Associations between MHC class I and susceptibility to HIV-2 disease progression
OBJECTIVES: Human immunodeficiency virus type 2 (HIV-2) progression to disease is significantly slower than that of human immunodeficiency virus type 1 (HIV-1). Genetic determinants for susceptibility to disease progression were hypothesized to play a more significant role in this infection compared with HIV-1. We sought to identify common human lymphocyte antigen (HLA) alleles in the Senegalese population and to compare HLA profiles between HIV-2-infected individuals with low and high risk for disease progression.
STUDY DESIGN/METHODS: We conducted a case-control study investigating possible associations between MHC class I genes and the risk of disease progression in HIV-2-infected individuals. The MHC class I genotype was molecularly defined using polymerase chain reaction with sequence specific primers (PCR-SSP) in 62 female sex workers from the Dakar, Senegal cohort. Lack of antibodies to the HIV-2 antigen p26 has been previously shown to predict disease progression and was used in this study as a surrogate marker. Twenty-one cases were identified lacking antibodies to p26, therefore at a higher risk of disease progression, and were compared with 41 p26 antibody-positive, randomly selected controls.
RESULTS: Statistical analysis showed that HLA B35 was significantly associated with lack of p26 antibodies, and higher risk of disease progression ( < 0.05). The same association was found for the self-defined class I haplotypes B35-Cw4 and A23-Cw 7 ( < 0.05). The HLA B 53 allele was associated with slower disease progression; however, this association was not statistically significant. We observed a trend whereby heterozygotes were at lower risk for HIV-2 disease progression, as previously reported in HIV-1 disease.
CONCLUSIONS: In this West African population, a distinct profile of HLA class I alleles was observed, and many of these appear to influence disease progression in HIV-2 infection.
| Medienart: |
Artikel |
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| Erscheinungsjahr: |
2002 |
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| Erschienen: |
2002 |
| Enthalten in: |
Zur Gesamtaufnahme - volume:5 |
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| Enthalten in: |
Journal of human virology - 5(2002), 1 vom: 01. Jan., Seite 1-7 |
| Sprache: |
Englisch |
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| Beteiligte Personen: |
Diouf, Khady [VerfasserIn] |
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| Anmerkungen: |
Date Completed 15.11.2002 Date Revised 24.11.2016 published: Print Citation Status MEDLINE |
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| Förderinstitution / Projekttitel: |
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| PPN (Katalog-ID): |
NLM121444635 |
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| 035 | |a (NLM)12352262 | ||
| 040 | |a DE-627 |b ger |c DE-627 |e rakwb | ||
| 041 | |a eng | ||
| 100 | 1 | |a Diouf, Khady |e verfasserin |4 aut | |
| 245 | 1 | 0 | |a Associations between MHC class I and susceptibility to HIV-2 disease progression |
| 264 | 1 | |c 2002 | |
| 336 | |a Text |b txt |2 rdacontent | ||
| 337 | |a ohne Hilfsmittel zu benutzen |b n |2 rdamedia | ||
| 338 | |a Band |b nc |2 rdacarrier | ||
| 500 | |a Date Completed 15.11.2002 | ||
| 500 | |a Date Revised 24.11.2016 | ||
| 500 | |a published: Print | ||
| 500 | |a Citation Status MEDLINE | ||
| 520 | |a OBJECTIVES: Human immunodeficiency virus type 2 (HIV-2) progression to disease is significantly slower than that of human immunodeficiency virus type 1 (HIV-1). Genetic determinants for susceptibility to disease progression were hypothesized to play a more significant role in this infection compared with HIV-1. We sought to identify common human lymphocyte antigen (HLA) alleles in the Senegalese population and to compare HLA profiles between HIV-2-infected individuals with low and high risk for disease progression | ||
| 520 | |a STUDY DESIGN/METHODS: We conducted a case-control study investigating possible associations between MHC class I genes and the risk of disease progression in HIV-2-infected individuals. The MHC class I genotype was molecularly defined using polymerase chain reaction with sequence specific primers (PCR-SSP) in 62 female sex workers from the Dakar, Senegal cohort. Lack of antibodies to the HIV-2 antigen p26 has been previously shown to predict disease progression and was used in this study as a surrogate marker. Twenty-one cases were identified lacking antibodies to p26, therefore at a higher risk of disease progression, and were compared with 41 p26 antibody-positive, randomly selected controls | ||
| 520 | |a RESULTS: Statistical analysis showed that HLA B35 was significantly associated with lack of p26 antibodies, and higher risk of disease progression ( < 0.05). The same association was found for the self-defined class I haplotypes B35-Cw4 and A23-Cw 7 ( < 0.05). The HLA B 53 allele was associated with slower disease progression; however, this association was not statistically significant. We observed a trend whereby heterozygotes were at lower risk for HIV-2 disease progression, as previously reported in HIV-1 disease | ||
| 520 | |a CONCLUSIONS: In this West African population, a distinct profile of HLA class I alleles was observed, and many of these appear to influence disease progression in HIV-2 infection | ||
| 650 | 4 | |a Journal Article | |
| 650 | 4 | |a Research Support, Non-U.S. Gov't | |
| 650 | 4 | |a Research Support, U.S. Gov't, Non-P.H.S. | |
| 650 | 4 | |a Research Support, U.S. Gov't, P.H.S. | |
| 650 | 7 | |a Gene Products, gag |2 NLM | |
| 650 | 7 | |a HIV Antibodies |2 NLM | |
| 650 | 7 | |a HIV Antigens |2 NLM | |
| 650 | 7 | |a HLA-B35 Antigen |2 NLM | |
| 650 | 7 | |a gag Gene Products, Human Immunodeficiency Virus |2 NLM | |
| 650 | 7 | |a gag protein p26, Human immunodeficiency virus |2 NLM | |
| 700 | 1 | |a Sarr, Abdoulaye Dieng |e verfasserin |4 aut | |
| 700 | 1 | |a Eisen, Geoffrey |e verfasserin |4 aut | |
| 700 | 1 | |a Popper, Stephen |e verfasserin |4 aut | |
| 700 | 1 | |a Mboup, Souleymane |e verfasserin |4 aut | |
| 700 | 1 | |a Kanki, Phyllis |e verfasserin |4 aut | |
| 773 | 0 | 8 | |i Enthalten in |t Journal of human virology |d 1997 |g 5(2002), 1 vom: 01. Jan., Seite 1-7 |w (DE-627)NLM097437964 |x 1090-9508 |7 nnns |
| 773 | 1 | 8 | |g volume:5 |g year:2002 |g number:1 |g day:01 |g month:01 |g pages:1-7 |
| 912 | |a GBV_USEFLAG_A | ||
| 912 | |a GBV_NLM | ||
| 951 | |a AR | ||
| 952 | |d 5 |j 2002 |e 1 |b 01 |c 01 |h 1-7 | ||