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Association between high aflatoxin B1 levels and high viral load in HIV-positive people

Identifieur interne : 000007 ( PascalFrancis/Corpus ); précédent : 000006; suivant : 000008

Association between high aflatoxin B1 levels and high viral load in HIV-positive people

Auteurs : P. E. Jolly ; S. Inusah ; B. Lu ; W. O. Ellis ; A. Nyarko ; T. D. Phillips ; J. H. Williams

Source :

RBID : Pascal:13-0349936

Descripteurs français

English descriptors

Abstract

Since both aflatoxin and the human immunodeficiency virus (HIV) cause immune suppression, chronic exposure to aflatoxin in HIV-positive people could lead to higher levels of virus replication. This study was conducted to examine the association between aflatoxin B1 albumin adduct (AF-ALB) levels and HIV viral load. Antiretroviral naive HIV-positive people (314) with median CD4 count of 574 cells/μl blood (mean ± standard deviation = 630±277) were recruited in Kumasi, Ghana. Sociodemographic and health data, and blood samples were collected from participants. The plasma samples were tested for AF-ALB and HIV viral load. Univariate logistic regression analysis was conducted using viral load (high/low) as the outcome and AF-ALB quartiles as exposure. Multivariable logistic regression analysis was performed between quartile AF-ALB, viral load and CD4 adjusting for sex, age, and year of HIV diagnosis. Both univariate and multivariable logistic regression showed that viral load increased as AF-ALB levels increased. By univariate analysis, high viral load was 2.3 times more likely among persons in the third AF-ALB quartile (95% confidence interval (CI): 1.13, 4.51), and 2.9 times more likely among persons in the fourth AF-ALB quartile (CI: 1.41, 5.88), compared to persons in the first quartile. In the multivariable model, persons in the fourth AF-ALB quartile were about 2.6 times more likely to have high viral loads than persons in the first quartile (CI: 1.19-5.69). When AF-ALB and viral load were log transformed and linear regression analysis conducted, the univariate linear regression analysis showed that for each pg/mg increase in AF-ALB, viral load increased by approximately 1.6 copies/ml (P=0.0006). The association was marginally significant in the adjusted linear regression model (i.e. for each pg/mg increase in AF-ALB, the mean viral load increased by approximately 1.3 copies/ml, P=0.073). These data show strong and consistent increases in HIV viral load with increasing AF-ALB levels. Since the median and mean CD4 were greater than 500 cells for participants in each AF-ALB quartile, the results indicate that the immune modulating and virus transcription effects of aflatoxin may occur quite early in HIV infection, even while the CD4 count is still above 500, resulting in higher viral loads.

Notice en format standard (ISO 2709)

Pour connaître la documentation sur le format Inist Standard.

