SidaSubSaharaV1, Istex, Corpus, bibRecord, 003557

High Frequency of Antiretroviral Drug Resistance among HIV-Infected Adults Receiving First-Line Highly Active Antiretroviral Therapy in N'Djamena, Chad

Identifieur interne : 003557 ( Istex/Corpus ); précédent : 003556; suivant : 003558

High Frequency of Antiretroviral Drug Resistance among HIV-Infected Adults Receiving First-Line Highly Active Antiretroviral Therapy in N'Djamena, Chad

Auteurs : Donato Koyalta ; Charlotte Charpentier ; Jatibi Beassamda ; Elisabeth Rey ; Ali Si-Mohamed ; Noël Djemadji-Oudjeil ; Laurent Bélec

Source :

Clinical Infectious Diseases [ 1058-4838 ] ; 2009-07-01.

RBID : ISTEX:A2B4843EF2F91111F5D9269E70B62FE1C285FA6D

Abstract

Antiretroviral drug resistance was evaluated in 88 adults infected with human immunodeficiency virus, most with subtype CRF11_cpx, who had received a first-line antiretroviral regimen for 6 months, in N'Djamena, Chad. A total of 47 patients (53%) had detectable viral load at month 6, and 56 (64%) had at least 1 antiretroviral resistance mutation observed.

Url:

https://api.istex.fr/document/A2B4843EF2F91111F5D9269E70B62FE1C285FA6D/fulltext/pdf

DOI: 10.1086/599611

Links to Exploration step

ISTEX:A2B4843EF2F91111F5D9269E70B62FE1C285FA6D

Le document en format XML

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<xref rid="aff3" ref-type="aff">3</xref>

</contrib>

<aff id="aff1"><label>1</label>
<institution>Reference Laboratory, Hôpital Général de Référence Nationale, N'</institution>
, <addr-line>Djamena, Chad</addr-line>
</aff>

<aff id="aff2"><label>2</label>
<institution>Laboratoire de Virologie, Hôpital Européen Georges Pompidou</institution>
, <addr-line>Paris, France</addr-line>
</aff>

<aff id="aff3"><label>3</label>
<institution>Faculté de Médecine Paris Descartes</institution>
, <addr-line>Paris, France</addr-line>
</aff>

<aff id="aff4"><label>4</label>
<institution>Service de Pharmacologie Clinique, Groupe Hospitalier Cochin Hôpital Saint-Vincent de Paul</institution>
, <addr-line>Paris, France</addr-line>
</aff>

</contrib-group>

<author-notes>

<corresp id="cor1">Reprints or correspondence: Dr. Charlotte Charpentier, Hôpital Européen Georges Pompidou, Laboratoire de Virologie, 20 rue Leblanc, 75015 Paris, France (<email>charlotte.charpentier@egp.aphp.fr</email>
).</corresp>

<fn fn-type="other"><label>a</label>
<p>D.K. and C.C. contributed equally to this article.</p>
</fn>

</author-notes>

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

<day>1</day>

<month>7</month>

<year>2009</year>

</pub-date>

<volume>49</volume>

<issue>1</issue>

<fpage>155</fpage>

<lpage>159</lpage>

<history>

<date date-type="received">

<day>16</day>

<month>12</month>

<year>2008</year>

</date>

<date date-type="accepted">

<day>7</day>

<month>2</month>

<year>2009</year>

</date>

</history>

<copyright-statement>© 2009 by the Infectious Diseases Society of America</copyright-statement>

<copyright-year>2009</copyright-year>

<abstract>

<p>Antiretroviral drug resistance was evaluated in 88 adults infected with human immunodeficiency virus, most with subtype CRF11_cpx, who had received a first-line antiretroviral regimen for 6 months, in N'Djamena, Chad. A total of 47 patients (53%) had detectable viral load at month 6, and 56 (64%) had at least 1 antiretroviral resistance mutation observed.</p>

