SidaSubSaharaV1, Istex, Corpus, bibRecord, 002976

Assessing Eosinophil Count as a Marker of Immune Activation among Human Immunodeficiency Virus—Infected Persons in Sub-Saharan Africa

Identifieur interne : 002976 ( Istex/Corpus ); précédent : 002975; suivant : 002977

Assessing Eosinophil Count as a Marker of Immune Activation among Human Immunodeficiency Virus—Infected Persons in Sub-Saharan Africa

Auteurs : T. L. Chorba ; J. Nkengasong ; T. H. Roels ; B. Monga ; C. Maurice ; M. Maran ; G. Djomand

Source :

Clinical Infectious Diseases [ 1058-4838 ] ; 2002-05-01.

RBID : ISTEX:7FAE7D625E8794159B964D9ACBDD0624915E1DA8

Abstract

In 611 human immunodeficiency virus—infected persons who had not yet begun to receive antiretroviral therapy, we evaluated the linear association between absolute eosinophil count (as a surrogate for immune response to helminthic infection) and CD4+ T cell count, and between absolute eosinophil count and log virus load. Overall, no significant correlations were observed between eosinophil count and CD4+ T cell count, or between eosinophil count and log virus load.

Url:

https://api.istex.fr/document/7FAE7D625E8794159B964D9ACBDD0624915E1DA8/fulltext/pdf

DOI: 10.1086/339940

Links to Exploration step

ISTEX:7FAE7D625E8794159B964D9ACBDD0624915E1DA8

Le document en format XML

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, <addr-line>Atlanta, Georgia</addr-line>
</aff>

<aff id="aff2"><label>2</label>
<institution>Global AIDS Program, Centers for Disease Control and Prevention</institution>
, <addr-line>Atlanta, Georgia</addr-line>
</aff>

<aff id="aff3"><label>3</label>
<institution>Division of HIV/AIDS Prevention, National Center for HIV, STD and TB Prevention, Centers for Disease Control and Prevention</institution>
, <addr-line>Atlanta, Georgia</addr-line>
</aff>

</contrib-group>

<author-notes>

<corresp id="cor1">Reprints or correspondence: Dr. Terence L. Chorba, Div. of STD Prevention, Centers for Disease Control and Prevention, Mailstop E-44, 1600 Clifton Rd. NE, Atlanta, GA 30333 (<email>TLC2@cdc.gov</email>
); or Dr. John Nkengasong, Projet RETRO-CI, B.P. 1712, Abidjan, Côte d'Ivoire (<email>JCN5@cdc.gov</email>
).</corresp>

<fn fn-type="current-aff" id="FN1"><label>a</label>
<p>Present affiliation: Global AIDS Program (T.H.R.) and Division of STD Prevention (T.L.C.), National Center for HIV, STD and TB Prevention, Centers for Disease Control and Prevention, Atlanta, Georgia.</p>
</fn>

</author-notes>

<pub-date pub-type="ppub">

<day>1</day>

<month>5</month>

<year>2002</year>

</pub-date>

<volume>34</volume>

<issue>9</issue>

<fpage>1264</fpage>

<lpage>1266</lpage>

<history>

<date date-type="received">

<day>24</day>

<month>7</month>

<year>2001</year>

</date>

<date date-type="rev-recd">

<day>4</day>

<month>12</month>

<year>2001</year>

</date>

</history>

<copyright-statement>© 2002 by the Infectious Diseases Society of America</copyright-statement>

<copyright-year>2002</copyright-year>

<abstract>

<p>In 611 human immunodeficiency virus—infected persons who had not yet begun to receive antiretroviral therapy, we evaluated the linear association between absolute eosinophil count (as a surrogate for immune response to helminthic infection) and CD4<sup>+</sup>
 T cell count, and between absolute eosinophil count and log virus load. Overall, no significant correlations were observed between eosinophil count and CD4<sup>+</sup>
 T cell count, or between eosinophil count and log virus load.</p>

</abstract>

</article-meta>

</front>

<body>

<p>A better understanding is needed as to why the HIV/AIDS epidemic in sub-Saharan Africa has been predominantly heterosexual, unlike the epidemic in Europe and North America. High virus loads may account, at least in part, for the higher rates of heterosexual transmission: in studies of discordant couples, the virus load was found to be the chief predictor of the risk of heterosexual transmission of HIV type 1 (HIV-1), as compared with other risk factors for heterosexual transmission, and transmission was found to be rare among persons with HIV RNA levels of µ1500 copies/mL [<xref rid="ref1" ref-type="bibr">1</xref>
]. In addition, both susceptibility to HIV infection [<xref rid="ref2" ref-type="bibr">2</xref>
] and increases in virus load (which lead to faster progression of HIV disease) [<xref rid="ref3" ref-type="bibr">3</xref>
] have been associated with common infections, including sexually transmitted infections [<xref rid="ref3" ref-type="bibr">3</xref>
], malaria [<xref rid="ref4" ref-type="bibr">4</xref>
], tuberculosis [<xref rid="ref5" ref-type="bibr">5</xref>
], and helminthic infections [<xref rid="ref6" ref-type="bibr">6</xref>
].</p>

