Using the Spearman test. Multiple group sample comparison was performed using

Using the Spearman test. Multiple group sample comparison was performed using the Kruskal-Wallis testImpact of Hepatitis B on Plasmodium Infectionswith Dunn’s multiple comparisons. P,0.05 was considered statistically significant.Plasmodium DNA PrevalenceDNA extracted from the 117 patient cellular fractions was tested for evidence of parasitemia (Table 2). Nested PCR identified 58 (49.6 ) pre-transfusion Madecassoside samples with detectable Plasmodium genome. Of these, 52 (90 ) carried single species P.falciparum infections; five (9 ) carried mixed infections of P.falciparum/ P.malariae and one (2 ) exhibited a mixed infection of P.falciparum/ P.ovale (Table 2). Quantitative PCR results were concordant with nested PCR in 55 samples (95 ), with the 18334597 Plasmodium identity of each amplicon confirmed by sequencing. The median level of parasitemia was 8.4610e+2 parasites/ml. Fifty-nine samples negative for Plasmodium DNA by NAT were retested with the HAPB real-time PCR and were found positive.Results HBV PrevalencePre-transfusion samples were collected from 154 blood recipients attending KATH in Kumasi, Ghana and tested for serological and molecular markers to determine HBV infection status. Thirty-seven samples were excluded from further analysis as they fulfilled exclusion criteria (see Materials and Methods). Of the 117 participants remaining in the study (Table 1), 22 1313429 (18.8 ) were reactive for HBsAg by rapid-test. All 22 samples were further characterized as HBsAg+/HBV DNA+ (median viral load: 2.1e2 IU/ml; range 3.8610e0?.9610e6 IU/ml). The 95 samples non-reactive for HBsAg by rapid test were re-tested by HBsAg EIA that identified 20 (21 ) as positive (median S/CO: 1.6; median viral load 1.0610e3 IU/ml; range 2.0610e2?1.0610e4 IU/ml). Overall, 42 (36 ) recipients were HBsAg positive by either rapid test or EIA (median age: 28.5 years) with 41 (98 ) positive by NAT with HBV DNA load ranging between 1.45610e+1 and 4.9610e+6 IU/ml (Table 2). All 42 were antiHBc reactive, despite one sample (0.8 ) being HBsAg+/HBV DNA(-). Of 75 HBsAg negative patient samples, 63 tested anti-HBc reactive. Of these, 56 (48 ) samples were identified as `HBV recovered’ (HBsAg2/anti-HBc+/HBV DNA(-)), whilst 7 (6 ) exhibited detectable levels of HBV DNA indicating occult HBV infection (OBI). The remaining 12 recipients (10 ) were characterized as HBsAg2/anti-HBc2/HBV DNA(-) and considered `HBV susceptible’ (Table 2). All 69 samples identified as HBV DNA negative by NAT, tested positive for Human Apoprotein B gene (HAPB) DNA (confirming their negative status). The 48 DNA positive samples were sequenced in the pre-S/S, S or BCP-PC regions and genotyped by phylogenetic analysis using a panel of genotyped samples from Genbank. All sequences clustered with genotype E (data not shown). All sequences have been submitted to Genbank under accession numbers JX982150?JX982218.Correlation between HBV Exposure and Plasmodium ParasitemiaIn order to study associations between HBV and Plasmodium, parasite density was stratified according to HBV status in the 117 samples (PHCCC Figure 1). In total, 49 samples (42 ) were positive for HBV (HBsAg and/or DNA) with 7 of these identified as occult HBV infections (HBsAg2/DNA+). Of these, 25/42 HBV positive and 4/7 OBI infected individuals exhibited parasitemia. These were compared to 29 HBV2/Plasmodium+ individuals, from a total of 68 (43 ) HBV negative participants (Figure 1). The difference between parasitemia levels in HBV infected (HBsAg+/ DNA+), HBV OBI a.Using the Spearman test. Multiple group sample comparison was performed using the Kruskal-Wallis testImpact of Hepatitis B on Plasmodium Infectionswith Dunn’s multiple comparisons. P,0.05 was considered statistically significant.Plasmodium DNA PrevalenceDNA extracted from the 117 patient cellular fractions was tested for evidence of parasitemia (Table 2). Nested PCR identified 58 (49.6 ) pre-transfusion samples with detectable Plasmodium genome. Of these, 52 (90 ) carried single species P.falciparum infections; five (9 ) carried mixed infections of P.falciparum/ P.malariae and one (2 ) exhibited a mixed infection of P.falciparum/ P.ovale (Table 2). Quantitative PCR results were concordant with nested PCR in 55 samples (95 ), with the 18334597 Plasmodium identity of each amplicon confirmed by sequencing. The median level of parasitemia was 8.4610e+2 parasites/ml. Fifty-nine samples negative for Plasmodium DNA by NAT were retested with the HAPB real-time PCR and were found positive.Results HBV PrevalencePre-transfusion samples were collected from 154 blood recipients attending KATH in Kumasi, Ghana and tested for serological and molecular markers to determine HBV infection status. Thirty-seven samples were excluded from further analysis as they fulfilled exclusion criteria (see Materials and Methods). Of the 117 participants remaining in the study (Table 1), 22 1313429 (18.8 ) were reactive for HBsAg by rapid-test. All 22 samples were further characterized as HBsAg+/HBV DNA+ (median viral load: 2.1e2 IU/ml; range 3.8610e0?.9610e6 IU/ml). The 95 samples non-reactive for HBsAg by rapid test were re-tested by HBsAg EIA that identified 20 (21 ) as positive (median S/CO: 1.6; median viral load 1.0610e3 IU/ml; range 2.0610e2?1.0610e4 IU/ml). Overall, 42 (36 ) recipients were HBsAg positive by either rapid test or EIA (median age: 28.5 years) with 41 (98 ) positive by NAT with HBV DNA load ranging between 1.45610e+1 and 4.9610e+6 IU/ml (Table 2). All 42 were antiHBc reactive, despite one sample (0.8 ) being HBsAg+/HBV DNA(-). Of 75 HBsAg negative patient samples, 63 tested anti-HBc reactive. Of these, 56 (48 ) samples were identified as `HBV recovered’ (HBsAg2/anti-HBc+/HBV DNA(-)), whilst 7 (6 ) exhibited detectable levels of HBV DNA indicating occult HBV infection (OBI). The remaining 12 recipients (10 ) were characterized as HBsAg2/anti-HBc2/HBV DNA(-) and considered `HBV susceptible’ (Table 2). All 69 samples identified as HBV DNA negative by NAT, tested positive for Human Apoprotein B gene (HAPB) DNA (confirming their negative status). The 48 DNA positive samples were sequenced in the pre-S/S, S or BCP-PC regions and genotyped by phylogenetic analysis using a panel of genotyped samples from Genbank. All sequences clustered with genotype E (data not shown). All sequences have been submitted to Genbank under accession numbers JX982150?JX982218.Correlation between HBV Exposure and Plasmodium ParasitemiaIn order to study associations between HBV and Plasmodium, parasite density was stratified according to HBV status in the 117 samples (Figure 1). In total, 49 samples (42 ) were positive for HBV (HBsAg and/or DNA) with 7 of these identified as occult HBV infections (HBsAg2/DNA+). Of these, 25/42 HBV positive and 4/7 OBI infected individuals exhibited parasitemia. These were compared to 29 HBV2/Plasmodium+ individuals, from a total of 68 (43 ) HBV negative participants (Figure 1). The difference between parasitemia levels in HBV infected (HBsAg+/ DNA+), HBV OBI a.

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