07 i1="03" i2="X" l="FRE">
<s0>Traitement</s0>
</fC07>
<fC07 i1="03" i2="X" l="ENG">
<s0>Treatment</s0>
</fC07>
<fC07 i1="03" i2="X" l="SPA">
<s0>Tratamiento</s0>
</fC07>
<fC07 i1="04" i2="X" l="FRE">
<s0>Virus immunodéficience humaine</s0>
<s2>NW</s2>
</fC07>
<fC07 i1="04" i2="X" l="ENG">
<s0>Human immunodeficiency virus</s0>
<s2>NW</s2>
</fC07>
<fC07 i1="04" i2="X" l="SPA">
<s0>Human immunodeficiency virus</s0>
<s2>NW</s2>
</fC07>
<fC07 i1="05" i2="X" l="FRE">
<s0>Lentivirus</s0>
<s2>NW</s2>
</fC07>
<fC07 i1="05" i2="X" l="ENG">
<s0>Lentivirus</s0>
<s2>NW</s2>
</fC07>
<fC07 i1="05" i2="X" l="SPA">
<s0>Lentivirus</s0>
<s2>NW</s2>
</fC07>
<fC07 i1="06" i2="X" l="FRE">
<s0>Retroviridae</s0>
<s2>NW</s2>
</fC07>
<fC07 i1="06" i2="X" l="ENG">
<s0>Retroviridae</s0>
<s2>NW</s2>
</fC07>
<fC07 i1="06" i2="X" l="SPA">
<s0>Retroviridae</s0>
<s2>NW</s2>
</fC07>
<fC07 i1="07" i2="X" l="FRE">
<s0>Virus</s0>
<s2>NW</s2>
</fC07>
<fC07 i1="07" i2="X" l="ENG">
<s0>Virus</s0>
<s2>NW</s2>
</fC07>
<fC07 i1="07" i2="X" l="SPA">
<s0>Virus</s0>
<s2>NW</s2>
</fC07>
<fC07 i1="08" i2="X" l="FRE">
<s0>Immunodéficit</s0>
<s5>37</s5>
</fC07>
<fC07 i1="08" i2="X" l="ENG">
<s0>Immune deficiency</s0>
<s5>37</s5>
</fC07>
<fC07 i1="08" i2="X" l="SPA">
<s0>Inmunodeficiencia</s0>
<s5>37</s5>
</fC07>
<fC07 i1="09" i2="X" l="FRE">
<s0>Immunopathologie</s0>
<s5>39</s5>
</fC07>
<fC07 i1="09" i2="X" l="ENG">
<s0>Immunopathology</s0>
<s5>39</s5>
</fC07>
<fC07 i1="09" i2="X" l="SPA">
<s0>Inmunopatología</s0>
<s5>39</s5>
</fC07>
<fC07 i1="10" i2="X" l="FRE">
<s0>Prévention</s0>
<s5>40</s5>
</fC07>
<fC07 i1="10" i2="X" l="ENG">
<s0>Prevention</s0>
<s5>40</s5>
</fC07>
<fC07 i1="10" i2="X" l="SPA">
<s0>Prevención</s0>
<s5>40</s5>
</fC07>
<fN21>
<s1>207</s1>
</fN21>
<fN44 i1="01">
<s1>OTO</s1>
</fN44>
<fN82>
<s1>OTO</s1>
</fN82>
</pA>
</standard>
</inist>
</record>

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