</abstract>

</article-meta>

</front>

<body>

<p>The availability of highly active antiretroviral therapy (HAART) has rapidly increased in sub-Saharan Africa, and this has led to the emergence of antiretroviral (ARV) drug resistance. The reported rates of drug resistance among patients who received ARV therapy in sub-Saharan Africa have shown large variation; rates are reported to be 3.7%–49% after 24–163 weeks ofHAART [<xref rid="ref1" ref-type="bibr">1</xref>
]. Numerous contributing factors may explain the differences among countries and among African cohorts, including variation in available health care systems, sociocultural factors associated with patient adherence to therapy, practices of prescribing ARV therapy, and access to biological monitoring [<xref rid="ref1" ref-type="bibr">1</xref>
], as well as the high level of human immunodeficiency virus (HIV) polymorphism that characterizes the virus circulating throughout sub-Saharan Africa [<xref rid="ref2" ref-type="bibr">2</xref>
].</p>

<p>Observational data on ARV drug resistance among patients receiving a first-line HAART are very scarce in central Africa and have previously been reported only in Cameroon [<xref rid="ref3" ref-type="bibr">3</xref>
, <xref rid="ref4" ref-type="bibr">4</xref>
]. In addition, Gody et al. [<xref rid="ref5" ref-type="bibr">5</xref>
] reported a high prevalence of ARV drug resistance among HIV-infected children treated in the Central African Republic. These reports prompted us to evaluate the frequency of ARV drug resistance among HIV-infected adults receiving first-line ARV therapy who were living in Chad, a country with a high prevalence of non-type B subtypes [<xref rid="ref6" ref-type="bibr">6</xref>
] and of circulating recombinant forms (CRFs) of HIV, especially CRF11_cpx. Chad is also characterized by poorly functioning medical systems and by various societal difficulties associated with the scaling up of ARV treatment access.</p>

<p><bold><italic>Patients and methods</italic>
</bold>
. Eighty-eight patients with HIV infection who attended the referral center for ARV therapy in the Hôpital Général de Référence Nationale (N'Djamena, Chad) were prospectively and consecutively included in our observational study in 2006. All patients were followed up for 6 months, in accordance with the World Health Organization (WHO) 2006 recommendations for ARV therapy in adults and adolescents in resource-limited settings [<xref rid="ref7" ref-type="bibr">7</xref>
], including 1 visit every month for delivery of ARV drugs, medical and biological monitoring, and observance counseling. All patients reported that they had not received any ARV drug combinations prior to enrollment and were given first-line ARV regimens: 81% received the generic fixed-dose formulation of stavudine, lamivudine, and nevirapine; and 19% received therapy containing nongeneric indinavir. The ARV regimens were not changed during the observation period.</p>

<p>After patients provided informal oral consent, a blood sample was obtained for measurement of CD4 cell count and HIV load (VERSANT HIV-1 RNA 3.0; Siemens Diagnostic Medical Solution). Measurements of plasma viral load were not available at baseline before initiation of treatment. The ARV drug resistance analysis was performed for all patients with a viral load >2.70 log<sub>10</sub>
copies/mL. ARV drug resistance was determined by sequencing of HIV reverse-transcriptase (RT) and protease genes, in accordance with the consensus technique of the Agence Nationale de Recherche sur le Sida et les hépatites virales (ANRS) [<xref rid="ref8" ref-type="bibr">8</xref>
]. Resistance-associated mutations in RT and protease genes were interpreted in accordance with the 2008 ANRS resistance algorithm ( http://www.hivfrenchresistance.org). GenBank accession numbers for the protease and RT gene sequences are FJ688173-FJ688209, respectively. HIV subtype was evaluated by comparing the polymerase sequence with consensus sequences with use of the Los Alamos HIV sequence database ( http://www.hiv.lanl.gov). Feedback from the results of HIV load testing and ARV drug resistance genotyping allows adaptation of ARV treatment. Plasma concentrations of nevirapine or indinavir were measured in plasma samples with use of a high-performance liquid chromatography assay.</p>

