GST genotypes distribution in study population.

<p>GST genotypes distribution in study population.</p

Electrophoresis of PCR products from the co-amplification of GSTM1, GSTT1 and the internal control, CYP1A1 gene.

<p>Ethidium bromide stained 2% agarose gel. N = negative control, M = 100bp molecular weight marker. Lanes 2, 6, 7, 18 and 21 were positive for GSTT1 deletion genotype. Lanes 1, 11, 15, 17, 19, 20 and 22 had GSTM1 deletion genotype. Lanes 9 and 10 represented individuals with a deletion of both genotypes. Lanes 3, 4, 5, 8, 12, 13, 14 and 16 had both genes present.</p

Basic demographic data of study population stratified by ART use.

<p>Basic demographic data of study population stratified by ART use.</p

Effect of GST polymorphism on GST enzyme activity.

<p>GST polymorphism was obtained by PCR amplification of the GSTM1 and GSTT1 genes, with CYP1A1 gene used as control. GST enzyme activity was assayed spectrophotometrically.</p

Image_3_Longitudinal analysis of microbiome composition in Ghanaians living with HIV-1.JPEG

Human immunodeficiency virus (HIV) 1 infection is known to cause gut microbiota dysbiosis. Among the causes is the direct infection of HIV-1 in gut-resident CD4+ T cells, causing a cascade of phenomena resulting in the instability of the gut mucosa. The effect of HIV infection on gut microbiome dysbiosis remains unresolved despite antiretroviral therapy. Here, we show the results of a longitudinal study of microbiome analysis of people living with HIV (PLWH). We contrasted the diversity and composition of the microbiome of patients with HIV at the first and second time points (baseline_case and six months later follow-up_case, respectively) with those of healthy individuals (baseline_control). We found that despite low diversity indices in the follow-up_case, the abundance of some genera was recovered but not completely, similar to baseline_control. Some genera were consistently in high abundance in PLWH. Furthermore, we found that the CD4+ T-cell count and soluble CD14 level were significantly related to high and low diversity indices, respectively. We also found that the abundance of some genera was highly correlated with clinical features, especially with antiretroviral duration. This includes genera known to be correlated with worse HIV-1 progression (Achromobacter and Stenotrophomonas) and a genus associated with gut protection (Akkermansia). The fact that a protector of the gut and genera linked to a worse progression of HIV-1 are both enriched may signify that despite the improvement of clinical features, the gut mucosa remains compromised.</p

Image_2_Longitudinal analysis of microbiome composition in Ghanaians living with HIV-1.JPEG

Human immunodeficiency virus (HIV) 1 infection is known to cause gut microbiota dysbiosis. Among the causes is the direct infection of HIV-1 in gut-resident CD4+ T cells, causing a cascade of phenomena resulting in the instability of the gut mucosa. The effect of HIV infection on gut microbiome dysbiosis remains unresolved despite antiretroviral therapy. Here, we show the results of a longitudinal study of microbiome analysis of people living with HIV (PLWH). We contrasted the diversity and composition of the microbiome of patients with HIV at the first and second time points (baseline_case and six months later follow-up_case, respectively) with those of healthy individuals (baseline_control). We found that despite low diversity indices in the follow-up_case, the abundance of some genera was recovered but not completely, similar to baseline_control. Some genera were consistently in high abundance in PLWH. Furthermore, we found that the CD4+ T-cell count and soluble CD14 level were significantly related to high and low diversity indices, respectively. We also found that the abundance of some genera was highly correlated with clinical features, especially with antiretroviral duration. This includes genera known to be correlated with worse HIV-1 progression (Achromobacter and Stenotrophomonas) and a genus associated with gut protection (Akkermansia). The fact that a protector of the gut and genera linked to a worse progression of HIV-1 are both enriched may signify that despite the improvement of clinical features, the gut mucosa remains compromised.</p

Image_1_Longitudinal analysis of microbiome composition in Ghanaians living with HIV-1.JPEG

Human immunodeficiency virus (HIV) 1 infection is known to cause gut microbiota dysbiosis. Among the causes is the direct infection of HIV-1 in gut-resident CD4+ T cells, causing a cascade of phenomena resulting in the instability of the gut mucosa. The effect of HIV infection on gut microbiome dysbiosis remains unresolved despite antiretroviral therapy. Here, we show the results of a longitudinal study of microbiome analysis of people living with HIV (PLWH). We contrasted the diversity and composition of the microbiome of patients with HIV at the first and second time points (baseline_case and six months later follow-up_case, respectively) with those of healthy individuals (baseline_control). We found that despite low diversity indices in the follow-up_case, the abundance of some genera was recovered but not completely, similar to baseline_control. Some genera were consistently in high abundance in PLWH. Furthermore, we found that the CD4+ T-cell count and soluble CD14 level were significantly related to high and low diversity indices, respectively. We also found that the abundance of some genera was highly correlated with clinical features, especially with antiretroviral duration. This includes genera known to be correlated with worse HIV-1 progression (Achromobacter and Stenotrophomonas) and a genus associated with gut protection (Akkermansia). The fact that a protector of the gut and genera linked to a worse progression of HIV-1 are both enriched may signify that despite the improvement of clinical features, the gut mucosa remains compromised.</p

Table_1_Longitudinal analysis of microbiome composition in Ghanaians living with HIV-1.DOCX

Human immunodeficiency virus (HIV) 1 infection is known to cause gut microbiota dysbiosis. Among the causes is the direct infection of HIV-1 in gut-resident CD4+ T cells, causing a cascade of phenomena resulting in the instability of the gut mucosa. The effect of HIV infection on gut microbiome dysbiosis remains unresolved despite antiretroviral therapy. Here, we show the results of a longitudinal study of microbiome analysis of people living with HIV (PLWH). We contrasted the diversity and composition of the microbiome of patients with HIV at the first and second time points (baseline_case and six months later follow-up_case, respectively) with those of healthy individuals (baseline_control). We found that despite low diversity indices in the follow-up_case, the abundance of some genera was recovered but not completely, similar to baseline_control. Some genera were consistently in high abundance in PLWH. Furthermore, we found that the CD4+ T-cell count and soluble CD14 level were significantly related to high and low diversity indices, respectively. We also found that the abundance of some genera was highly correlated with clinical features, especially with antiretroviral duration. This includes genera known to be correlated with worse HIV-1 progression (Achromobacter and Stenotrophomonas) and a genus associated with gut protection (Akkermansia). The fact that a protector of the gut and genera linked to a worse progression of HIV-1 are both enriched may signify that despite the improvement of clinical features, the gut mucosa remains compromised.</p

Phylogenetic analysis of influenza B Yamagata lineage using the HA genes.

Bootstrap values over 80% are indicated on the tree. Red represents the WHO vaccine candidate virus genome, pink represents reference Ghanaian specimens sequenced at the Francis Crick Institute, blue represents the sequences we identified, green represents the deletion sub-group, Amino acid changes in black represent those within HA1, with violet representing changes in the HA2.</p

Lineage specific markers of influenza B HA gene.

Multiple sequence alignment was carried out using ClustalW in BioEdit with a boostrap replicates of 1000 in line with Edgar [16]. Influenza B/Brisbane/60/2008 was used as the reference sequence for B/Victoria lineages while B/Wisconsin/1/2010, Clade 3 and B/Massachusetts/2/2012, Clade 2 were used as the reference sequence for B Yamagata lineages. Influenza B virus lineage-specific markers (nts 522, 540–542, 548, 549, 555, 558 and 568) are shown in yellow, whereas the clade specific markers (nts 538, 562 and 589) have been highlighted as green.</p