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)

We report a patient with human immunodeficiency virus (HIV) infection and disabling psoriatic arthritis who was treated with auranofin. Her skin lesions and arthritis resolved after auranofin treatment and she has remained free of opportunistic infections during 24 mo followup. Her CD4 count during oral gold therapy showed a significant, sustained increase in CD4 cells. The literature on the effect of gold compounds on HIV infectivity and HIV reverse transcriptase is reviewed.
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PMID:Treatment of HIV associated psoriatic arthritis with oral gold. 889 67

Highly active antiretroviral therapy (HAART) has resulted in decreased mortality and morbidity from the acquired immune deficiency syndrome caused by the human immunodeficiency virus (HIV). Drug resistance and toxicity of HAART has led to the search for novel inhibitors of HIV infection. Gold-based compounds have shown promising activity against a wide range of clinical conditions and microorganism infections including HIV-1. A typical example is auranofin which resulted in an elevated CD4+ T-cell count in an HIV patient being treated for psoriatic arthritis. In addition, reports exist on gold-based inhibitors of reverse transcriptase (RT), protease (PR) and viral entry of host cells. These and other characteristics of gold-based HIV drugs are reviewed here.
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PMID:HIV therapeutic possibilities of gold compounds. 2012 92

The aim of this study was to assess the potential clinical implications of Chlamydophila pneumoniae in patients with acute and chronic arthritic diseases and to investigate whether blood monocytes might reflect a concomitant synovial or persistent systemic infection. C. pneumoniae was investigated with advanced PCR and reverse transcriptase (RT) PCR techniques targeting different genes and combined with cell line cultures, in synovial fluid (SF) and peripheral blood mononuclear cell (PBMC) specimens collected from 28 patients with arthritis. Five out of twenty-eight patients (17.8%) were found to have C. pneumoniae DNA in either SF or PBMC specimens. Their diagnosis was reactive arthritis (ReA), S.A.P.H.O syndrome, psoriatic arthritis, undifferentiated oligoarthritis (UOA) and ankylosing spondylitis (AS). Specimens from patients with UOA and AS had also mRNA transcripts but those from AS yielded C. pneumoniae growth after co-culture. Moreover, C. pneumoniae DNA levels measured by Real-Time PCR (LightCycler) were higher in PBMC specimens compared to those found in SF at the end of antibiotic treatment. C. pneumoniae may have a role as triggering factor also in chronic arthritides including AS. The combined use of culture and molecular tools increases detection rates and improves the overall sensitivity, suggesting their potential use to detect C. pneumoniae. The different kinetics of bacterial DNA at both peripheral and synovial levels should be taken into consideration when monitoring and evaluating the effectiveness of antibiotic treatment.
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PMID:Detection of Chlamydophila pneumoniae in patients with arthritis: significance and diagnostic value. 2038 12

Psoriatic arthritis (PsA) is a seronegative, inflammatory joint disease associated with psoriasis. In most patients with PsA, skin lesions precede arthritis; however, the causality of skin inflammation for the development of arthritis remains unclear. Gp130F759/F759 knock-in (F759) mice develop autoimmune arthritis after 1 year of age through persistent signal transducer and activator of transcription 3 (Stat3) activation due to impairment in SOCS3-dependent negative regulation. Here, we crossed F759 mice with K5.Stat3C transgenic mice, in which keratinocytes express constitutive active Stat3 (Stat3C), leading to generation of psoriasis-like skin change. F759 mice harboring the K5.Stat3C transgene not only had aggravated skin lesions but also spontaneously developed arthritis with high penetrance in adjacent paws as early as 3 weeks of age. The joint lesions included swelling of the peripheral paws and nail deformities contiguous with the skin lesions, closely resembling PsA. Histopathologic study revealed enthesitis and bone erosions, with mononuclear cell infiltrates. Quantitative reverse transcriptase-PCR (RT-PCR), immunohistochemical analyses, and flow cytometry showed upregulation of the IL-23/T helper type 17 (Th17) pathway in affected joints. Furthermore, enforced generation of psoriasis-like skin inflammation by topical treatment with 12-O-tetradecanoylphorbol-13-acetate (TPA) in F759 mice induced swelling of the underlying joints. This animal model renders psoriatic inflammation as the driver of arthritis and helps to further understand the pathogenesis of PsA.
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PMID:Psoriatic inflammation facilitates the onset of arthritis in a mouse model. 2526 86