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Antiretroviral therapy during the earliest stage of acute HIV infection (Fiebig I) might minimize establishment of a latent HIV reservoir and thereby facilitate viremic control after analytical treatment interruption. We show that 8 participants, who initiated treatment during Fiebig I and were treated for a median of 2.8 years, all experienced rapid viral load rebound following analytical treatment interruption, indicating that additional strategies are required to control or eradicate HIV. Initiation of antiretroviral therapy in the first 2 weeks of HIV infection fails to prevent resurgence of virus after stopping treatment, indicating early establishment of a resilient viral reservoir.

Hepatic stellate cells (HSCs) mediate hepatitis C virus (HCV)–related liver fibrosis, and increased HSC activation in human immunodeficiency virus (HIV)/HCV coinfection may be associated with accelerated fibrosis. We examined the level of HSC activation in HIV/HCV-coinfected and HCV-monoinfected subjects and its relationship to the level of activation and gene expression of peripheral immune cells in coinfected subjects. HSC activation levels positively correlated with peripheral CD4+ and CD8+ T cell immune activation and were associated with enhanced interleukin-15 (IL-15) gene expression, suggesting a pathogenic role for IL-15–driven immunomediated hepatic fibrosis. Future strategies that reduce immune activation and HSC activation may delay progression of liver fibrosis

Studies conducted in the Laboratory of Immunopathogenesis and Bioinformatics have shown that high endogenous levels of interferon stimulated genes (IFSGs) are correlated with (1) Human Immunodeficiency Virus (HIV) viremia and (2) poor response to HCV therapy in HIV-infected patients coinfected with Hepatitis C virus (HCV). To this end, the study evaluated the QuantigenePlex (QGP) branch DNA with a bead cross multiple analyte profiling (bDNA/xMAP) assay from Panomics along with singleplex real-time PCR (rt-PCR) and Affymetrix GeneChip® microarrays to assess IFSG expression levels. Samples included peripheral blood mononuclear cells (PBMCs) from healthy controls treated in vitro or in vivo with or without Interferon (IFN) alpha-2-beta and from patients who are infected with HIV alone or co-infected with HCV. The QGP bDNA/xMAP bead assay provides accurate high-sample-throughput expression analysis of dozens of genes in the fraction of time over rt-PCR and microarray analysis. It also has a narrower approach and is less expensive than microarray studies and similar in expense to rt-PCR. The work presented here validated a high-sample-throughput system that determines the expression level of 10-30 IFN response genes in hundreds of samples using the QGP platform. The application of this system to clinical studies has already provided a better understanding of the relationship between IFSG expression levels and HIV and HCV disease stages.