Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: 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)

The purposes of this study were to elucidate the role of cytokine upregulation in the pathogenesis of rabies encephalitis and to compare the detection of Negri bodies with that of rabies protein by immunohistochemistry and rabies RNA by reverse transcriptase (RT) in situ PCR for its diagnosis. Negri bodies were evident in 4/7 of the documented rabies cases; viral protein and viral RNA were detected in each case. The average number of rabies-infected cells, determined by counting 150 neurons in serial sections in areas where viral protein was evident, with the three different detection methods was: Negri bodies (<1/150), immunohistochemistry (4/150), and RT in situ PCR (49/150). No rabies protein or RNA was detected in four control brain tissues that were read with the rabies cases in a blinded fashion. The ratio of cells expressing tumor necrosis factor alpha (TNFalpha) or inducible nitric oxide synthetase (iNOS) to 1 SSI-1/SOCS-1 (suppressors of cytokine signaling) expression, which is a novel class of negative feedback regulators of cytokine receptor signaling, was markedly increased only in the areas where many viral infected cells were present. Colabeling experiments showed that most of the cells expressing iNOS or TNFalpha were not virally infected, but rather adjacent to rabies-infected neurons. We conclude that RT in situ PCR for rabies virus is the most accurate test for the determination of viral load in rabies encephalitis. Further, the disease is characterized by massive viral infection of neurons in a markedly focal distribution in conjunction with a concomitant upregulation of cytokine expression in adjacent, noninfected cells that may be due, in part, to SOCS downregulation.
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PMID:Molecular detection of rabies encephalitis and correlation with cytokine expression. 1538 58

Measles inclusion body encephalitis (MIBE) is a disease of the immunocompromised host and typically occurs within 1 year of acute measles infection or vaccination. We report a 13-year-old boy who had chronic granulomatous disease and presented 38 days after stem cell transplantation with afebrile focal seizures that progressed despite multiple anticonvulsants. After an extensive diagnostic evaluation, brain biopsy was performed, revealing numerous intranuclear inclusion bodies consistent with paramyxovirus nucleocapsids. Measles studies including reverse transcriptase-polymerase chain reaction and viral growth confirmed measles virus, genotype D3. Immunohistochemistry was positive for measles nucleoprotein. Despite intravenous ribavirin therapy, the patient died. MIBE has not been described in stem cell recipients but is a disease of immunocompromised hosts and typically occurs within 1 year of measles infection, exposure, or vaccination. Our case is unusual as neither the patient nor the stem cell donor had apparent recent measles exposure or vaccination, and neither had recent travel to measles-endemic regions. The patient had an erythematous rash several weeks before the neurologic symptoms; however, skin biopsy was consistent with graft-versus-host disease, and immunohistochemistry studies for measles nucleoprotein were negative. As measles genotype D3 has not been seen in areas where the child lived since his early childhood, the possibility of an unusually long latency period between initial measles infection and MIBE is raised. In addition, this case demonstrates the utility of brain biopsy in the diagnosis of encephalitis of unknown cause in the immunocompromised host.
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PMID:A new complication of stem cell transplantation: measles inclusion body encephalitis. 1552 95

Carcasses of 13 red-tailed hawks (RTHAs) and 11 Cooper's hawks (COHAs) were tested for West Nile virus (WNV) using WNV-specific reverse transcriptase-polymerase chain reaction (RT-PCR) on fresh brain tissue and WNV-specific immunohistochemistry (IHC) on various organs. Ten COHAs (91%) and 11 RTHAs (85%) were positive for WNV RNA by RT-PCR. All 11 COHAs (100%) and 10 RTHAs (77%) were positive for WNV antigen by IHC. A triad of inflammatory lesions, including chronic lymphoplasmacytic and histiocytic encephalitis, endophthalmitis, and myocarditis, was common in both species. In COHAs, the heart (54%), cerebrum (50%), and eye (45%) were the organs that most commonly contained WNV antigen. The amount of WNV antigen was usually small. In RTHAs, the kidney (38%), cerebrum (38%), cerebellum (38%), and eye (36%) were the organs most commonly containing WNV antigen. Unlike COHAs, larger amounts of WNV antigen were present in the cerebrum of RTHAs. WNV antigen was detected in similar cell populations in both species, including neurons of brain, spinal cord, and retina, pigmented epithelial cells of the retina, epithelial cells of renal medullary tubules, cardiomyocytes, endothelial cells and smooth muscle cells of arteries, dendritic cells of splenic lymph follicles, exocrine pancreatic cells, adrenal cells, and keratinocytes of the skin. The study presents strong evidence that WNV can cause a chronic fatal disease in RTHAs and COHAs. The lesion distribution of WNV infection in both species is variable, but inflammatory lesions are common, and a triad of lesions including encephalitis, myocarditis, and endophthalmitis is indicative of WNV infection in both species.
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PMID:Pathologic findings in red-tailed hawks (Buteo jamaicensis) and Cooper's hawks (Accipiter cooper) naturally infected with West Nile virus. 1552 79

