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HIV Infection and the Incidence of Malaria Among HIV-Exposed Children from Tanzania

Identifieur interne : 001700 ( Pmc/Corpus ); précédent : 001699; suivant : 001701

HIV Infection and the Incidence of Malaria Among HIV-Exposed Children from Tanzania

Auteurs : Amara E. Ezeamama ; Donna Spiegelman ; Ellen Hertzmark ; Ronald J. Bosch ; Karim P. Manji ; Christopher Duggan ; Roland Kupka ; Melanie W. Lo ; James O. Okuma ; Rodrick Kisenge ; Said Aboud ; Wafaie W. Fawzi

Source :

RBID : PMC:3415816

Abstract

Objective

To determine whether human immunodeficiency virus (HIV) infection is associated with increased risk of malaria incidence and recurrence in children.

Methods

Newborn infants of HIV-infected mothers were enrolled at 6 weeks and followed for 2 years. HIV status was assessed by enzyme-linked immunosorbant assay and confirmed by HIV DNA polymerase chain reaction. Malaria was defined as (1) physician-diagnosed clinical malaria; (2) probable malaria, in which laboratory testing is requested for parasitemia; and (3) blood smear–confirmed malaria. Cox proportional hazards models estimated hazard ratios (HRs) for development of first and second malaria episodes, and generalized estimating equation models estimated malaria rate differences per 100-child-years in relation to time-updated HIV status.

Results

Child HIV infection was associated with clinical (HR, 1.34; 95% confidence interval [CI], 1.12–1.61), probable (HR, 1.47; 95% CI, 1.19–1.81), and confirmed (HR, 1.67; 95% CI, 1.18–2.36) malaria episodes. Per 100 child-years, HIV-infected children experienced 88 (95% CI, 65–113), 36 (95% CI, 19–53), and 20 (95% CI, 9–31) more episodes of clinical, probable, and confirmed malaria episodes, respectively, than HIV-uninfected children. Among children with ≥1 malaria episodes, those with HIV infection developed second clinical (HR, 1.28; 95% CI, 1.04–1.57), probable (HR, 1.60; 95% CI, 1.26–2.14), and confirmed (HR, 2.27; 95% CI, 1.06–3.89) malaria sooner than HIV-uninfected children.

Conclusions

HIV infection is a risk factor for the development of malaria. Proactive malaria disease prevention and treatment is warranted for all children, particularly those with HIV infection in settings of coendemicity.


