Clinical symptoms reported in subjects with PARV4 infection.

<p>Papers are listed in alphabetical order by first author.</p>a<p>Denominator presented is the number of individuals positive for PARV4 (extrapolated from total number of subjects studied in each paper), except for Simmons et al. <a href="http://www.plospathogens.org/article/info:doi/10.1371/journal.ppat.1004036#ppat.1004036-Simmons1" target="_blank">[9]</a>, where denominator is number with HIV.</p>b<p>Other infectious causes of the clinical syndrome were excluded.</p>c<p>Other pathogens were also present which may have explained the clinical syndrome.</p><p>CNS = central nervous system; CSF = cerebrospinal fluid; IDU = injecting drug user; LFTs = liver function tests.</p

Prevalence of HBsAg and HBeAg from 37 studies of HBV drug resistance in Africa.

<p>Prevalence of HBsAg and HBeAg from 37 studies of HBV drug resistance in Africa.</p

HBV drug resistance associated mutations (RAMs), vaccine escape mutations (VEMs) and mutations associated with Hepatitis B immunoglobulin (HBIg) resistance.

<p>HBV genes are shown in the coloured ovals. TDF = tenofovir, ETV = entecavir, 3TC = lamivudine. This figure incorporates data from eight studies; three were identified by the systematic review presented in this manuscript [<a href="http://www.plosntds.org/article/info:doi/10.1371/journal.pntd.0006629#pntd.0006629.ref012" target="_blank">12</a>–<a href="http://www.plosntds.org/article/info:doi/10.1371/journal.pntd.0006629#pntd.0006629.ref014" target="_blank">14</a>] and five from the wider literature [<a href="http://www.plosntds.org/article/info:doi/10.1371/journal.pntd.0006629#pntd.0006629.ref007" target="_blank">7</a>,<a href="http://www.plosntds.org/article/info:doi/10.1371/journal.pntd.0006629#pntd.0006629.ref015" target="_blank">15</a>–<a href="http://www.plosntds.org/article/info:doi/10.1371/journal.pntd.0006629#pntd.0006629.ref018" target="_blank">18</a>].</p

HBV drug resistant mutations (RAMs) identified from HBV genome sequences from Africa downloaded from the Hepatitis B Virus database (https://hbvdb.ibcp.fr/) [36] and GenBank database (http://hvdr.bioinf.wits.ac.za/alignments/) [37].

<p>HBV drug resistant mutations (RAMs) identified from HBV genome sequences from Africa downloaded from the Hepatitis B Virus database (<a href="https://hbvdb.ibcp.fr/" target="_blank">https://hbvdb.ibcp.fr/</a>) [<a href="http://www.plosntds.org/article/info:doi/10.1371/journal.pntd.0006629#pntd.0006629.ref036" target="_blank">36</a>] and GenBank database (<a href="http://hvdr.bioinf.wits.ac.za/alignments/" target="_blank">http://hvdr.bioinf.wits.ac.za/alignments/</a>) [<a href="http://www.plosntds.org/article/info:doi/10.1371/journal.pntd.0006629#pntd.0006629.ref037" target="_blank">37</a>].</p

Annotated map to summarise HBV drug resistance associated mutations (RAMs) and vaccine escape mutations (VEMs).

<p>Mutations identified from 33 studies of African cohorts published between 2007 and 2017 (inclusive). Four studies identified by our systematic literature review were not represented here as they did not report any RAMs. Full details of each citation can be found in <a href="http://www.plosntds.org/article/info:doi/10.1371/journal.pntd.0006629#pntd.0006629.t001" target="_blank">Table 1</a>.</p

Prevalence of HBV resistance associated mutations (RAMs) in Pol/RT proteins among HBV infected patients in Africa.

<p>These data are derived from 27 studies of HBV drug resistance in Africa published between 2007 and 2017 (inclusive). The countries represented are listed in alphabetical order. A detailed summary of RAMs identified from each study is presented (<a href="http://www.plosntds.org/article/info:doi/10.1371/journal.pntd.0006629#pntd.0006629.g002" target="_blank">Fig 2</a>, <a href="http://www.plosntds.org/article/info:doi/10.1371/journal.pntd.0006629#pntd.0006629.s006" target="_blank">S4 Table</a>, <a href="http://www.plosntds.org/article/info:doi/10.1371/journal.pntd.0006629#pntd.0006629.s007" target="_blank">S5 Table</a>). Prevalence of RAMs for a specific country was determined by grouping all studies from that country that reported a specific mutation. We used all individuals who tested HBsAg positive to generate a denominator in order to provide a conservative estimate of RAM prevalence, and the numerator was the total number of individuals with that specific mutation from these studies. A: treatment naïve; B: treatment experienced.</p

Cohort characteristics.

<p>Cohort characteristics.</p

Cohort characteristics.

<p>Cohort characteristics.</p

HLA associations with the remaining 15-mer OLP’s in CMV pp65, IE-1 and IE-2 that were targeted by ≥4% of the study cohort.

<p>HLA associations with the remaining 15-mer OLP’s in CMV pp65, IE-1 and IE-2 that were targeted by ≥4% of the study cohort.</p

Immunodominant CMV-specific CD8+ T-cell responses within pp65, IE-1 and IE-2 measured by IFN-g ELISpot assay for CMV+ subjects.

<p>(A) Percentage responders to each protein-covering peptide pool. (B) Percentage responders among 152 CMV+ individuals to pp65 15mer overlapping peptides that were targeted by >4% of the study population. (C) Percentage responders among 95 CMV+ individuals to IE-1 15mer overlapping peptides that were targeted by >3% of the study population. (D) Percentage responders among 92 CMV+ individuals to IE-2 15mer overlapping peptides that were targeted by >3% of the study population.</p