Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:2.7.7.49 (reverse transcriptase)
 31,746 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Chronic viral infection has been implicated in the pathogenesis of B-cell lymphoma, and hepatitis C virus (HCV) infects lymphocytes. Chronic infection with HCV may result in B-cell proliferation. Individuals infected with hepatitis C are often co-infected with the RNA virus GB virus type C. Studies from Europe where hepatitis C infection is more common than in North America have shown a high prevalence of hepatitis C infection in patients with B-cell lymphoma. The aim of this study was to establish the prevalence of HCV and GBV-C infection in patients with B-cell lymphoma in an area of low HCV prevalence. One hundred patients with B-cell lymphoma (10 high grade, 46 intermediate grade, and 44 low grade) and 100 controls with nonhematological malignancies were studied. Serum was analyzed for HCV antibodies by third generation enzyme-linked immunosorbant assay, and HCV RNA and GBV-C RNA was analyzed by reverse transcriptase PCR. None of the controls or lymphoma patients had antibodies to HCV. HCV RNA was undetected in 60 out of 100 lymphoma patients tested. GBV-C RNA was detected in the serum of 5 out of 100 (5%) of lymphoma patients and in 3 out of 100 (3%) controls. Hepatitis C and GBV-C are, therefore, unlikely to play a major role in the pathogenesis of B-cell lymphoma in North America.
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PMID:No association between hepatitis C and B-cell lymphoma. 1049 Mar 76

Chronic infection and resulting inflammation promote tumor development and progression, and Toll-like receptors (TLRs) may play an important role in this process. The aim of this study was to determine whether CpG oligonucleotides (CpG-ODN), which are Toll-like receptor 9 (TLR9) agonists, can promote inflammatory cytokines release from the prostate cancer PC-3 cells through activation of nuclear factor-kappaB (NF-kappaB). Flow cytometry, semiquantitative real-time reverse transcriptase-polymerase chain reaction, enzyme-linked immunosorbent assay, and immunofluorescence analysis were used to detect the transforming growth factor-beta1 (TGF-beta1) and interleukin-8 (IL-8) release and NF-kappaB activation in PC-3 cells after CpG-ODN stimulation. CpG-ODN promoted the expression and secretion of immunosuppressive cytokines TGF-beta1 and IL-8 from PC-3 cells. In addition, after CpG-ODN stimulation, NF-kappaB nuclear translocation was also observed in PC-3 cells, contributing to CpG-induced upregulation of IL-8 and TGF-beta1. Thus, TLR9 agonists may promote IL-8 and TGF-beta1 production in human prostate cancer cells through NF-kappaB activation.
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PMID:Toll-like receptor 9 agonists promote IL-8 and TGF-beta1 production via activation of nuclear factor kappaB in PC-3 cells. 1959 55

Chronic infection of hepatitis B virus (HBV) presents one of the serious public health challenges worldwide. Current treatment of chronic hepatitis B (CHB) is limited, and is composed of interferon and nucleoside/nucleotide reverse transcriptase inhibitors (NRTI). Interferon is poorly tolerated and is only responsive in a small fraction of CHB patients and NRTIs often face the problem of emergence of drug resistance during long-term treatment. The current treatment of CHB can be improved in several ways including genotyping mutations associated with drug resistance before treatment to guide the choice of NRTIs and suitable combinations among NRTIs and interferon. It is important to continue research in the identification of novel therapeutic targets in the life cycle of HBV or in the host immune system to stimulate the development of new antiviral agents and immunotherapies. Several antiviral agents targeting HBV entry, cccDNA, capsid formation, viral morphogenesis and virion secretion, as well as two therapeutic vaccines are currently being evaluated in preclinical studies or in clinical trials to assess their anti-HBV efficacy.
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PMID:Development of novel therapeutics for chronic hepatitis B. 2096 Mar 2