pA  
A01 01  1    @0 1875-0710
A05       @2 6
A06       @2 3
A08 01  1  ENG  @1 Association between high aflatoxin B1 levels and high viral load in HIV-positive people
A09 01  1  ENG  @1 WMF meets IUPAC Conference: 7th Conference of The World Mycotoxin Forum® and the XIIIth IUPAC International Symposium on Mycotoxins and Phycotoxins, Rotterdam, Netherlands, 5-9 November 2012
A11 01  1    @1 JOLLY (P. E.)
A11 02  1    @1 INUSAH (S.)
A11 03  1    @1 LU (B.)
A11 04  1    @1 ELLIS (W. O.)
A11 05  1    @1 NYARKO (A.)
A11 06  1    @1 PHILLIPS (T. D.)
A11 07  1    @1 WILLIAMS (J. H.)
A14 01      @1 University of Alabama at Birmingham, Department of Epidemiology, School of Public Health, 1665 University Boulevard, RPHB 217 @2 Birmingham, AL 35294-0022 @3 USA @Z 1 aut. @Z 2 aut. @Z 3 aut.
A14 02      @1 Kwame Nkrumah University of Science and Technology @2 Kumasi @3 GHA @Z 4 aut.
A14 03      @1 Kumasi South Regional Hospital @2 Kumasi @3 GHA @Z 5 aut.
A14 04      @1 Department of Veterinary Integrative Biosciences, Texas A&M University, Mail Stop 4458 @2 College Station, TX 77843 @3 USA @Z 6 aut.
A14 05      @1 College of Agricultural and Environmental Sciences, University of Georgia, 1109 Experiment St @2 Griffin, GA 30223 @3 USA @Z 7 aut.
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A44       @0 0000 @1 © 2013 INIST-CNRS. All rights reserved.
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A47 01  1    @0 13-0349936
A60       @1 P @2 C
A61       @0 A
A64 01  1    @0 World mycotoxin journal : (Print)
A66 01      @0 NLD
C01 01    ENG  @0 Since both aflatoxin and the human immunodeficiency virus (HIV) cause immune suppression, chronic exposure to aflatoxin in HIV-positive people could lead to higher levels of virus replication. This study was conducted to examine the association between aflatoxin B1 albumin adduct (AF-ALB) levels and HIV viral load. Antiretroviral naive HIV-positive people (314) with median CD4 count of 574 cells/μl blood (mean ± standard deviation = 630±277) were recruited in Kumasi, Ghana. Sociodemographic and health data, and blood samples were collected from participants. The plasma samples were tested for AF-ALB and HIV viral load. Univariate logistic regression analysis was conducted using viral load (high/low) as the outcome and AF-ALB quartiles as exposure. Multivariable logistic regression analysis was performed between quartile AF-ALB, viral load and CD4 adjusting for sex, age, and year of HIV diagnosis. Both univariate and multivariable logistic regression showed that viral load increased as AF-ALB levels increased. By univariate analysis, high viral load was 2.3 times more likely among persons in the third AF-ALB quartile (95% confidence interval (CI): 1.13, 4.51), and 2.9 times more likely among persons in the fourth AF-ALB quartile (CI: 1.41, 5.88), compared to persons in the first quartile. In the multivariable model, persons in the fourth AF-ALB quartile were about 2.6 times more likely to have high viral loads than persons in the first quartile (CI: 1.19-5.69). When AF-ALB and viral load were log transformed and linear regression analysis conducted, the univariate linear regression analysis showed that for each pg/mg increase in AF-ALB, viral load increased by approximately 1.6 copies/ml (P=0.0006). The association was marginally significant in the adjusted linear regression model (i.e. for each pg/mg increase in AF-ALB, the mean viral load increased by approximately 1.3 copies/ml, P=0.073). These data show strong and consistent increases in HIV viral load with increasing AF-ALB levels. Since the median and mean CD4 were greater than 500 cells for participants in each AF-ALB quartile, the results indicate that the immune modulating and virus transcription effects of aflatoxin may occur quite early in HIV infection, even while the CD4 count is still above 500, resulting in higher viral loads.
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C03 06  X  ENG  @0 Mycotoxin @5 28
C03 06  X  SPA  @0 Micotoxina @5 28
C07 01  X  FRE  @0 Toxine
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A30 03  1  ENG  @1 IUPAC International Symposium on Mycotoxins and Phycotoxins @2 13 @3 Rotterdam NLD @4 2012-11-05

Format Inist (serveur)