<p><bold><italic>Results</italic>
</bold>
. After 6 months of receiving an ARV regimen, the median CD4 cell count was 288 cells/mm<sup>3</sup>
(range, 30–960 cells/mm<sup>3</sup>
) (<xref rid="tab1" ref-type="fig">table 1</xref>
). HIV load was below the detection limit (50 copies/mL) in 41 (47%) of 88 patients. The median viral load among the remaining patients was 4.69 log<sub>10</sub>
copies/mL (range, 1.72–5.70 copies/mL). ARV drug resistance profiles were assessed in 38 patients who had a viral load >2.70 log<sub>10</sub>
copies/mL (<xref rid="tab1" ref-type="fig">table 1</xref>
). RT and protease gene sequences were obtained for 33 and 37 samples, respectively. The most prevalent HIV form was CRF11_cpx, which was detected in 8 (26%) of 31 patients whose HIV subtype was determined. Other HIV subtypes were observed, including subtype D in 5 patients (16%), CRF02_AG in 4 patients (13%), CRF12_BF in 4 patients (13%), CRF06_cpx in 3 patients (10%), CRF14_BG in 3 patients (10%), CRF01_AE in 2 patients (6%), and subtype G in 2 patients (6%). In 2 (6%) of 33 sequences examined, HIV subtype could not be classified because of the complexity of the recombination events detected.</p>

<p>Wild-type virus was detected in 13 patients (39%), including 8 patients who had high viral load measurements (>5 log<sub>10</sub>
copies/mL) and undetectable nevirapine or indinavirconcentrations, which likely suggests discontinuation of ARV treatment.</p>

<p>Twenty-one (64%) of 33 patients for whom the RT gene was sequenced exhibited virus with mutations that confer resistance to at least 1 ARV drug. The most frequently detected ARV drug resistance mutation was the M184V/I mutation, which was detected in 18 samples (55%). ARV drug-resistant virus harboring thymidine analogue-mutations (TAMs), which are associated with resistance to zidovudine and stavudine, were detected in 4 patients (12%); these mutations were indicative of the TAM-2 pathway, because the T215F mutation was present in all cases.</p>

<p>Mutations associated with resistance to nonnucleoside RT inhibitors (NNRTI) were found in 17 (52%) of 33 sequences obtained. A total of 28 NNRTI resistance mutations were detected in the 17 sequences (median mutations per sequence, 2; range, 1–3 mutations). The K103N/S mutation occurred most frequently and was detected in 8 (47%) of the 17 sequences that harbored NNRTI resistance mutations, whereas the Y181C mutation was detected in 6 sequences (35%). The V106I mutation, described as a natural polymorphism in HIV non-B subtypes, was found in 3 patients (3%), including 2 who were infected with subtype D. In our study, the prevalence of resistance to etravirine, a recent second-generation NNRTI, was found to be 3.6% among NNRTI-experienced patients, because 1 sample exhibited 3 mutations that are associated with a possible resistance to etravirine.</p>

<p>All protease sequences exhibited at least 2 mutations that are associated with resistance to protease inhibitors (median mutations per sequence, 5; range, 2–9 mutations). The majority of these mutations have been described elsewhere as non-B subtype polymorphisms [<xref rid="ref9" ref-type="bibr">9</xref>
]. Major protease inhibitor resistance mutations (M46I, L76V, V82A/T, I84V, and L90M) were detected in 5 (38%) of the 13 indinavir-treated patients. Interestingly, HIV protease sequences for 4 (14%) of 28 protease inhibitor-naive patients for whom sequences were available demonstrated possible resistance to saquinavir according to the ANRS algorithm, because the mutations L10I/V, I15V, and K20I/R were present. Two of the latter patients were infected with CRF12_BF, and the remaining 2 patients were infected with unclassified HIV subtypes.</p>

<p>Overall, among the 33 patients for whom both HIV RT and protease sequences were available, 21 (64%) were infected with virus that was resistant to 1 drug in their treatment, 14 (42%) were infected with virus that was resistant to 2 drugs in their treatment, and 3 (9%) were infected with virus that was resistant to all 3 drugs in their ARV therapy.</p>