A total of 191 adult sand flies belonging to the genus Sergentomyia were collected from seven villages in Karimnagar and Warangal districts of Andhra Pradesh State, India, after an outbreak of encephalitis due to Chandipura virus (CHPV). Fifteen pools, each containing two specimens, were tested by reverse transcriptase-polymerase chain reaction and sequencing. One pool of Sergentomyia from Kolanur village in Karimnagar District was positive for CHPV.
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PMID:Detection of chandipura virus from sand flies in the genus Sergentomyia (Diptera: Phlebotomidae) at Karimnagar District, Andhra Pradesh, India. 1596 4

Eastern equine encephalitis (EEE) was diagnosed in a flock of African penguins. Diagnosis was based on history and clinical signs and confirmed via serologic testing, virus isolation, reverse transcriptase-polymerase chain reaction (RT-PCR) assay, and histologic examination. Clinical signs in penguins included anorexia, behavior changes, depression, regurgitation, ataxia, recumbency, and seizures, and some penguins did not have any clinical signs. Mean +/- SD number of days that affected penguins had clinical signs was 12 +/- 5 days. Abnormalities initially detected on CBC included heterophilic leukocytosis and anemia; lymphocytosis and monocytosis were detected later. Plasma biochemical abnormalities included high activities of aspartate amino-transferase and creatine kinase, hyponatremia, hypochloremia, hyperglycemia, and high concentrations of globulin, triglycerides, and cholesterol. Mean +/- SD number of days required for resolution of CBC and plasma biochemical abnormalities was 67 +/- 24 days after the onset of clinical signs. Treatment consisted of supportive therapy. All penguins survived with the exception of one that was euthanatized; histopathologic findings were consistent with encephalitis. Results of RT-PCR assays performed on tissue from the right cerebrum of the penguin that was euthanatized were positive for EEE viral RNA. An inability to isolate virus several weeks after illness suggested successful viral clearance in recovered penguins. To the authors' knowledge, EEE infection in any penguin species has not been reported.
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PMID:Eastern equine encephalitis in a flock of African penguins maintained at an aquarium. 1598 91

The carcasses of 25 great horned owls and 12 goshawks were investigated for West Nile virus (WNV) infection by immunohistochemistry (IHC) performed on various organs, including brain, spinal cord, heart, kidney, eye, bone marrow, spleen, liver, lungs, pancreas, intestine, and proventriculus, using a WNV-antigen-specific monoclonal antibody and by WNV-specific reverse transcriptase-polymerase chain reaction (RT-PCR), performed on fresh brain tissue only. WNV infection was diagnosed by IHC in all owls and all goshawks. WNV-specific RT-PCR amplified WNV-RNA in the brain of all goshawks but only 12 owls (48%). Cachexia was a common macroscopic finding associated with WNV infection in owls (76%). Myocarditis was occasionally macroscopically evident in goshawks (33%). Microscopically, inflammatory lesions, including lymphoplasmacytic and histiocytic encephalitis, myocarditis, endophthalmitis, and pancreatitis were present in both species but were more common and more severe in goshawks than in owls. The most characteristic brain lesion in owls was the formation of glial nodules, in particular in the molecular layer of the cerebellum, while encephalitis affecting the periventricular parenchyma of the cerebral cortex was common in the goshawks. In owls, WNV-antigen-positive cells were present usually only in very small numbers per organ. Kidney (80%), heart (39%), and cerebellum (37%) were the organs that most commonly contained WNV antigen in owls. WNV antigen was frequently widely distributed in the organs of infected goshawks, with increased amounts of WNV antigen in the heart and the cerebrum. Spleen (75%), cerebellum (66%), heart (58%), cerebrum (58%), and eye (50%) were often WNV-antigen positive in goshawks. In contrast with the goshawks, WNV antigen was not present in cerebral and retinal neurons of owls. WNV infection appears to be capable of causing fatal disease in great horned owls and goshawks. However, the distribution and severity of histologic lesions, the antigen distribution in the various organs, and the amount of antigen varied among both species. Therefore, the diagnostician may choose organs for histology and immunohistochemistry as well as RT-PCR depending on the investigated species in order to avoid false-negative results.
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PMID:Pathologic and immunohistochemical findings in goshawks (Accipiter gentilis) and great horned owls (Bubo virginianus) naturally infected with West Nile virus. 1609 31

We report West Nile virus (WNV) RNA in urine collected from a patient with encephalitis 8 days after symptom onset. Viral RNA was detected by reverse transcriptase-polymerase chain reaction (RT-PCR). Sequence and phylogenetic analysis confirmed the PCR product to have > or = 99% similarity to the WNV strain NY 2000-crow3356.
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PMID:West Nile virus detection in urine. 1610 23

