Figure 4

<p><b>A)</b> Gel electrophoresis of the conventional PCR amplification products showing the undigested 384-bp OPV amplicon DNA ladder (lane 1); negative controls (lanes 2–3); human specimens from 13 patients of the Bena Tshiadi healthcare district (lanes 4–13 and 15–18), and from 1 patient of the Yangala healthcare district (lane 14). <b>B)</b><i>BsrGI</i> digestion profile of 384-bp MPXV amplicons: banding patterns with 210- and 174-bp fragments.</p

Multiple alignment of 14 kD DNA targets and design of primers and probes for the qPCR assay.

<p>Primers for qPCR and for the conventional PCR are shown in plain boxes whereas the pan-orthopoxvirus and specific variola virus probes are highlighted in a dashed boxes. The monkepoxvirus specific SNP (C→T) is arrowed. The pyrosequencing probe is indicated by a plain arrow.</p

Map of West Kasai Province.

<p>Areas affected by rash illness outbreaks are highlighted as follows: ▴: Bena Tshiadi healthcare zone (13 patients in 7 different villages). All cases were confirmed as monkeypox cases. Hourglass Symbol: Yangala healthcare zone (8 patients clustered in Tshikongo village). All were confirmed as varicella cases.♦: Ndesha healthcare zone in the outskirts of Kananga (3 patients clustered in Lubuyi village, several kilometers north of Kananga city). All were confirmed as varicella cases.</p

Blotting papers showing six 6 spots with dried liquid exudate from pustules collected in one patient.

<p>One spot (arrow) was removed and processed for DNA-based identification of causative agents of the rash illness.</p

DNA-based identification of causative agents of rash illness outbreaks (2008 and 2009) in West Kasai province.

<p>Legend: Patients originated from the following healthcare districts: Bena Tshiadi, 1–13; Yangala, 14–22; Ndesha, 23–25.</p

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Illustrative example of neurodisability in konzo.

<p>(A) Spastic stance in a boy severely affected by konzo. (B) Depiction of deficits at KABC-II cognition testing. (C) Deficits in fine motor control at the BOT-2 testing.</p

Age, biochemical measures and neurocognitive proficiency scores by konzo status.

<p>Children with konzo had low concentrations of serum albumin, plasma SCN, and neurology proficiency scores. They had, however, higher concentrations of serum triglycerides and 8,12-iso-iPF2<b>α</b>-VI isoprostane relative to those with no konzo.</p><p>Age, biochemical measures and neurocognitive proficiency scores by konzo status.</p

Spearman coefficients (p-value) for correlations between concentrations of isoprostanes, triglycerides, albumin, and neurocognitive proficiency scores (N = 32).

<p>Of all the forms of isoprostanes, only 8,12-iso-iPF2<b>α</b>-VI isoprostane had serum concentrations that consistently and negatively correlated with concentrations of serum albumin and neurology proficiency scores. Concentrations of serum albumin positively correlated with neurology proficiency scores in contrast to the trend for concentrations of triglycerides that negatively correlated with proficiency scores.</p><p>Spearman coefficients (p-value) for correlations between concentrations of isoprostanes, triglycerides, albumin, and neurocognitive proficiency scores (N = 32).</p

Correlations between motor/cognition performance scores and levels of serum isoprostanes.

<p>Low motor or cognition performance significantly correlated with high concentrations of 8,12-iso-iPF2alpha-VI isoprostane in children affected by konzo. (A) MPI (mental processing index) also referred to as KABC-II scores in main text versus serum level of 8,12-iso-iPF2α-VI isoprostane (triangles  =  konzo children, r = −0.78, p = 0.00; circles  =  non-konzo children, r = −0.24, p = 0.47). (B) BOT-2 scores versus serum level of 8,12-iso-iPF2α-VI isoprostane (triangles  =  konzo children, r = −0.63, p<0.01; circles  =  non-konzo children, r = −0.06, p = 0.86).</p