<p><bold><italic>Discussion</italic>
</bold>
. In the present observational study on ARV drug resistance among patients who had received 6 months of HAART in Chad, nearly one-half of the patients had undetectable HIV loads and demonstrated successful ARV treatment, whereas the remaining patients had detectable viral loads, with the majority infected with ARV drug-resistant HIV. A minority of patients with detectable viral loads had no detected resistance mutations and undetectable ARV drug concentrations, likely suggesting a lack of treatment adherence. Thus, the prevalence of virological failure among the patients who effectively received their ARV regimens was particularly high in this hospital cohort (64%). The prevalence of ARV drug resistance mutations in patients who experienced virological failure corresponded to the respective usage of particular ARV drugs; 55% were receiving nucleoside RT inhibitors; 52% were receiving NNRTIs, and 13% were receiving protease inhibitors. Considering the patients who experienced virological failure and those who did not take their ARV treatment, the rate of unsuccessful health care of patients may be estimated to be 53%. Although it was not assessed in our study, the insufficiency of the health care system in Chad and the significant difficulties in obtaining adequate adherence to therapy in Central Africa [<xref rid="ref5" ref-type="bibr">5</xref>
] may have contributed to the high rate of therapeutic failure. The National AIDS Program in Chad tried to apply the WHO recommendations for HIV care in developing countries [<xref rid="ref7" ref-type="bibr">7</xref>
]; our observations confirm the operational difficulties encountered in the implementation of ARV drug access programs in developing countries that have poor conditions at the start. Furthermore, these results highlight the value of virological monitoring of ARV drug-treated patients by assessing plasma HIV load at least once per year, even in patients receiving first-line therapy, as is now recommended by the WHO [<xref rid="ref7" ref-type="bibr">7</xref>
].</p>

<p>The genetic diversity of HIV strains constitutes a huge challenge for ARV therapy strategies and monitoring, especially considering that most HIV studies related to ARV drug design and viral susceptibility were performed using subtype B virus. Previous studies have suggested no significant difference of HIV non-B subtypes in term of virological response to ARV drugs [<xref rid="ref10" ref-type="bibr">10</xref>
,<xref rid="ref11" ref-type="bibr">11</xref>
]. However, the complexity of diversity increases, because HIV non-B subtypes are not a unique entity but are comprised of 8 subtypes and >40 CRFs [<xref rid="ref12" ref-type="bibr">12</xref>
], and other studies have primarily assessed ARV drug resistance with use of 3 types of HIV: subtype C, CRF02_AG, and CRF06_cpx [<xref rid="ref13" ref-type="bibr">13</xref>
-<xref rid="ref15" ref-type="bibr">15</xref>
]. In the present study, a high genetic diversity was observed among sequenced HIV, as has been reported elsewhere for circulating HIV strains in Chad [<xref rid="ref6" ref-type="bibr">6</xref>
]. In addition, a high frequency of natural polymorphisms was present in therapeutic viral targets, particularly in the protease gene. To what extent such common polymorphisms may impact virological outcomes is currently unknown, but different prevalences of drug resistance mutations among CRF02_AG and CRF06_cpx HIV forms have recently been reported in Burkina Faso [<xref rid="ref14" ref-type="bibr">14</xref>
]. In addition, natural polymorphisms can possibly impact the interpretation of resistance genotyping [<xref rid="ref16" ref-type="bibr">16</xref>
]. In our study, 4 protease inhibitor-naive patients, including 2 infected with a CRF12_BF virus, were infected with virus that was possibly resistant to saquinavir. We have reported similar observations among children infected with CRF11_cpx HIV elsewhere [<xref rid="ref5" ref-type="bibr">5</xref>
]. Whether these genotypic resistance profiles are effectively associated with phenotypic resistance warrants further evaluation, because the genotype interpretation algorithm could differ according to the subtype [<xref rid="ref16" ref-type="bibr">16</xref>
]. Taken together, these findings emphasize the necessity to increase the amount of data available for non-B subtypes of HIV, with the aim of improving the reliability of ARV drug resistance interpretation rules for non-B subtypes.</p>