<p>Of the factors that can influence transmission and progression of HIV infection, the contribution of helminthic infections to the spread of HIV has not been fully explored. Tissue-dwelling and intestinal helminthic infections occur predominantly in tropical regions and rural areas of the world where sanitation and personal hygiene are poor and where education and resources to control these parasites are lacking [<xref rid="ref7" ref-type="bibr">7</xref>
]. Both tissue-dwelling and intestinal helminthic infections result in an expansion of the T helper (Th2) lymphocyte subset (with a resultant increase in serum IgE levels, eosinophils, and mast cells) [<xref rid="ref8" ref-type="bibr">8</xref>
, <xref rid="ref9" ref-type="bibr">9</xref>
] and a shift in cytokine balance toward a Th2-type response [<xref rid="ref10" ref-type="bibr">10</xref>
]. Indeed, high levels of immune activation with high levels of serum IgE have been reported in young Thai workers in Israel [<xref rid="ref11" ref-type="bibr">11</xref>
]. Furthermore, in studies of HIV-infected Ethiopian immigrants in Israel, egg secretion in stool has been directly correlated with virus load, and eradication of helminths has been found to significantly decrease virus load [<xref rid="ref6" ref-type="bibr">6</xref>
]. However, in another study of sugar-estate residents in Ethiopia, HIV-positive and HIV-negative persons were found, in general, to have similar rates of carriage of intestinal parasites, although amoebic parasites were more commonly found in HIV-positive persons than in HIV-negative persons [<xref rid="ref12" ref-type="bibr">12</xref>
].</p>

<p>In an attempt to determine the extent to which potential helminth infection—induced immune activation may contribute to the HIV epidemic observed in sub-Saharan Africa, we evaluated the correlation between eosinophilia (as a surrogate for immune response to helminthic infection) and CD4<sup>+</sup>
 T cell counts and that between eosinophilia and HIV loads in HIV-infected persons who had not yet started receiving antiretroviral therapy.</p>

<p><bold><italic>Method</italic>
</bold>
. From 5 October 1998 through 28 December 2000, 2748 antiretroviral-naive HIV-positive patients were evaluated for treatment in the Joint United Nations Programme on HIV/AIDS (UNAIDS) HIV Drug Access Initiative in Abidjan, the largest city in Côte d'Ivoire. All patients were seen at any 1 of 7 clinics that participated in this initiative. These clinics included university hospital departments of infectious diseases (in Treichville), pediatrics (in Yopougon), and pulmonary diseases (in Cocody); an outpatient tuberculosis treatment center (in Adjamé); a military hospital (in Abobo); a Ministry of Health outpatient AIDS clinic (Unite de soins ambulatoires et conseil [USAC]; Treichville); and a private outpatient AIDS clinic (the Centre Intégré de Recherches Biocliniques d'Abidjan [CIRBA]). After they consulted the clinic for treatment, patients provided blood samples for testing for clinical purposes. In all, 741 patients underwent appropriate initial laboratory evaluation and started to receive an antiretroviral treatment during the study period; of these patients, 611 were µ15 years old. Routine laboratory data for these 611 patients were used for our analyses.</p>

<p>Laboratory evaluation included verification of HIV serologic status, a routine complete blood cell count, virus load determination, and a CD4<sup>+</sup>
 T cell count, all of which were performed at the Projet RETRO-CI laboratory in Abidjan. This laboratory is maintained by the US Centers for Disease Control and Prevention (CDC; Atlanta), in conjunction with the Côte d'Ivoire Ministry of Health, and it participates routinely in the CDC's proficiency testing programs. Whole blood samples were collected into EDTA (K3) tubes (Becton Dickinson). Within 4 h of the time that the blood sample was obtained, plasma was separated from cells by centrifugation at 200<italic>g</italic>
, aliquoted, and stored at -70°C.</p>

<p>We determined HIV antibody status using an ELISA-based testing algorithm [<xref rid="ref13" ref-type="bibr">13</xref>
]. For HIV type-specific serodiagnosis, we used a synthetic peptide line immunoassay (Peptilav 1–2; Sanofi Diagnostics). Eosinophil (eosinophilic granulocyte) counts, in cells per microliter, were determined using complete blood cell counts on EDTA samples, by use of Coulter Max M (Coultronics France SA).</p>

