Chloroplast genome sequencing analysis of CCMP452 (West Atlantic) and NIES293 (West Pacific) strains-4

45 to 50 kb. This DNA is used to generate a fosmid library which is selectively screened for cpDNA-containing clones, which are then sequenced, annotated and assembled.<p><b>Copyright information:</b></p><p>Taken from "Chloroplast genome sequencing analysis of CCMP452 (West Atlantic) and NIES293 (West Pacific) strains"</p><p>http://www.biomedcentral.com/1471-2164/9/211</p><p>BMC Genomics 2008;9():211-211.</p><p>Published online 8 May 2008</p><p>PMCID:PMC2410131.</p><p></p

Chloroplast genome sequencing analysis of CCMP452 (West Atlantic) and NIES293 (West Pacific) strains-3

<p><b>Copyright information:</b></p><p>Taken from "Chloroplast genome sequencing analysis of CCMP452 (West Atlantic) and NIES293 (West Pacific) strains"</p><p>http://www.biomedcentral.com/1471-2164/9/211</p><p>BMC Genomics 2008;9():211-211.</p><p>Published online 8 May 2008</p><p>PMCID:PMC2410131.</p><p></p

Chloroplast genome sequencing analysis of CCMP452 (West Atlantic) and NIES293 (West Pacific) strains-5

G: small inverted (red) and tandem (blue) repeats; Third ring: sequence comparison to the other genome, including SNPs (blue), small insertions (green), deletions (red) and regions of extremely poor alignment (orange); Fourth ring: Location and size of fosmid clones color coded according to their orientation: supports depicted isoform (green), supports alternate isoform (pink), uninformative (black); Fifth ring: location of inverted repeats, large and small single copy domains. Red bar depicts location of 8 kb region inverted in CCMP452 relative to NIES293; inner circle: GC content.<p><b>Copyright information:</b></p><p>Taken from "Chloroplast genome sequencing analysis of CCMP452 (West Atlantic) and NIES293 (West Pacific) strains"</p><p>http://www.biomedcentral.com/1471-2164/9/211</p><p>BMC Genomics 2008;9():211-211.</p><p>Published online 8 May 2008</p><p>PMCID:PMC2410131.</p><p></p

Chloroplast genome sequencing analysis of CCMP452 (West Atlantic) and NIES293 (West Pacific) strains-2

Ce in large and small single copy regions.<p><b>Copyright information:</b></p><p>Taken from "Chloroplast genome sequencing analysis of CCMP452 (West Atlantic) and NIES293 (West Pacific) strains"</p><p>http://www.biomedcentral.com/1471-2164/9/211</p><p>BMC Genomics 2008;9():211-211.</p><p>Published online 8 May 2008</p><p>PMCID:PMC2410131.</p><p></p

Chloroplast genome sequencing analysis of CCMP452 (West Atlantic) and NIES293 (West Pacific) strains-1

G: small inverted (red) and tandem (blue) repeats; Third ring: sequence comparison to the other genome, including SNPs (blue), small insertions (green), deletions (red) and regions of extremely poor alignment (orange); Fourth ring: Location and size of fosmid clones color coded according to their orientation: supports depicted isoform (green), supports alternate isoform (pink), uninformative (black); Fifth ring: location of inverted repeats, large and small single copy domains. Red bar depicts location of 8 kb region inverted in CCMP452 relative to NIES293; inner circle: GC content.<p><b>Copyright information:</b></p><p>Taken from "Chloroplast genome sequencing analysis of CCMP452 (West Atlantic) and NIES293 (West Pacific) strains"</p><p>http://www.biomedcentral.com/1471-2164/9/211</p><p>BMC Genomics 2008;9():211-211.</p><p>Published online 8 May 2008</p><p>PMCID:PMC2410131.</p><p></p

Chloroplast genome sequencing analysis of CCMP452 (West Atlantic) and NIES293 (West Pacific) strains-0