Url:
DOI: 10.1093/infdis/jis234
PubMed: 22457274
PubMed Central: 3415816

Links to Exploration step

PMC:3415816

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,
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<div type="abstract" xml:lang="en">
<sec>
<title>Objective</title>
<p>To determine whether human immunodeficiency virus (HIV) infection is associated with increased risk of malaria incidence and recurrence in children.</p>
</sec>
<sec>
<title>Methods</title>
<p>Newborn infants of HIV-infected mothers were enrolled at 6 weeks and followed for 2 years. HIV status was assessed by enzyme-linked immunosorbant assay and confirmed by HIV DNA polymerase chain reaction. Malaria was defined as (1) physician-diagnosed clinical malaria; (2) probable malaria, in which laboratory testing is requested for parasitemia; and (3) blood smear–confirmed malaria. Cox proportional hazards models estimated hazard ratios (HRs) for development of first and second malaria episodes, and generalized estimating equation models estimated malaria rate differences per 100-child-years in relation to time-updated HIV status.</p>
</sec>
<sec>
<title>Results</title>
<p>Child HIV infection was associated with clinical (HR, 1.34; 95% confidence interval [CI], 1.12–1.61), probable (HR, 1.47; 95% CI, 1.19–1.81), and confirmed (HR, 1.67; 95% CI, 1.18–2.36) malaria episodes. Per 100 child-years, HIV-infected children experienced 88 (95% CI, 65–113), 36 (95% CI, 19–53), and 20 (95% CI, 9–31) more episodes of clinical, probable, and confirmed malaria episodes, respectively, than HIV-uninfected children. Among children with ≥1 malaria episodes, those with HIV infection developed second clinical (HR, 1.28; 95% CI, 1.04–1.57), probable (HR, 1.60; 95% CI, 1.26–2.14), and confirmed (HR, 2.27; 95% CI, 1.06–3.89) malaria sooner than HIV-uninfected children.</p>
</sec>
<sec>
<title>Conclusions</title>
<p>HIV infection is a risk factor for the development of malaria. Proactive malaria disease prevention and treatment is warranted for all children, particularly those with HIV infection in settings of coendemicity.</p>
</sec>
</div>
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<journal-id journal-id-type="nlm-ta">J Infect Dis</journal-id>
<journal-id journal-id-type="iso-abbrev">J. Infect. Dis</journal-id>
<journal-id journal-id-type="publisher-id">jinfdis</journal-id>
<journal-id journal-id-type="hwp">jinfdis</journal-id>
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<journal-title>The Journal of Infectious Diseases</journal-title>
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<issn pub-type="epub">1537-6613</issn>
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<article-id pub-id-type="publisher-id">jis234</article-id>
<article-categories>
<subj-group subj-group-type="heading">
<subject>Major Articles and Brief Reports</subject>
<subj-group subj-group-type="heading">
<subject>HIV/AIDS</subject>
</subj-group>
</subj-group>
<series-title>Editor's choice</series-title>
</article-categories>
<title-group>
<article-title>HIV Infection and the Incidence of Malaria Among HIV-Exposed Children from Tanzania</article-title>
</title-group>
<contrib-group>
<contrib contrib-type="author">
<name>
<surname>Ezeamama</surname>
<given-names>Amara E.</given-names>
</name>
<xref ref-type="aff" rid="af1">1</xref>
</contrib>
<contrib contrib-type="author">
<name>
<surname>Spiegelman</surname>
<given-names>Donna</given-names>
</name>
<xref ref-type="aff" rid="af2">2</xref>
<xref ref-type="aff" rid="af3">3</xref>
</contrib>
<contrib contrib-type="author">
<name>
<surname>Hertzmark</surname>
<given-names>Ellen</given-names>
</name>
<xref ref-type="aff" rid="af3">3</xref>
</contrib>
<contrib contrib-type="author">
<name>
<surname>Bosch</surname>
<given-names>Ronald J.</given-names>
</name>
<xref ref-type="aff" rid="af3">3</xref>
<xref ref-type="aff" rid="af4">4</xref>
</contrib>
<contrib contrib-type="author">
<name>
<surname>Manji</surname>
<given-names>Karim P.</given-names>
</name>
<xref ref-type="aff" rid="af5">5</xref>
</contrib>
<contrib contrib-type="author">
<name>
<surname>Duggan</surname>
<given-names>Christopher</given-names>
</name>
<xref ref-type="aff" rid="af1">1</xref>
<xref ref-type="aff" rid="af6">6</xref>
</contrib>
<contrib contrib-type="author">
<name>
<surname>Kupka</surname>
<given-names>Roland</given-names>
</name>
<xref ref-type="aff" rid="af1">1</xref>
<xref ref-type="aff" rid="af7">7</xref>
</contrib>
<contrib contrib-type="author">
<name>
<surname>Lo</surname>
<given-names>Melanie W.</given-names>
</name>
<xref ref-type="aff" rid="af8">8</xref>
</contrib>
<contrib contrib-type="author">
<name>
<surname>Okuma</surname>
<given-names>James O.</given-names>
</name>
<xref ref-type="aff" rid="af1">1</xref>
</contrib>
<contrib contrib-type="author">
<name>
<surname>Kisenge</surname>
<given-names>Rodrick</given-names>
</name>
<xref ref-type="aff" rid="af5">5</xref>
</contrib>
<contrib contrib-type="author">