<p>HIV RNA load was quantified in plasma by use of the Amplicor HIV-1 Monitor test, version 1.5 (Roche Diagnostics Systems). This assay accurately quantifies HIV-1 subtype A/G recombinant viruses, which are the predominant subtypes in Côte d'Ivoire [<xref rid="ref14" ref-type="bibr">14</xref>
, <xref rid="ref15" ref-type="bibr">15</xref>
]. The lower limit of detection of this assay is 200 copies/mL. CD4<sup>+</sup>
 T cell counts, in cells per microliter, were determined with a 3-color flow cytometric measurement of fresh peripheral whole blood samples by use of a FACScan flow cytometer (Becton Dickinson). All assays were performed according to the methods recommended by the manufacturers.</p>

<p>Spearman rank-correlation analysis [<xref rid="ref16" ref-type="bibr">16</xref>
] was performed to assess the linear associations between absolute eosinophil count and CD4<sup>+</sup>
 T cell count and between absolute eosinophil count and log virus load. Because of reported sex-specific differences in CD4<sup>+</sup>
 T cell counts that have been observed in patients with certain HIV loads [<xref rid="ref17" ref-type="bibr">17</xref>
–<xref rid="ref19" ref-type="bibr">19</xref>
], we also performed Spearman rank-correlation analyses to assess the overall linear association between absolute eosinophil count and log virus load for male and female patients. Stratification according to CD4<sup>+</sup>
 T cell count was consistent with the CDC's 1993 revised classification system for HIV infection and expanded AIDS surveillance case definition criteria [<xref rid="ref20" ref-type="bibr">20</xref>
]: CD4<sup>+</sup>
 T cell counts, 0–199 cells/µL, 200–499 cells/µL, and ≥500 cells/µL.</p>

<p><bold><italic>Result</italic>
</bold>
. Of the 611 patients, 341 (56%) were male. The median patient age was 36 years (interquartile range [IQR], 31–43 years). For the 611 patients, the median absolute eosinophil count was 155 cells/µL (IQR, 64–368 cells/µL), the median CD4<sup>+</sup>
 T cell count was 115 cells/µL (IQR, 22–243 cells/µL), and the median HIV-1 RNA load was 5.6 log<sub>10</sub>
 copies/mL (IQR, 4.8–6.0 log<sub>10</sub>
 copies/mL). The median absolute eosinophil count value was well within the range of normal values reported elsewhere [<xref rid="ref21" ref-type="bibr">21</xref>
].</p>

<p>No significant correlation was observed overall between eosinophil count and CD4<sup>+</sup>
 T cell count (<italic>r</italic>
<sup>2</sup>
, 0.04; <italic>P</italic>
 = 0.28) or between eosinophil count and log virus load (<italic>r</italic>
<sup>2</sup>
, 0.008; <italic>P</italic>
 = 0.85). No significant correlations were observed between eosinophil count and virus load after stratification by sex and CD4<sup>+</sup>
 T cell count (<xref rid="tab1" ref-type="fig">table 1</xref>
).</p>

<p><bold><italic>Discussio</italic>
</bold>
. Although helminthic infections can be credited with contributing enormously to morbidity among populations in sub-Saharan Africa [<xref rid="ref22" ref-type="bibr">22</xref>
, <xref rid="ref23" ref-type="bibr">23</xref>
], the data presented here do not indicate that eosinophil counts are associated with virus loads or CD4<sup>+</sup>
 T cell counts in persons infected with HIV. However, although there has been considerable interest in immune activation as a potential contributor to the spread of HIV infection in Africa [<xref rid="ref2" ref-type="bibr">2</xref>
, <xref rid="ref3" ref-type="bibr">3</xref>
, <xref rid="ref24" ref-type="bibr">24</xref>
, <xref rid="ref25" ref-type="bibr">25</xref>
], the relationship between body burden of infection and immune activation is not necessarily linear.</p>

<p>The intravascular half-life of eosinophils is ∼2 h [<xref rid="ref26" ref-type="bibr">26</xref>
], and the development and terminal differentiation of eosinophils in humans is IL-5 dependent [<xref rid="ref27" ref-type="bibr">27</xref>
]. In murine models of helminthic infection, the major source of IL-5 is the T helper subset, Th2 [<xref rid="ref27" ref-type="bibr">27</xref>
]. Although it remains unclear whether Th2-derived responses (including the increase in IgE levels, eosinophils, and mast cells) have an important role in the protective immune response to helminths in humans [<xref rid="ref8" ref-type="bibr">8</xref>
], eosinophil count (as a potential surrogate marker for helminth-induced immune activation) was not correlated with CD4<sup>+</sup>
 T cell count or HIV load in the data presented here.</p>

