Project description:Molecular basis for CNS dysfunction in simian immunodeficiency virus-infected rhesus monkeys. We used microarrays to identify differentially expressed genes in chronic simian immunodeficiency virus-infected rhesus monkeys. Frontal lobe samples were obtained from control and SIV infected animals for RNA extraction and hybridization on Affymetrix microarrays. We sought to better understand the gene that changes in gene expression with SIV infection in the frontal lobe.
Project description:Cannabinoid administration before and after simian immunodeficiency virus (SIV)-inoculation ameliorated disease progression and decreased inflammation in male rhesus macaques. Δ9-tetrahydrocannabinol (Δ9-THC) did not increase viral load in brain tissue or produce additive neuropsychological impairment in SIV-infected macaques. To determine if the neuroimmunomodulation of Δ9-THC involved differential microRNA (miR) expression, miR expression in the striatum of uninfected macaques receiving vehicle (VEH) or Δ9-THC (THC) and SIV-infected macaques administered either vehicle (VEH/SIV) or Δ9-THC (THC/SIV) was profiled using next generation deep sequencing.
Project description:Antiretroviral treatment regimens can effectively control HIV replication and some aspects of disease progression. However, molecular events in end-organ diseases such as central nervous system (CNS) disease are not yet fully understood, and routine eradication of latent reservoirs is not yet in reach. Regulatory RNAs have emerged as important participants in HIV disease pathogenesis. Using brain tissue from the simian immunodeficiency virus (SIV) model of HIV disease, we profiled messenger RNAs (mRNAs) and circular RNAs (circRNAs), seeking to identify possible networks of RNA interaction in SIV infection and neuroinflammation.
Project description:Antiretroviral treatment regimens can effectively control HIV replication and some aspects of disease progression. However, molecular events in end-organ diseases such as central nervous system (CNS) disease are not yet fully understood, and routine eradication of latent reservoirs is not yet in reach. Brain tissue-derived extracellular vesicles (bdEVs) act locally in the source tissue and may indicate molecular mechanisms in HIV CNS pathology. Regulatory RNAs from EVs have emerged as important participants in HIV disease pathogenesis. Using brain tissue and bdEVs from the simian immunodeficiency virus (SIV) model of HIV disease, we profiled messenger RNAs (mRNAs) and microRNAs (miRNAs), seeking to identify possible networks of RNA interaction in SIV infection and neuroinflammation.
Project description:Molecular basis for CNS dysfunction in simian immunodeficiency virus-infected rhesus monkeys. We used microarrays to identify differentially expressed genes in chronic simian immunodeficiency virus-infected rhesus monkeys.
Project description:Rhesus macaques (RMs) inoculated with live-attenuated Rev-Independent Nef¯ simian immunodeficiency virus (Rev-Ind Nef¯SIV) as adults or neonates controlled viremia to undetectable levels and showed no signs of immunodeficiency over 6-8 years of follow-up. We tested the capacity of this live-attenuated virus to protect RMs against pathogenic, heterologous SIVsmE660 challenges Blood PBMC Time after SIV infection: 2 weeks post SIV infection Infection:Rev-Ind Nef¯SIV
Project description:Strain 68-1–derived Rhesus Cytomegalovirus (RhCMV) vectors expressing simian immunodeficiency virus (SIV) proteins (RhCMV/SIV) are able to elicit and maintain cellular immune responses that stringently control and subsequently clear a mucosal challenge with highly pathogenic SIV in 50-60% of vaccinated rhesus monkeys (RMs). Here, we utilize whole blood transcriptomic profiling to identify host responses correlated to RhCMV/SIV efficacy.
