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

---

Query: EC:2.7.7.49 (reverse transcriptase)
31,746 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Little is known about the relationship between recovery from acute viral encephalitis and the clearance of viral genetic material from the central nervous system. In a mouse model of Sindbis virus encephalitis, we have previously shown that clearance of infectious virus is mediated by antibody-induced restriction of viral gene expression rather than by cytotoxic destruction of virally infected cells. To explore whether Sindbis virus genomes persist in mouse brain after the clearance of infectious virus, we used reverse transcriptase-polymerase chain reaction amplification methods to detect Sindbis virus RNA in brain samples from immunocompetent BALB/c and antibody-treated immunodeficient scid/CB17 mice. RNA sequences from both the nonstructural region (NSP1 gene) and structural regions (E2 gene) of Sindbis virus were detected in the brains of all BALB/c and antibody-treated scid mice examined at 1, 2, and 3 months after infection. Additional BALB/c mouse brains were also positive at 8, 12, and 17 months after infection. To determine whether persistent RNA was capable of resuming unrestricted replication in the absence of the continuous presence of antiviral antibodies, viral titers were measured in the brains of scid mice at 1, 2, 3, and 6 months after antibody treatment. Viral reactivation was seen in scid mice treated with hyperimmune serum or a low dose of monoclonal antibody to the E2 envelope glycoprotein, but not in mice treated with a high dose of monoclonal antibody to E2. Replication of infectious virus isolated from scid mouse brain could be restricted by repeat treatment with immune serum, indicating that viral reactivation is not due to antibody-escape mutations. These results demonstrate that Sindbis virus can persist long term in a nonproductive form in mouse brain and suggest that the humoral immune response plays an important role in preventing viral reactivation.
...
PMID:Persistence of viral RNA in mouse brains after recovery from acute alphavirus encephalitis. 138 64

We have used the reverse transcriptase-polymerase chain reaction technique to gain insight into the pathogenesis of encephalitis caused by Borna disease virus (BDV). RNA specific for BDV was first detected in the olfactory bulb of intranasally infected rats at 6 days postinfection (p.i.). At 14 days p.i., high levels of BDV RNA were found in all brain regions, and at 26 days p.i., BDV-specific RNA was also present in the eye, nasal mucosa, and facial skin. In the chronic phase of the disease, BDV RNA was identified in many peripheral organs but not in blood. Analysis of brain tissue for the presence of cytokine mRNAs revealed that the mRNA levels of interleukin-6 (IL-6), tumor necrosis factor alpha, and IL-1 alpha had increased sharply at 14 and 26 days p.i. These cytokine mRNAs reached maximum levels at the peak of inflammatory reactions and decreased drastically in the chronic phase of the disease. Although IL-2 mRNA was also found in normal brain, it was markedly increased in BDV-infected brain at 14 days p.i. Expression of gamma interferon (IFN-gamma) mRNA, which was not observed in normal rat brain, was detected at 14 days p.i. and reached a maximum level at 38 days p.i. IL-2 and IFN-gamma mRNA expression correlated with expression of CD4 and CD8 mRNAs, indicating that both CD4+ and CD8+ T lymphocytes are induced in the early stages of BDV infection. Since IFN-gamma and CD8 mRNA levels were still highly elevated in the chronic phase of Borna disease, it is likely that CD8+ T lymphocytes act to reduce inflammation and to ameliorate neurological signs during the chronic phase of infection.
...
PMID:Kinetics of virus spread and changes in levels of several cytokine mRNAs in the brain after intranasal infection of rats with Borna disease virus. 173 Nov 17

We summarize the pathogenesis of animal lentiviruses (visna-maedi virus, caprine arthritis and encephalitis virus, and equine infectious anemia virus), which have raised considerable interest since the discovery of human lentiviruses. The human lentiviruses possess structural, genetic, and clinical properties similar to those of animal lentiviruses. We describe the different mechanisms of and the principal work on reverse transcriptase inhibitors of animal lentiviruses, such as HPA-23, phosphonoformate, or 2',3'-dideoxynucleosides. Animal viruses of this family may serve as models for infection with human lentiviruses such as human immunodeficiency virus, the etiologic agent of AIDS.
...
PMID:Animal lentivirus replication and reverse transcriptase inhibitors. 247 76