<name>
<surname>Aboud</surname>
<given-names>Said</given-names>
</name>
<xref ref-type="aff" rid="af5">5</xref>
<xref ref-type="aff" rid="af9">9</xref>
</contrib>
<contrib contrib-type="author">
<name>
<surname>Fawzi</surname>
<given-names>Wafaie W.</given-names>
</name>
<xref ref-type="aff" rid="af1">1</xref>
</contrib>
</contrib-group>
<aff id="af1">
<label>1</label>
<addr-line>Department of Nutrition</addr-line>
</aff>
<aff id="af2">
<label>2</label>
<addr-line>Department of Epidemiology</addr-line>
</aff>
<aff id="af3">
<label>3</label>
<addr-line>Department of Biostatistics</addr-line>
</aff>
<aff id="af4">
<label>4</label>
<addr-line>Center for Biostatistics in AIDS Research</addr-line>
,
<institution>Harvard School of Public Health</institution>
</aff>
<aff id="af5">
<label>5</label>
<addr-line>Department of Pediatrics and Child Health, School of Medicine</addr-line>
</aff>
<aff id="af6">
<label>6</label>
<addr-line>Division of Gastroenterology and Nutrition</addr-line>
,
<institution>Children's Hospital</institution>
,
<addr-line>Boston, Massachusetts</addr-line>
</aff>
<aff id="af7">
<label>7</label>
<addr-line>United Nations Children's Fund</addr-line>
,
<institution>Regional Office for West and Central Africa</institution>
,
<addr-line>Dakar</addr-line>
,
<country>Senegal</country>
</aff>
<aff id="af8">
<label>8</label>
<institution>University of Minnesota Medical School</institution>
, Minneapolis</aff>
<aff id="af9">
<label>9</label>
<addr-line>Department of Microbiology and Immunology</addr-line>
,
<institution>Muhimbili University of Health and Allied Sciences</institution>
,
<addr-line>Dar es Salaam</addr-line>
,
<country>Tanzania</country>
</aff>
<author-notes>
<fn>
<p>Presented in part: Rank Prize Funds Minisymposium on Nutrition and HIV, Windermere, United Kingdom, 2–5 March 2009.</p>
</fn>
<corresp>Correspondence: Amara E. Ezeamama, PhD, Department of Nutrition, Harvard School of Public Health, 667 Huntington Ave, Bldg 2, Room 302, Boston, MA 02115 (
<email>aezeamam@hsph.harvard.edu</email>
).</corresp>
</author-notes>
<pub-date pub-type="ppub">
<day>15</day>
<month>5</month>
<year>2012</year>
</pub-date>
<pub-date pub-type="epub">
<day>28</day>
<month>3</month>
<year>2012</year>
</pub-date>
<volume>205</volume>
<issue>10</issue>
<fpage>1486</fpage>
<lpage>1494</lpage>
<history>
<date date-type="received">
<day>12</day>
<month>8</month>
<year>2011</year>
</date>
<date date-type="accepted">
<day>16</day>
<month>11</month>
<year>2011</year>
</date>
</history>
<permissions>
<copyright-statement>© The Author 2012. Published by Oxford University Press on behalf of the Infectious Diseases Society of America. All rights reserved. For Permissions, please e-mail: journals.permissions@oup.com.</copyright-statement>
<copyright-year>2012</copyright-year>
</permissions>
<self-uri content-type="pdf" xlink:type="simple" xlink:href="jis234.pdf"></self-uri>
<abstract>
<sec>
<title>Objective</title>
<p>To determine whether human immunodeficiency virus (HIV) infection is associated with increased risk of malaria incidence and recurrence in children.</p>
</sec>
<sec>
<title>Methods</title>
<p>Newborn infants of HIV-infected mothers were enrolled at 6 weeks and followed for 2 years. HIV status was assessed by enzyme-linked immunosorbant assay and confirmed by HIV DNA polymerase chain reaction. Malaria was defined as (1) physician-diagnosed clinical malaria; (2) probable malaria, in which laboratory testing is requested for parasitemia; and (3) blood smear–confirmed malaria. Cox proportional hazards models estimated hazard ratios (HRs) for development of first and second malaria episodes, and generalized estimating equation models estimated malaria rate differences per 100-child-years in relation to time-updated HIV status.</p>
</sec>
<sec>
<title>Results</title>
<p>Child HIV infection was associated with clinical (HR, 1.34; 95% confidence interval [CI], 1.12–1.61), probable (HR, 1.47; 95% CI, 1.19–1.81), and confirmed (HR, 1.67; 95% CI, 1.18–2.36) malaria episodes. Per 100 child-years, HIV-infected children experienced 88 (95% CI, 65–113), 36 (95% CI, 19–53), and 20 (95% CI, 9–31) more episodes of clinical, probable, and confirmed malaria episodes, respectively, than HIV-uninfected children. Among children with ≥1 malaria episodes, those with HIV infection developed second clinical (HR, 1.28; 95% CI, 1.04–1.57), probable (HR, 1.60; 95% CI, 1.26–2.14), and confirmed (HR, 2.27; 95% CI, 1.06–3.89) malaria sooner than HIV-uninfected children.</p>
</sec>
<sec>
<title>Conclusions</title>
<p>HIV infection is a risk factor for the development of malaria. Proactive malaria disease prevention and treatment is warranted for all children, particularly those with HIV infection in settings of coendemicity.</p>
</sec>
</abstract>
<counts>
<page-count count="28"></page-count>
</counts>
</article-meta>
</front>
</pmc>
</record>

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