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)

New data were presented at the 15th Conference on Retroviruses and Opportunistic Infections that further support the importance of considering the neuroeffectiveness of antiretroviral drugs when designing treatment regimens. Two studies linked antiretroviral therapy that had estimates of better neuroeffectiveness with better global neuropsychologic outcomes in life. A third study linked estimates of better antiretroviral therapy neuroeffectiveness, particularly nonnucleoside analogue reverse transcriptase inhibitors, with a lower prevalence of HIV-associated brain pathology at death. Additional findings presented at the conference focused on the correlates of HIV-associated neurocognitive disorders (HAND) and peripheral neuropathy. Supporting the concept that viral factors influence the pathogenesis of HAND, high frequencies of HAND were identified in people infected with HIV subtype D and in people infected with subtype B and having brain-specific mutations in V3 of gp160. Supporting the importance of host correlates of HAND, important data from a macaque study identified a strong link between a major histocompatibility complex class I allele, Mane-A*10, and simian immunodeficiency virus encephalitis. Supporting the importance of comorbidities in determining risk for HAND, high levels of lipopolysaccharide in blood, likely derived from the HIV-injured intestine and bacterial translocation, were linked to HAND. Coinfections with JC virus or Treponema pallidum were topics of other presentations, identifying a prognostic marker for PML (better CD8+ cytotoxic T-lymphocyte responses were associated with survival) and a diagnostic one for neurosyphilis (CXCL13 levels in CSF).
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PMID:Highlights of the 15th Conference on Retroviruses and Opportunistic Infections. Neurologic complications of HIV disease and their treatment. 1844 79

Mucopolysaccharidosis (MPS) IIIB is a lysosomal storage disease with severe neurological manifestations due to alpha-N-acetylglucosaminidase (NaGlu) deficiency. The mechanism of neuropathology in MPS IIIB is unclear. This study investigates the role of immune responses in neurological disease of MPS IIIB in mice. By means of gene expression microarrays and real-time quantitative reverse transcriptase-polymerase chain reaction, we demonstrated significant up-regulation of numerous immune-related genes in MPS IIIB mouse brain involving a broad range of immune cells and molecules, including T cells, B cells, microglia/macrophages, complement, major histocompatibility complex class I, immunoglobulin, Toll-like receptors, and molecules essential for antigen presentation. The significantly enlarged spleen and lymph nodes in MPS IIIB mice were due to an increase in splenocytes/lymphocytes, and functional assays indicated that the T cells were activated. An autoimmune component to the disease was further suggested by the presence of putative autoantigen or autoantigens in brain extracts that reacted specifically with serum IgG from MPS IIIB mice. We also demonstrated for the first time that immunosuppression with prednisolone alone can significantly slow the central nervous system disease progression. Our data indicate that immune responses contribute greatly to the neuropathology of MPS IIIB and should be considered as an adjunct treatment in future therapeutic developments for optimal therapeutic effect.
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PMID:Innate and adaptive immune activation in the brain of MPS IIIB mouse model. 1974 28

Induction of an antigenically broad and vigorous primary T-cell immune response by myeloid dendritic cells (DC) in blood and tissues could be important for an effective prophylactic or therapeutic vaccine to human immunodeficiency virus type 1 (HIV-1). Here we show that a primary CD8(+) T-cell response can be induced by HIV-1 peptide-loaded DC derived from blood monocytes of HIV-1-negative adults and neonates (moDC) and by Langerhans cells (LC) and interstitial, dermal-intestinal DC (idDC) derived from CD34(+) stem cells of neonatal cord blood. Optimal priming of single-cell gamma interferon (IFN-gamma) production by CD8(+) T cells required CD4(+) T cells and was broadly directed to multiple regions of Gag, Env, and Nef that corresponded to known and predicted major histocompatibility complex class I epitopes. Polyfunctional CD8(+) T-cell responses, defined as single-cell production of more than one cytokine (IFN-gamma, interleukin 2, or tumor necrosis factor alpha), chemokine (macrophage inhibitory factor 1beta), or cytotoxic degranulation marker CD107a, were primed by moDC, LC, and idDC to HIV-1 Gag and reverse transcriptase epitopes, as well as to Epstein-Barr virus and influenza A virus epitopes. Thus, three major types of blood and tissue myeloid DC targeted by HIV-1, i.e., moDC, LC, and idDC, can prime multispecific, polyfunctional CD8(+) T-cell responses to HIV-1 and other viral antigens.
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PMID:Primary human immunodeficiency virus type 1-specific CD8+ T-cell responses induced by myeloid dendritic cells. 1935 76

Abacavir is a nucleoside reverse transcriptase inhibitor used for combination antiretroviral therapy for treating human immunodeficiency virus (HIV) infection. An adverse effect from abacavir is a treatment-limiting hypersensitivity reaction, which can be severe and potentially life-threatening. Abacavir-induced hypersensitivity reaction has been associated with the presence of the major histocompatibility complex class I allele HLA-B*5701. A screening test for the HLA-B*5701 allele can assist clinicians to identify patients who are at risk of developing a hypersensitivity reaction to abacavir.
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PMID:HLA-B*5701 testing to predict abacavir hypersensitivity. 2115 80


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