Maedi-visna is a slow virus infection of sheep leading to a progressing lymphoproliferative disease which is invariably fatal. It affects multiple organs, but primarily the lungs where it causes interstitial pneumonia (maedi). Infection of the central nervous system was commonly observed in Icelandic sheep (visna), infection of mammary glands (hard udder) in sheep in Europe and the USA, and infection of the joints in sheep in the USA. The name ovine progressive pneumonia (OPP) is commonly used in the USA and ovine lentivirus (OvLV) infection is also a name used for maedi-visna. A related infection of goats, caprine arthritis-encephalitis (CAE), is common in Europe and the USA. The natural transmission of maedi-visna is mostly by the respiratory route, but also to newborn lambs by colostrum and milk. Intrauterine transmission seems to be rare and venereal transmission is not well documented. Macrophages are the major target cells of maedi-visna virus (MVV), but viral replication is greatly restricted in the animal host, apparently due to a posttranscriptional block. The low-grade viral production in infected tissues can explain the slow course of the disease in sheep. The lesions in maedi-visna consist of infiltrates of lymphocytes, plasma cells, and macrophages, and are detectable shortly after experimental transmission. Several studies indicate that the lesions are immune mediated and that cytotoxic T-lymphocytes may be important effector cells. The persistence of the MVV infection is explained by a reservoir of latently infected blood and bone marrow monocytes, which migrate into the target organs and mature into macrophages with proviral DNA transcription, but limited replication of virus. The MVV particles are morphologically similar to those of other retroviruses and the mode of replication follows the same general pattern. The genome organization and gene regulation resembles that of other lentiviruses. In addition to gag, pol and env, MVV has three auxiliary genes (tat, rev and vif), which seem to have similar functions as in other lentiviruses, with a possible exception of the tat gene. A determination of the 9200 nucleotide sequence of the MVV genome shows a close relationship to CAE virus, but limited sequence homology with other lentiviruses, and only in certain conserved domains of the reverse transcriptase and possibly in the surface protein. MVV infection in sheep and HIV-1 infection in humans have a number of features in common such as a long preclinical period following transmission, and a slow development of multiorgan disease with fatal outcome. A brief early acute phase, which is terminated by the immune response, is also an interesting common feature. Like HIV-1, MVV is macrophage tropic and the early stages of the HIV-1 infection which affect the central nervous system and the lungs are in many ways comparable to maedi-visna. In contrast to HIV-1, MVV does not infect T-lymphocytes and does not cause T-cell depletion and immunodeficiency. This is responsible for the difference in the late stages of the HIV-1 and MVV infections and the final clinical outcome. Despite limited sequence homology, certain proteins of MVV and HIV-1 show structural and functional similarities. Studies of MVV may therefore help in the search for new drugs against lentiviruses, including HIV-1.
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PMID:Maedi-visna virus and its relationship to human immunodeficiency virus. 1642 63

Nipah virus (NiV), a member of the Paramyxoviridae family, causes a zoonotic infection in which the reservoir, the fruit bat, may pass the infection to pigs and eventually to humans. In humans, the infection leads to encephalitis with >40 to 70% mortality. We have previously shown that polyclonal antibody directed to either one of two glycoproteins, G (attachment protein) or F (fusion protein), can protect hamsters from a lethal infection. In the present study, we have developed monoclonal antibodies (MAbs) to both glycoproteins and assessed their ability to protect animals against lethal NiV infection. We show that as little as 1.2 mug of an anti-G MAb protected animals, whereas more than 1.8 mug of anti-F MAb was required to completely protect the hamsters. High levels of either anti-G or anti-F MAbs gave a sterilizing immunity, whereas lower levels could protect against a fatal infection but resulted in an increase in anti-NiV antibodies starting 18 days after the viral challenge. Using reverse transcriptase PCR, the presence of NiV in the different organs could not be observed in MAb-protected animals. When the MAbs were given after infection, partial protection (50%) was observed with the anti-G MAbs when the animals were inoculated up to 24 h after infection, but administration of the anti-F MAbs protected some animals (25 to 50%) inoculated later during the infection. Our studies suggest that immunotherapy could be used for people who are exposed to NiV infections.
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PMID:Antibody prophylaxis and therapy against Nipah virus infection in hamsters. 1643 53

Free-living amoebae of the genus Acanthamoeba are causative agents of granulomatous amebic encephalitis and amebic keratitis. Because the virulence of Acanthamoeba culbertsoni cultured in the laboratory is restored by consecutive brain passages, we examined the genes induced in mouse brain-passaged A. culbertsoni by differential display reverse transcriptase polymerase chain reaction (DDRT-PCR). Enhanced A. culbertsoni virulence was observed during the second mouse brain passage, i.e., infected mouse mortality increased from 5% to 70%. Ten cDNAs induced during mouse brain passage were identified by DDRT-PCR and this was confirmed by northern blot analysis. BlastX searches of these cDNAs indicated the upregulations of genes encoding predictive NADH-dehydrogenase, proteasomal ATPase, and GDP-mannose pyrophosphorylase B, which have previously been reported to be associated with A. culbertsoni virulence factors.
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PMID:Identification of differentially expressed cDNAs in Acanthamoeba culbertsoni after mouse brain passage. 1651 77


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