Pan troglodytes
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA138049 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Hepatitis A virus (HAV) is a hepatotropic human picornavirus that has been associated only with acute infection. Its pathogenesis is not well understood since there have been few recent studies in animal models using modern methodologies. We characterized HAV infections in three chimpanzees, quantifying viral RNA by qRT-PCR and examining critical aspects of the innate immune response including intrahepatic interferon-stimulated gene expression. We compared these infection profiles with similar studies of chimpanzees infected with hepatitis C virus (HCV), a hepatotropic flavivirus that frequently causes persistent infection. Surprisingly, HAV-infected animals exhibited very limited induction of type I interferon-stimulated genes in the liver compared to chimpanzees with acute resolving HCV infection, despite similar levels of viremia and 100-fold greater quantities of viral RNA in the liver. Minimal ISG15 and IFIT1 responses peaked 1-2 weeks after HAV challenge, then subsided despite continuing high hepatic viral loads. An acute inflammatory response at 3-4 weeks correlated with the appearance of virus-specific antibodies, and both apoptosis and proliferation of hepatocytes. Despite this, HAV RNA persisted in the liver for months, remaining present long after its clearance from serum and feces and revealing dramatic differences in the kinetics of clearance in the three compartments. Viral RNA was detected in the liver for significantly longer (35 to >48 weeks) than HCV RNA in animals with acute resolving HCV infection (10-20 weeks). Collectively, these findings suggest that early HAV infection is far stealthier than HCV infection and represents a distinctly different paradigm in viral-host interactions within the liver. Chimpanzee liver was biopsied during an acute HAV infection. Chimp 1 and 2 had two baseline samples. Chimp 3 used the baselines from chimps 1 and 2. Chimp 1 had 8 samples during the HAV acute infection. Chimp 2 had 9 samples during the HAV acute infection. Chimp 3 had 4 samples during the HAV acute infection.
2011-03-09 | E-GEOD-27850 | biostudies-arrayexpress
Project description:Hepatitis A virus (HAV) is a hepatotropic human picornavirus that has been associated only with acute infection. Its pathogenesis is not well understood since there have been few recent studies in animal models using modern methodologies. We characterized HAV infections in three chimpanzees, quantifying viral RNA by qRT-PCR and examining critical aspects of the innate immune response including intrahepatic interferon-stimulated gene expression. We compared these infection profiles with similar studies of chimpanzees infected with hepatitis C virus (HCV), a hepatotropic flavivirus that frequently causes persistent infection. Surprisingly, HAV-infected animals exhibited very limited induction of type I interferon-stimulated genes in the liver compared to chimpanzees with acute resolving HCV infection, despite similar levels of viremia and 100-fold greater quantities of viral RNA in the liver. Minimal ISG15 and IFIT1 responses peaked 1-2 weeks after HAV challenge, then subsided despite continuing high hepatic viral loads. An acute inflammatory response at 3-4 weeks correlated with the appearance of virus-specific antibodies, and both apoptosis and proliferation of hepatocytes. Despite this, HAV RNA persisted in the liver for months, remaining present long after its clearance from serum and feces and revealing dramatic differences in the kinetics of clearance in the three compartments. Viral RNA was detected in the liver for significantly longer (35 to >48 weeks) than HCV RNA in animals with acute resolving HCV infection (10-20 weeks). Collectively, these findings suggest that early HAV infection is far stealthier than HCV infection and represents a distinctly different paradigm in viral-host interactions within the liver.
2011-03-09 | GSE27850 | GEO
Project description:Viral metagenome in feces from chimpanzees in China
| PRJNA473023 | ENA
Project description:We aim, among other things, to characterize olfactory receptor (OR) genes wich are differentially expressed between olfactory epithelium (OE) and other organ tissues, in chimpanzees (Pan troglodytes), and to make comparisons with human data from a previous series using the same platform. Keywords: Comparative
2008-10-01 | GSE11156 | GEO
Project description:Pathogenesis of hepatitis E and hepatitis C in chimpanzees: Similarities and differences
| PRJNA127725 | ENA
Project description:Chimpanzees with chronic Hepatitis C infection treated with LNA-antimiR-122.
2010-10-01 | E-MEXP-2375 | biostudies-arrayexpress
Project description:We aim, among other things, to characterize olfactory receptor (OR) genes wich are differentially expressed between olfactory epithelium (OE) and other organ tissues, in chimpanzees (Pan troglodytes), and to make comparisons with human data from a previous series using the same platform. Keywords: Comparative Four OE samples and eight non-OE samples, including two samples of the following tissues: heart, liver, lung, and testis.
2008-10-01 | E-GEOD-11156 | biostudies-arrayexpress
Project description:Pan troglodytes troglodytes Targeted Locus (Loci)
| PRJNA245255 | ENA
Project description:Hepatitis A virus (HAV), an hepatotropic picornavirus, is a common cause of acute hepatitis in human populations. Although responsible for considerable morbidity and mortality, the mechanisms underlying HAV-mediated liver injury are poorly understood. Ifnar1-/- mice are susceptible to HAV and when infected recapitulate cardinal features of hepatitis A in humans, including serum ALT elevation, hepatocellular apoptosis, and intrahepatic inflammatory cell infiltrates. In contrast, Mavs-/- mice, while equally permissive for infection, experience no liver injury. Previous studies indicate that HAV pathogenesis in Ifnar1-/- mice is dependent upon MAVS-IRF3 signaling, but leave unresolved the role of IRF3-mediated transcription versus non-transcriptional pro-apoptotic activity of activated IRF3 in HAV-induced liver disease. Here, we compared the intrahepatic transcriptomes of HAV-infected naïve Mavs-/- and Ifnar1-/- mice using high throughput RNA sequencing, and characterized IRF3-mediated transcriptional responses associated with hepatocyte apoptosis and liver inflammation.
2021-08-18 | GSE166353 | GEO