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HBV genotypes and drug resistance mutations in antiretroviral treatment-naïve and treatment-experienced HBV-HIV co-infected patients

Identifieur interne : 000385 ( Pmc/Corpus ); précédent : 000384; suivant : 000386

HBV genotypes and drug resistance mutations in antiretroviral treatment-naïve and treatment-experienced HBV-HIV co-infected patients

Auteurs : Timothy N. A. Archampong ; Ceejay L. Boyce ; Margaret Lartey ; Kwamena W. Sagoe ; Adjoa Obo-Akwa ; Ernest Kenu ; Jason T. Blackard ; Awewura Kwara

Source :

RBID : PMC:5106338

Abstract

Background

The presence of hepatitis B virus (HBV) resistance mutations upon initiation or during antiretroviral therapy (ART) in HIV co-infected patients is an important determinant of treatment response. The main objective of the study was to determine the prevalence of HBV resistance mutations in antiretroviral treatment-naïve and treatment-experienced HBV-HIV co-infected Ghanaian patients with detectable HBV viremia.

Methods

HBV-HIV co-infected patients who were ART-naïve or had received at least 9 months of lamivudine (3TC)-containing ART were enrolled in a cross-sectional study. Demographic and clinical data were collected and HBV DNA quantified. Partial HBV sequences were amplified by PCR and sequenced bi-directionally to obtain a 2.1-2.2 kb fragment for phylogenetic analysis of HBV genotypes and evaluation of drug resistance mutations.

Results

Of the 100 HBV-HIV co-infected study patients, 75 were successfully PCR-amplified, and 63 were successfully sequenced. Of these 63 patients, 27 (42.9%) were ART-experienced, and 58 (92.1%) had HBV genotype E. No resistance mutations were observed in the 36 ART-naïve patients, while 21 (77.8%) of 27 treatment-experienced patients had resistance mutations. All patients with resistance mutations had no tenofovir (TDF) in their regimens, and 80% of them had HIV RNA < 40 copies/mL. The 3TC resistance mutations rtL180M and rtM204V were observed in 10 (47.6%) of the 21 patients, while 5 patients (23.8%) had rtV173, rtL80I, and rtM204V mutations.

Discussion

A high proportion of HBV-HIV co-infected patients with detectable viremia on 3TC-containing ART had resistance mutations despite good ART adherence as determined by HIV RNA suppression. This study emphasizes the need for dual therapy as part of a fully suppressive ART in all HBV-HIV co-infected patients in Ghana.