NO : PASCAL 13-0349936 INIST
ET : Association between high aflatoxin B1 levels and high viral load in HIV-positive people
AU : JOLLY (P. E.); INUSAH (S.); LU (B.); ELLIS (W. O.); NYARKO (A.); PHILLIPS (T. D.); WILLIAMS (J. H.)
AF : University of Alabama at Birmingham, Department of Epidemiology, School of Public Health, 1665 University Boulevard, RPHB 217/Birmingham, AL 35294-0022/Etats-Unis (1 aut., 2 aut., 3 aut.); Kwame Nkrumah University of Science and Technology/Kumasi/Ghana (4 aut.); Kumasi South Regional Hospital/Kumasi/Ghana (5 aut.); Department of Veterinary Integrative Biosciences, Texas A&M University, Mail Stop 4458/College Station, TX 77843/Etats-Unis (6 aut.); College of Agricultural and Environmental Sciences, University of Georgia, 1109 Experiment St/Griffin, GA 30223/Etats-Unis (7 aut.)
DT : Publication en série; Congrès; Niveau analytique
SO : World mycotoxin journal : (Print); ISSN 1875-0710; Pays-Bas; Da. 2013; Vol. 6; No. 3; Pp. 255-261; Bibl. 1 p.1/4
LA : Anglais
EA : Since both aflatoxin and the human immunodeficiency virus (HIV) cause immune suppression, chronic exposure to aflatoxin in HIV-positive people could lead to higher levels of virus replication. This study was conducted to examine the association between aflatoxin B1 albumin adduct (AF-ALB) levels and HIV viral load. Antiretroviral naive HIV-positive people (314) with median CD4 count of 574 cells/μl blood (mean ± standard deviation = 630±277) were recruited in Kumasi, Ghana. Sociodemographic and health data, and blood samples were collected from participants. The plasma samples were tested for AF-ALB and HIV viral load. Univariate logistic regression analysis was conducted using viral load (high/low) as the outcome and AF-ALB quartiles as exposure. Multivariable logistic regression analysis was performed between quartile AF-ALB, viral load and CD4 adjusting for sex, age, and year of HIV diagnosis. Both univariate and multivariable logistic regression showed that viral load increased as AF-ALB levels increased. By univariate analysis, high viral load was 2.3 times more likely among persons in the third AF-ALB quartile (95% confidence interval (CI): 1.13, 4.51), and 2.9 times more likely among persons in the fourth AF-ALB quartile (CI: 1.41, 5.88), compared to persons in the first quartile. In the multivariable model, persons in the fourth AF-ALB quartile were about 2.6 times more likely to have high viral loads than persons in the first quartile (CI: 1.19-5.69). When AF-ALB and viral load were log transformed and linear regression analysis conducted, the univariate linear regression analysis showed that for each pg/mg increase in AF-ALB, viral load increased by approximately 1.6 copies/ml (P=0.0006). The association was marginally significant in the adjusted linear regression model (i.e. for each pg/mg increase in AF-ALB, the mean viral load increased by approximately 1.3 copies/ml, P=0.073). These data show strong and consistent increases in HIV viral load with increasing AF-ALB levels. Since the median and mean CD4 were greater than 500 cells for participants in each AF-ALB quartile, the results indicate that the immune modulating and virus transcription effects of aflatoxin may occur quite early in HIV infection, even while the CD4 count is still above 500, resulting in higher viral loads.
CC : 002B03J
FD : Association; Aflatoxine B1; Albumine; Ghana; Virus immunodéficience humaine; Mycotoxine
FG : Toxine; Afrique; Lentivirus; Retroviridae; Virus
ED : Association; Aflatoxin B1; Albumin; Ghana; Human immunodeficiency virus; Mycotoxin
EG : Toxin; Africa; Lentivirus; Retroviridae; Virus
SD : Asociación; Aflatoxina B1; Albúmina; Ghana; Human immunodeficiency virus; Micotoxina
LO : INIST-28127.354000503683990050
ID : 13-0349936