45 to 50 kb. This DNA is used to generate a fosmid library which is selectively screened for cpDNA-containing clones, which are then sequenced, annotated and assembled.<p><b>Copyright information:</b></p><p>Taken from "Chloroplast genome sequencing analysis of CCMP452 (West Atlantic) and NIES293 (West Pacific) strains"</p><p>http://www.biomedcentral.com/1471-2164/9/211</p><p>BMC Genomics 2008;9():211-211.</p><p>Published online 8 May 2008</p><p>PMCID:PMC2410131.</p><p></p

Liver macrophage-associated inflammation correlates with SIV burden and is substantially reduced following cART

<div><p>Liver disease is a leading contributor to morbidity and mortality during HIV infection, despite the use of combination antiretroviral therapy (cART). The precise mechanisms of liver disease during HIV infection are poorly understood partially due to the difficulty in obtaining human liver samples as well as the presence of confounding factors (e.g. hepatitis co-infection, alcohol use). Utilizing the simian immunodeficiency virus (SIV) macaque model, a controlled study was conducted to evaluate the factors associated with liver inflammation and the impact of cART. We observed an increase in hepatic macrophages during untreated SIV infection that was associated with a number of inflammatory and fibrosis mediators (TNFα, CCL3, TGFβ). Moreover, an upregulation in the macrophage chemoattractant factor CCL2 was detected in the livers of SIV-infected macaques that coincided with an increase in the number of activated CD16+ monocyte/macrophages and T cells expressing the cognate receptor CCR2. Expression of Mac387 on monocyte/macrophages further indicated that these cells recently migrated to the liver. The hepatic macrophage and T cell levels strongly correlated with liver SIV DNA levels, and were not associated with the levels of 16S bacterial DNA. Utilizing <i>in situ</i> hybridization, SIV-infected cells were found primarily within portal triads, and were identified as T cells. Microarray analysis identified a strong antiviral transcriptomic signature in the liver during SIV infection. In contrast, macaques treated with cART exhibited lower levels of liver macrophages and had a substantial, but not complete, reduction in their inflammatory profile. In addition, residual SIV DNA and bacteria 16S DNA were detected in the livers during cART, implicating the liver as a site on-going immune activation during antiretroviral therapy. These findings provide mechanistic insights regarding how SIV infection promotes liver inflammation through macrophage recruitment, with implications for in HIV-infected individuals.</p></div

Increased number of macrophages and T cells observed in the liver during SIV infection.

<p>CD68 macrophages and CD3 T cells were enumerated in the liver of uninfected, chronically SIV-infected, and chronically SIV-infected, cART infant or adult rhesus macaques by immunofluorescence microscopy. <b>A)</b> Fluorescent images at 600x (left image, scale bar = 10 um) and 100x (right image, scale bar = 100 um) depicting specific staining for macrophages (red) and T cells (green) in the liver (blue indicates nuclei). For quantification, eight random fields in the liver were imaged under 100x magnification and then analyzed by ImageJ software. <b>B)</b> Quantification of eight random fields of view for each animal to enumerate CD3 T cells by ImageJ Cell Counter analysis with adult and infant macaques graphed separately (top and bottom panels, respectively). <b>C)</b> Quantification CD68 macrophages in eight random fields of view for each animal using ImageJ Particle analysis. Data are graphed as the mean ± SEM. Statistical significance between groups was determined Mann Whitney T tests.</p

Top differentially expressed genes in SIV+ adult macaques.

<p>Top differentially expressed genes in SIV+ adult macaques.</p

T cells are the primary cellular subset infected with SIV in the liver.

<p><b>A-B)</b> Liver tissue sections from SIV-infected untreated macaques were assessed for SIV RNA+ cells (red) by <i>in situ</i> RNAscope technology followed by antibody staining with CD3 to identify T cells (green) and CD68 to identify macrophages (pink). Nuclei were stained with Dapi (blue). SIV RNA+ signal was predominately found associated with CD3 T cells (A) and in rare cases CD68 macrophages (B).</p