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)

Experimental intravenous challenge of 8-week-old kittens with the feline immunodeficiency virus Maryland isolate (FIV-MD) was investigated for its ability to infect the central nervous system (CNS) and induce neurologic abnormalities. Six cats were inoculated with 1,000 TCID50 units of FIV-MD isolate, with six age-matched cats serving as uninfected controls. Clinical and immunological evaluation documented that challenged cats developed immunodeficiency and growth delay. Neurologic examination revealed an abnormal stereotypic motor behavior consisting of repetitive, compulsive roaming that developed as early as 4 weeks postinfection (PI) and persisted throughout the 16-month study in three cats. Serial neuroelectrodiagnostic evaluation revealed persistent abnormal electroencephalographic recordings in three infected cats. Serial evoked potential (EP) recordings at 3, 8, and 12 months PI demonstrated significantly prolonged interpeak latencies III-V at 3 months PI and I-III at 12 months PI for brainstem EP recordings. Alterations of visual EPs were detected only at the 3-month time period. Retinocortical time, however, was significantly different from that in control cats at 3 and 12 months PI. Magnetic resonance imaging evaluation of FIV-MD-infected cats at 12 months PI revealed cortical atrophy, mild ventricular enlargement, and discrete white matter lesions. At 16 months PI, however, histopathological examination of brain tissue indicated only mild lesions limited to satellitosis and perivascular lymphocytic infiltrates. Virus was detected in the CNS by reverse transcriptase, immunofluorescence, and antigen capture. Evaluation of the cerebrospinal fluid revealed intrathecal anti-FIV-MD antibody despite lack of detectable viremia in five challenged cats. Collectively, these findings demonstrate the induction of virus-associated neurologic disease following parenteral FIV challenge in conjunction with an immunodeficiency state. The nature of the nervous system infection is analogous to HIV-1 pediatric encephalopathy.
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PMID:AIDS-associated encephalopathy with experimental feline immunodeficiency virus infection. 838 49

Intravenous infection of cats with feline immunodeficiency virus was used as a model system to study activation of virus replication in brain-resident microglial cells in vitro. Virus release by ramified microglial cells isolated from subclinically infected animals was detectable in cell-free tissue culture supernatant only by reverse transcription and nested PCR of gag-specific RNA sequences and not by virion-associated reverse transcriptase activity. In contrast, cocultivation of in vivo-infected microglial cells with mitogen-activated peripheral blood mononuclear cells (PBMC) regularly allows detection of high virus yields in cell-free tissue culture fluid. Besides uptake and multiplication of microglia-derived virus in PBMC, release of virus from microglia is stimulated by cell contact with PBMC. The data suggest that T lymphocytes patrolling the central nervous system could reactivate the semilatent state of lentiviruses in microglial cells in the course of clinically silent central nervous system infection.
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PMID:In vitro activation of feline immunodeficiency virus in ramified microglial cells from asymptomatically infected cats. 1148 54

An 18-year-old woman presented with a progressively worsening headache, photophobia feverishness and vomiting. Three weeks previously she had returned to the UK from a trip to Peru. At presentation, she had clinical signs of meningism. On admission, blood tests showed a mild lymphopenia, with a normal C reactive protein and white cell count. Chest X-ray and CT of the head were normal. Cerebrospinal fluid (CSF) microscopy was normal. CSF protein and glucose were in the normal range. MRI of the head and cerebral angiography were also normal. Subsequent molecular testing of CSF detected enterovirus RNA by reverse transcriptase PCR. The patient's clinical syndrome correlated with her virological diagnosis and no other cause of her symptoms was found. Her symptoms were self-limiting and improved with supportive management. This case illustrates an important example of viral central nervous system infection presenting clinically as meningitis but with normal CSF microscopy.
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PMID:Confirmed viral meningitis with normal CSF findings. 2503 43