Url:
DOI: 10.3851/IMP3055
PubMed: 27167598
PubMed Central: 5106338

Links to Exploration step

PMC:5106338

Le document en format XML

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<title>Background</title>
<p id="P1">The presence of hepatitis B virus (HBV) resistance mutations upon initiation or during antiretroviral therapy (ART) in HIV co-infected patients is an important determinant of treatment response. The main objective of the study was to determine the prevalence of HBV resistance mutations in antiretroviral treatment-naïve and treatment-experienced HBV-HIV co-infected Ghanaian patients with detectable HBV viremia.</p>
</sec>
<sec id="S2">
<title>Methods</title>
<p id="P2">HBV-HIV co-infected patients who were ART-naïve or had received at least 9 months of lamivudine (3TC)-containing ART were enrolled in a cross-sectional study. Demographic and clinical data were collected and HBV DNA quantified. Partial HBV sequences were amplified by PCR and sequenced bi-directionally to obtain a 2.1-2.2 kb fragment for phylogenetic analysis of HBV genotypes and evaluation of drug resistance mutations.</p>
</sec>
<sec id="S3">
<title>Results</title>
<p id="P3">Of the 100 HBV-HIV co-infected study patients, 75 were successfully PCR-amplified, and 63 were successfully sequenced. Of these 63 patients, 27 (42.9%) were ART-experienced, and 58 (92.1%) had HBV genotype E. No resistance mutations were observed in the 36 ART-naïve patients, while 21 (77.8%) of 27 treatment-experienced patients had resistance mutations. All patients with resistance mutations had no tenofovir (TDF) in their regimens, and 80% of them had HIV RNA < 40 copies/mL. The 3TC resistance mutations rtL180M and rtM204V were observed in 10 (47.6%) of the 21 patients, while 5 patients (23.8%) had rtV173, rtL80I, and rtM204V mutations.</p>
</sec>
<sec id="S4">
<title>Discussion</title>
<p id="P4">A high proportion of HBV-HIV co-infected patients with detectable viremia on 3TC-containing ART had resistance mutations despite good ART adherence as determined by HIV RNA suppression. This study emphasizes the need for dual therapy as part of a fully suppressive ART in all HBV-HIV co-infected patients in Ghana.</p>
</sec>
</div>
</front>
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<front>
<journal-meta>
<journal-id journal-id-type="nlm-journal-id">9815705</journal-id>
<journal-id journal-id-type="pubmed-jr-id">21447</journal-id>
<journal-id journal-id-type="nlm-ta">Antivir Ther</journal-id>
<journal-id journal-id-type="iso-abbrev">Antivir. Ther. (Lond.)</journal-id>
<journal-title-group>
<journal-title>Antiviral therapy</journal-title>
</journal-title-group>
<issn pub-type="ppub">1359-6535</issn>
<issn pub-type="epub">2040-2058</issn>
</journal-meta>
<article-meta>
<article-id pub-id-type="pmid">27167598</article-id>
<article-id pub-id-type="pmc">5106338</article-id>
<article-id pub-id-type="doi">10.3851/IMP3055</article-id>
<article-id pub-id-type="manuscript">NIHMS796471</article-id>
<article-categories>
<subj-group subj-group-type="heading">
<subject>Article</subject>
</subj-group>
</article-categories>
<title-group>
<article-title>HBV genotypes and drug resistance mutations in antiretroviral treatment-naïve and treatment-experienced HBV-HIV co-infected patients</article-title>
</title-group>
<contrib-group>
<contrib contrib-type="author">
<name>
<surname>Archampong</surname>
<given-names>Timothy N. A.</given-names>
</name>
<xref ref-type="aff" rid="A1">1</xref>
<xref ref-type="aff" rid="A2">2</xref>
<xref rid="FN2" ref-type="author-notes">*</xref>
</contrib>
<contrib contrib-type="author">
<name>
<surname>Boyce</surname>
<given-names>Ceejay L.</given-names>
</name>
<xref ref-type="aff" rid="A3">3</xref>
<xref rid="FN2" ref-type="author-notes">*</xref>
</contrib>
<contrib contrib-type="author">
<name>
<surname>Lartey</surname>
<given-names>Margaret</given-names>
</name>
<xref ref-type="aff" rid="A1">1</xref>
<xref ref-type="aff" rid="A2">2</xref>
</contrib>
<contrib contrib-type="author">
<name>
<surname>Sagoe</surname>
<given-names>Kwamena W.</given-names>
</name>
<xref ref-type="aff" rid="A4">4</xref>
</contrib>
<contrib contrib-type="author">
<name>
<surname>Obo-Akwa</surname>
<given-names>Adjoa</given-names>
</name>
<xref ref-type="aff" rid="A1">1</xref>
</contrib>
<contrib contrib-type="author">
<name>
<surname>Kenu</surname>
<given-names>Ernest</given-names>
</name>
<xref ref-type="aff" rid="A2">2</xref>
<xref ref-type="aff" rid="A5">5</xref>
</contrib>