</body>

<back>

<ack>

<title>Acknowledgments</title>

<p><bold><italic>Financial support</italic>
</bold>
. Hôpital Général de Référence Nationale and Association pour la Recherche en Infectiologie.</p>

<p><bold><italic>Potential conflicts of interest</italic>
</bold>
. All authors: no conflicts</p>

</ack>

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<fig position="float" id="tab1">

<label>Table 1</label>

<caption>

<p>Characteristics and antiretroviral drug resistance mutations detected by genotypic analysis in 37 human immunodeficiency virus (HIV)-infected adult patients living in Chad, for whom plasma HIV load was detectable after 6 months of receiving a first-line antiretroviral regimen, according to the 2006 revised recommendations of the World Health Organization.</p>

</caption>

<graphic mimetype="image" xlink:href="49-1-155-tbl001.tif"></graphic>

</fig>

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<fn-group>

<fn fn-type="presented-at" id="FN1"><p>Presented in part: 15th International Conference on AIDS and STIs in Africa, Dakar, Senegal, 3–7 December 2008 (abstract 356).</p>
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<name type="personal"><namePart type="given">Donato</namePart>
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<affiliation>Reference Laboratory, Hôpital Général de Référence Nationale, N', Djamena, Chad</affiliation>
<role><roleTerm type="text">author</roleTerm>
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<name type="personal" displayLabel="corresp"><namePart type="given">Charlotte</namePart>
<namePart type="family">Charpentier</namePart>
<affiliation>Laboratoire de Virologie, Hôpital Européen Georges Pompidou, Paris, France</affiliation>
<affiliation>Faculté de Médecine Paris Descartes, Paris, France</affiliation>
<affiliation>E-mail: charlotte.charpentier@egp.aphp.fr</affiliation>
<affiliation>Reprints or correspondence: Dr. Charlotte Charpentier, Hôpital Européen Georges Pompidou, Laboratoire de Virologie, 20 rue Leblanc, 75015 Paris, France</affiliation>
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<name type="personal"><namePart type="given">Jatibi</namePart>
<namePart type="family">Beassamda</namePart>
<affiliation>Reference Laboratory, Hôpital Général de Référence Nationale, N', Djamena, Chad</affiliation>
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<name type="personal"><namePart type="given">Elisabeth</namePart>
<namePart type="family">Rey</namePart>
<affiliation>Faculté de Médecine Paris Descartes, Paris, France</affiliation>
<affiliation>Service de Pharmacologie Clinique, Groupe Hospitalier Cochin Hôpital Saint-Vincent de Paul, Paris, France</affiliation>
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<name type="personal"><namePart type="given">Ali</namePart>
<namePart type="family">Si-Mohamed</namePart>
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<affiliation>Faculté de Médecine Paris Descartes, Paris, France</affiliation>
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<name type="personal"><namePart type="given">Noël</namePart>
<namePart type="family">Djemadji-Oudjeil</namePart>
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<name type="personal"><namePart type="given">Laurent</namePart>
<namePart type="family">Bélec</namePart>
<affiliation>Laboratoire de Virologie, Hôpital Européen Georges Pompidou, Paris, France</affiliation>
<affiliation>Faculté de Médecine Paris Descartes, Paris, France</affiliation>
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<abstract>Antiretroviral drug resistance was evaluated in 88 adults infected with human immunodeficiency virus, most with subtype CRF11_cpx, who had received a first-line antiretroviral regimen for 6 months, in N'Djamena, Chad. A total of 47 patients (53%) had detectable viral load at month 6, and 56 (64%) had at least 1 antiretroviral resistance mutation observed.</abstract>
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High Frequency of Antiretroviral Drug Resistance among HIV-Infected Adults Receiving First-Line Highly Active Antiretroviral Therapy in N'Djamena, Chad

High Frequency of Antiretroviral Drug Resistance among HIV-Infected Adults Receiving First-Line Highly Active Antiretroviral Therapy in N'Djamena, Chad

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