Links to Exploration step

Pascal:13-0349936

Le document en format XML

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<div type="abstract" xml:lang="en">Since both aflatoxin and the human immunodeficiency virus (HIV) cause immune suppression, chronic exposure to aflatoxin in HIV-positive people could lead to higher levels of virus replication. This study was conducted to examine the association between aflatoxin B
<sub>1</sub>
albumin adduct (AF-ALB) levels and HIV viral load. Antiretroviral naive HIV-positive people (314) with median CD4 count of 574 cells/μl blood (mean ± standard deviation = 630±277) were recruited in Kumasi, Ghana. Sociodemographic and health data, and blood samples were collected from participants. The plasma samples were tested for AF-ALB and HIV viral load. Univariate logistic regression analysis was conducted using viral load (high/low) as the outcome and AF-ALB quartiles as exposure. Multivariable logistic regression analysis was performed between quartile AF-ALB, viral load and CD4 adjusting for sex, age, and year of HIV diagnosis. Both univariate and multivariable logistic regression showed that viral load increased as AF-ALB levels increased. By univariate analysis, high viral load was 2.3 times more likely among persons in the third AF-ALB quartile (95% confidence interval (CI): 1.13, 4.51), and 2.9 times more likely among persons in the fourth AF-ALB quartile (CI: 1.41, 5.88), compared to persons in the first quartile. In the multivariable model, persons in the fourth AF-ALB quartile were about 2.6 times more likely to have high viral loads than persons in the first quartile (CI: 1.19-5.69). When AF-ALB and viral load were log transformed and linear regression analysis conducted, the univariate linear regression analysis showed that for each pg/mg increase in AF-ALB, viral load increased by approximately 1.6 copies/ml (P=0.0006). The association was marginally significant in the adjusted linear regression model (i.e. for each pg/mg increase in AF-ALB, the mean viral load increased by approximately 1.3 copies/ml, P=0.073). These data show strong and consistent increases in HIV viral load with increasing AF-ALB levels. Since the median and mean CD4 were greater than 500 cells for participants in each AF-ALB quartile, the results indicate that the immune modulating and virus transcription effects of aflatoxin may occur quite early in HIV infection, even while the CD4 count is still above 500, resulting in higher viral loads.</div>
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<s1>Kwame Nkrumah University of Science and Technology</s1>
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</fA14>
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<s1>International Union of Pure and Applied Chemistry (IUPAC)</s1>
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<s0>World mycotoxin journal : (Print)</s0>
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<s0>Since both aflatoxin and the human immunodeficiency virus (HIV) cause immune suppression, chronic exposure to aflatoxin in HIV-positive people could lead to higher levels of virus replication. This study was conducted to examine the association between aflatoxin B
<sub>1</sub>
albumin adduct (AF-ALB) levels and HIV viral load. Antiretroviral naive HIV-positive people (314) with median CD4 count of 574 cells/μl blood (mean ± standard deviation = 630±277) were recruited in Kumasi, Ghana. Sociodemographic and health data, and blood samples were collected from participants. The plasma samples were tested for AF-ALB and HIV viral load. Univariate logistic regression analysis was conducted using viral load (high/low) as the outcome and AF-ALB quartiles as exposure. Multivariable logistic regression analysis was performed between quartile AF-ALB, viral load and CD4 adjusting for sex, age, and year of HIV diagnosis. Both univariate and multivariable logistic regression showed that viral load increased as AF-ALB levels increased. By univariate analysis, high viral load was 2.3 times more likely among persons in the third AF-ALB quartile (95% confidence interval (CI): 1.13, 4.51), and 2.9 times more likely among persons in the fourth AF-ALB quartile (CI: 1.41, 5.88), compared to persons in the first quartile. In the multivariable model, persons in the fourth AF-ALB quartile were about 2.6 times more likely to have high viral loads than persons in the first quartile (CI: 1.19-5.69). When AF-ALB and viral load were log transformed and linear regression analysis conducted, the univariate linear regression analysis showed that for each pg/mg increase in AF-ALB, viral load increased by approximately 1.6 copies/ml (P=0.0006). The association was marginally significant in the adjusted linear regression model (i.e. for each pg/mg increase in AF-ALB, the mean viral load increased by approximately 1.3 copies/ml, P=0.073). These data show strong and consistent increases in HIV viral load with increasing AF-ALB levels. Since the median and mean CD4 were greater than 500 cells for participants in each AF-ALB quartile, the results indicate that the immune modulating and virus transcription effects of aflatoxin may occur quite early in HIV infection, even while the CD4 count is still above 500, resulting in higher viral loads.</s0>