<p>Th2-derived responses may themselves be specific, as well as being stimulus specific, and the immunologic mechanisms that result in the helminth-induced Th2-derived response of eosinophilia may have a certain independence from those Th2-derived mechanisms that affect the dynamics of HIV replication. In addition, intravascular eosinophil counts may not be well correlated with the body burden of helminths; eosinophilia is not a constant feature of helminthic infection, and the absence of elevated eosinophil levels does not exclude the presence of helminths [<xref rid="ref28" ref-type="bibr">28</xref>
, <xref rid="ref29" ref-type="bibr">29</xref>
]. Elevation of eosinophil counts in response to helminthic infection is less commonly seen among persons from endemic areas who have had life-long exposure to such infections than they are among persons who have recently been infected for the first time [<xref rid="ref30" ref-type="bibr">30</xref>
, <xref rid="ref31" ref-type="bibr">31</xref>
]. Unfortunately, in this study, we had no direct measure of the presence or burden of helminthic infection. The fact that the median eosinophil count in the study population was well within the normal range for a Western population may indicate the nonrepresentativeness of the study population, with respect to the presence or absence of helminthic infection. Alternatively, if the study population was representative of West African adults with respect to helminthic infection, the low median eosinophil count may indicate that intravascular eosinophil counts are a poor marker for helminth-induced immune activation.</p>

<p>Subsequent studies to evaluate the potential correlation between helminthic infection and HIV transmission and susceptibility in sub-Saharan Africa should examine serum IgE levels, the presence of mastocytosis, levels of cytokines, and other direct and indirect measures of the body burden of and the immune response to helminthic infection. As cohorts are developed for potential vaccination trials, advantage should be taken of opportunities to evaluate more directly the contribution of helminthic infection to HIV transmission and susceptibility.</p>

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<caption><p><bold>Spearman-rank correlation between absolute eosinophil count and log HIV type 1 (HIV-1) RNA level among antiretroviralnaive HIV-infected patients, by sex and CD4<sup>+</sup>
 T cell count.</bold>
</p>
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<affiliation>Global AIDS Program, Centers for Disease Control and Prevention, Atlanta, Georgia</affiliation>
<affiliation>E-mail: TLC2@cdc.gov</affiliation>
<affiliation>Reprints or correspondence: Dr. Terence L. Chorba, Div. of STD Prevention, Centers for Disease Control and Prevention, Mailstop E-44, 1600 Clifton Rd. NE, Atlanta, GA 30333</affiliation>
<affiliation>E-mail: TLC2@cdc.gov</affiliation>
<description>aPresent affiliation: Global AIDS Program (T.H.R.) and Division of STD Prevention (T.L.C.), National Center for HIV, STD and TB Prevention, Centers for Disease Control and Prevention, Atlanta, Georgia.</description>
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<name type="personal"><namePart type="given">J.</namePart>
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<affiliation>Projet RETRO-CI, Abidjan, Côte d'Ivoire;, Atlanta, Georgia</affiliation>
<affiliation>Division of HIV/AIDS Prevention, National Center for HIV, STD and TB Prevention, Centers for Disease Control and Prevention, Atlanta, Georgia</affiliation>
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<affiliation>Division of HIV/AIDS Prevention, National Center for HIV, STD and TB Prevention, Centers for Disease Control and Prevention, Atlanta, Georgia</affiliation>
<description>aPresent affiliation: Global AIDS Program (T.H.R.) and Division of STD Prevention (T.L.C.), National Center for HIV, STD and TB Prevention, Centers for Disease Control and Prevention, Atlanta, Georgia.</description>
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<name type="personal"><namePart type="given">B.</namePart>
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<name type="personal"><namePart type="given">G.</namePart>
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<abstract>In 611 human immunodeficiency virus—infected persons who had not yet begun to receive antiretroviral therapy, we evaluated the linear association between absolute eosinophil count (as a surrogate for immune response to helminthic infection) and CD4+ T cell count, and between absolute eosinophil count and log virus load. Overall, no significant correlations were observed between eosinophil count and CD4+ T cell count, or between eosinophil count and log virus load.</abstract>
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Assessing Eosinophil Count as a Marker of Immune Activation among Human Immunodeficiency Virus—Infected Persons in Sub-Saharan Africa

Assessing Eosinophil Count as a Marker of Immune Activation among Human Immunodeficiency Virus—Infected Persons in Sub-Saharan Africa

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