35 research outputs found

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

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    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_3_Longitudinal analysis of microbiome composition in Ghanaians living with HIV-1.JPEG

    No full text
    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

    No full text
    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

    No full text
    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

    Additional file 4 of Probing SARS-CoV-2-positive plasma to identify potential factors correlating with mild COVID-19 in Ghana, West Africa

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    Additional file 4. Cytokine concentration levels in COVID-19 patients. Comparison of cytokine concentration levels between COVID-19 symptomatic, asymptomatic patients, pre-COVID-19 health participants, COVID-19 pandemic health individuals and COVID-19 non-survivors. The cytokine concentration levels were measured from plasma of COVID-19 symptomatic (n = 29) and asymptomatic (n = 29), individuals, pre-COVID-19 health participants (100), COVID-19 pandemic health individuals (33) and COVID-19 non-survivors (2). The median quantity of the cytokines is shown by a horizontal line across the scatter plot while the lower and upper dotted lines represent the 25th and 75th percentiles, respectively. Statistical significance between symptomatic and asymptomatic patients were determined by a Kruskal-Wallis test with Dunn’s post hoc. (*: p 0.05)

    Lineage specific markers of influenza B HA gene.

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    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

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

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    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
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