<contrib contrib-type="author">
<name>
<surname>Blackard</surname>
<given-names>Jason T.</given-names>
</name>
<xref ref-type="aff" rid="A3">3</xref>
</contrib>
<contrib contrib-type="author">
<name>
<surname>Kwara</surname>
<given-names>Awewura</given-names>
</name>
<xref ref-type="aff" rid="A6">6</xref>
<xref ref-type="aff" rid="A7">7</xref>
</contrib>
</contrib-group>
<aff id="A1">
<label>1</label>
Department of Medicine and Therapeutics, School of Medicine and Dentistry, College of Health Sciences, University of Ghana, Accra, Ghana</aff>
<aff id="A2">
<label>2</label>
Korle-Bu Teaching Hospital, Accra, Ghana</aff>
<aff id="A3">
<label>3</label>
Division of Digestive Disease, University of Cincinnati College of Medicine, Cincinnati, OH, USA</aff>
<aff id="A4">
<label>4</label>
Department of Medical Microbiology, School of Biomedical and Allied Health Sciences, College of Health Sciences, University of Ghana, Accra, Ghana</aff>
<aff id="A5">
<label>5</label>
School of Public Health, College of Health Sciences, University of Ghana</aff>
<aff id="A6">
<label>6</label>
Warren Alpert Medical School of Brown University, Providence, RI, USA</aff>
<aff id="A7">
<label>7</label>
The Miriam Hospital, Providence, RI, USA</aff>
<author-notes>
<corresp id="FN1">Corresponding author: Timothy N. A. Archampong; Lecturer, Department of Medicine and Therapeutics, School of Medicine and Dentistry, College of Health Sciences, University of Ghana; PO Box 4236, Korle-Bu, Accra, Ghana,
<email>tnaa@doctors.net.uk</email>
; Tel: 00233-203039841</corresp>
<fn id="FN2" fn-type="equal">
<label>*</label>
<p>These authors contributed equally to this manuscript</p>
</fn>
</author-notes>
<pub-date pub-type="nihms-submitted">
<day>22</day>
<month>6</month>
<year>2016</year>
</pub-date>
<pub-date pub-type="epub">
<day>11</day>
<month>5</month>
<year>2016</year>
</pub-date>
<pub-date pub-type="ppub">
<year>2017</year>
</pub-date>
<pub-date pub-type="pmc-release">
<day>10</day>
<month>3</month>
<year>2017</year>
</pub-date>
<volume>22</volume>
<issue>1</issue>
<fpage>13</fpage>
<lpage>20</lpage>
<pmc-comment>elocation-id from pubmed: 10.3851/IMP3055</pmc-comment>
<abstract>
<sec id="S1">
<title>Background</title>
<p id="P1">The presence of hepatitis B virus (HBV) resistance mutations upon initiation or during antiretroviral therapy (ART) in HIV co-infected patients is an important determinant of treatment response. The main objective of the study was to determine the prevalence of HBV resistance mutations in antiretroviral treatment-naïve and treatment-experienced HBV-HIV co-infected Ghanaian patients with detectable HBV viremia.</p>
</sec>
<sec id="S2">
<title>Methods</title>
<p id="P2">HBV-HIV co-infected patients who were ART-naïve or had received at least 9 months of lamivudine (3TC)-containing ART were enrolled in a cross-sectional study. Demographic and clinical data were collected and HBV DNA quantified. Partial HBV sequences were amplified by PCR and sequenced bi-directionally to obtain a 2.1-2.2 kb fragment for phylogenetic analysis of HBV genotypes and evaluation of drug resistance mutations.</p>
</sec>
<sec id="S3">
<title>Results</title>
<p id="P3">Of the 100 HBV-HIV co-infected study patients, 75 were successfully PCR-amplified, and 63 were successfully sequenced. Of these 63 patients, 27 (42.9%) were ART-experienced, and 58 (92.1%) had HBV genotype E. No resistance mutations were observed in the 36 ART-naïve patients, while 21 (77.8%) of 27 treatment-experienced patients had resistance mutations. All patients with resistance mutations had no tenofovir (TDF) in their regimens, and 80% of them had HIV RNA < 40 copies/mL. The 3TC resistance mutations rtL180M and rtM204V were observed in 10 (47.6%) of the 21 patients, while 5 patients (23.8%) had rtV173, rtL80I, and rtM204V mutations.</p>
</sec>
<sec id="S4">
<title>Discussion</title>
<p id="P4">A high proportion of HBV-HIV co-infected patients with detectable viremia on 3TC-containing ART had resistance mutations despite good ART adherence as determined by HIV RNA suppression. This study emphasizes the need for dual therapy as part of a fully suppressive ART in all HBV-HIV co-infected patients in Ghana.</p>
</sec>
</abstract>
<kwd-group>
<kwd>Hepatitis B virus</kwd>
<kwd>HIV</kwd>
<kwd>co-infection</kwd>
<kwd>Ghana</kwd>
<kwd>Africa</kwd>
<kwd>genotype</kwd>
<kwd>drug resistance</kwd>
</kwd-group>
</article-meta>
</front>
</pmc>
</record>

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