</fC01>
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<s5>01</s5>
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<s0>Human immunodeficiency virus</s0>
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<s2>NW</s2>
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<s0>Lentivirus</s0>
<s2>NW</s2>
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<s0>Lentivirus</s0>
<s2>NW</s2>
</fC07>
<fC07 i1="04" i2="X" l="FRE">
<s0>Retroviridae</s0>
<s2>NW</s2>
</fC07>
<fC07 i1="04" i2="X" l="ENG">
<s0>Retroviridae</s0>
<s2>NW</s2>
</fC07>
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<s0>Retroviridae</s0>
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<s2>NW</s2>
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<fC07 i1="05" i2="X" l="SPA">
<s0>Virus</s0>
<s2>NW</s2>
</fC07>
<fN21>
<s1>329</s1>
</fN21>
</pA>
<pR>
<fA30 i1="01" i2="1" l="ENG">
<s1>WMF meets IUPAC Conference</s1>
<s3>Rotterdam NLD</s3>
<s4>2012-11-05</s4>
</fA30>
<fA30 i1="02" i2="1" l="ENG">
<s1>Conference of The World Mycotoxin Forum</s1>
<s2>7</s2>
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<s1>IUPAC International Symposium on Mycotoxins and Phycotoxins</s1>
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<s4>2012-11-05</s4>
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<server>
<NO>PASCAL 13-0349936 INIST</NO>
<ET>Association between high aflatoxin B
<sub>1</sub>
levels and high viral load in HIV-positive people</ET>
<AU>JOLLY (P. E.); INUSAH (S.); LU (B.); ELLIS (W. O.); NYARKO (A.); PHILLIPS (T. D.); WILLIAMS (J. H.)</AU>
<AF>University of Alabama at Birmingham, Department of Epidemiology, School of Public Health, 1665 University Boulevard, RPHB 217/Birmingham, AL 35294-0022/Etats-Unis (1 aut., 2 aut., 3 aut.); Kwame Nkrumah University of Science and Technology/Kumasi/Ghana (4 aut.); Kumasi South Regional Hospital/Kumasi/Ghana (5 aut.); Department of Veterinary Integrative Biosciences, Texas A&M University, Mail Stop 4458/College Station, TX 77843/Etats-Unis (6 aut.); College of Agricultural and Environmental Sciences, University of Georgia, 1109 Experiment St/Griffin, GA 30223/Etats-Unis (7 aut.)</AF>
<DT>Publication en série; Congrès; Niveau analytique</DT>
<SO>World mycotoxin journal : (Print); ISSN 1875-0710; Pays-Bas; Da. 2013; Vol. 6; No. 3; Pp. 255-261; Bibl. 1 p.1/4</SO>
<LA>Anglais</LA>
<EA>Since both aflatoxin and the human immunodeficiency virus (HIV) cause immune suppression, chronic exposure to aflatoxin in HIV-positive people could lead to higher levels of virus replication. This study was conducted to examine the association between aflatoxin B
<sub>1</sub>
albumin adduct (AF-ALB) levels and HIV viral load. Antiretroviral naive HIV-positive people (314) with median CD4 count of 574 cells/μl blood (mean ± standard deviation = 630±277) were recruited in Kumasi, Ghana. Sociodemographic and health data, and blood samples were collected from participants. The plasma samples were tested for AF-ALB and HIV viral load. Univariate logistic regression analysis was conducted using viral load (high/low) as the outcome and AF-ALB quartiles as exposure. Multivariable logistic regression analysis was performed between quartile AF-ALB, viral load and CD4 adjusting for sex, age, and year of HIV diagnosis. Both univariate and multivariable logistic regression showed that viral load increased as AF-ALB levels increased. By univariate analysis, high viral load was 2.3 times more likely among persons in the third AF-ALB quartile (95% confidence interval (CI): 1.13, 4.51), and 2.9 times more likely among persons in the fourth AF-ALB quartile (CI: 1.41, 5.88), compared to persons in the first quartile. In the multivariable model, persons in the fourth AF-ALB quartile were about 2.6 times more likely to have high viral loads than persons in the first quartile (CI: 1.19-5.69). When AF-ALB and viral load were log transformed and linear regression analysis conducted, the univariate linear regression analysis showed that for each pg/mg increase in AF-ALB, viral load increased by approximately 1.6 copies/ml (P=0.0006). The association was marginally significant in the adjusted linear regression model (i.e. for each pg/mg increase in AF-ALB, the mean viral load increased by approximately 1.3 copies/ml, P=0.073). These data show strong and consistent increases in HIV viral load with increasing AF-ALB levels. Since the median and mean CD4 were greater than 500 cells for participants in each AF-ALB quartile, the results indicate that the immune modulating and virus transcription effects of aflatoxin may occur quite early in HIV infection, even while the CD4 count is still above 500, resulting in higher viral loads.</EA>
<CC>002B03J</CC>
<FD>Association; Aflatoxine B1; Albumine; Ghana; Virus immunodéficience humaine; Mycotoxine</FD>
<FG>Toxine; Afrique; Lentivirus; Retroviridae; Virus</FG>
<ED>Association; Aflatoxin B1; Albumin; Ghana; Human immunodeficiency virus; Mycotoxin</ED>
<EG>Toxin; Africa; Lentivirus; Retroviridae; Virus</EG>
<SD>Asociación; Aflatoxina B1; Albúmina; Ghana; Human immunodeficiency virus; Micotoxina</SD>
<LO>INIST-28127.354000503683990050</LO>
<ID>13-0349936</ID>
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