The human immunodeficiency virus is a member of the lentivirus subfamily of the retrovirus family. Retroviruses are RNA viruses which code for an RNA-dependent DNA polymerase (reverse transcriptase), which transcribes the RNA genome into a DNA provirus which, on integration with the host DNA, directs the synthesis of new virions. The RNA genome consists of a gag gene, which codes for the viral core proteins, a pol gene, which codes for the reverse transcriptase, an env gene, which codes for the glycoproteins of the viral envelope, and several genes (tat, rev, vif, vpr, and nef), that code for regulatory proteins. At each end of the genome are long terminal repeats, that contain regulatory elements for transcription. There are 3 subfamilies of Retroviridae (Oncovirinae, Spumavirinae, and Lentiverinae). The Lentiverinae ("slow viruses") include the bovine immunodeficiency virus (BIV), the feline immunodeficiency virus (FIV), the human immunodeficiency viruses (HIV), and the simian immunodeficiency viruses (SIV). SIV has been isolated from macaques (mac), African green monkeys (agm), sooty mangabeys (sm), and mandrills (mnd). Only SIVmac causes an AIDS-like disease in its natural host, but it is genetically closer to HIV-2 than to HIV-1. SIVsm causes an AIDS-like disease in macaques, but not in the sooty mangabey. Monkeys infected with SIV develop diarrhea, wasting, decrease in T4 lymphocytes, lymphadenopathy, development of giant cells, and encephalitis, as well as opportunistic infections. Kaposi's sarcoma, however, has not been found in SIV-infected primates. Virus is recovered from peripheral blood mononuclear cells and the brain. SIV models are useful for understanding the natural history of primate lentiviruses, for defining the pathogenesis of AIDS, and for developing vaccines. The ideal model would be one in which HIV causes AIDS, but so far only chimpanzees and gibbons have successfully been infected with HIV-1, and although virus, is recovered from peripheral blood mononuclear cells of chimpanzees within 2 weeks of infection, and 2 animals have lost antibodies to the p24 protein, none has so far developed clinical AIDS. Attempts to develop vaccines to immunize chimpanzees are continuing. Nonprimate lentiviruses include the visna virus, the feline immunodeficiency virus, and the bovine immunodeficiency virus. The visna virus infects fibroblasts by fusion of the viral envelope with the plasma membrane of the fibroblast; it infects macrophages by endocytosis. Infected macrophages regulate the production and dissemination of viral particles. The feline immunodeficiency virus infects T-lymphocytes of cats and produces oral, gastrointestinal and respiratory pathology as well as lymphadenopathy and opportunistic infections. Bovine immunodeficiency-like virus causes a generalized lymphadenopathy similar to that seen in AIDS-related complex.
...
PMID:Animal models for HIV infection and AIDS: memorandum from a WHO meeting. 285 Jan 18

Suramin sodium is a reverse transcriptase inhibitor with in vitro activity against the human immunodeficiency virus (HIV), the causative agent of acquired immunodeficiency syndrome (AIDS). Ninety-eight patients with AIDS manifest as opportunistic infections (n = 38), AIDS with Kaposi's sarcoma (n = 38), AIDS-related complex (n = 20), or AIDS-associated non-Hodgkin's lymphoma (NHL) (n = 2) were treated with suramin sodium at 0.5, 1.0, or 1.5 g/wk for six weeks followed by maintenance therapy with 0.5 or 1.0 g/wk. Of 72 patients who were HIV culture positive before therapy and were assessable for subsequent HIV culture 40% became culture negative during treatment, with no apparent correlation between virus recovery and serum suramin concentration. No immunologic improvement was noted. One complete clinical remission was noted in a patient with Kaposi's sarcoma and stage IV NHL. Seven minor clinical responses were also noted. Toxic reactions were generally reversible, and included fever (78%), rash (48%), malaise (43%), nausea (34%), neurologic symptoms (33%), and vomiting (20%). Suramin-induced neutropenia was noted in 26%, thrombocytopenia in 12%, a serum creatinine level of 180 mumol/L or higher (greater than or equal to 2.1 mg/dL) in 12%, liver dysfunction in 14%, and clinical and/or laboratory evidence of adrenal insufficiency in 23%. Sixteen patients died while receiving suramin or within three weeks of discontinuation of drug therapy due to infection (n = 6), hepatic failure (n = 3), pulmonary Kaposi's sarcoma (n = 2), AIDS encephalitis (n = 2), AIDS-associated NHL (n = 1), iatrogenic hemo-pneumothorax (n = 1), or pulmonary disease of uncertain etiology. Suramin as currently administered cannot be recommended as effective therapy for AIDS.
...
PMID:Suramin therapy in AIDS and related disorders. Report of the US Suramin Working Group. 365 Mar 39

A syncytium-forming agent with reverse transcriptase activity was isolated in cell culture from materials collected from 19 Michigan goats and 1 goat recently imported from California. Syncytia formation could be maintained by subpassaging cells or filtered supernate from infected cultures with caprine fetal synovial membrane indicator cells. Electron microscopy by negative staining with ammonium molybdate revealed 100-nm retrovirus-like particles morphologically identified as caprine arthritis-encephalitis virus. The agent was recovered from synovial membrane explants, synovial fluid, colostrum cells, and peripheral blood mononuclear cells of clinically arthritic goats. Samples were collected from 9 Michigan goat herds, and virus was isolated from 7 of these herds.
...
PMID:Caprine arthritis-encephalitis virus isolated from Michigan goats. 620 29

DNA from mouse cells chronically infected with tick-borne encephalitis (TBE) virus was treated with restrictases, the resulting fragments were fractionated by size by gel electrophoresis, denaturated, and transferred from gel on nitro-cellulose filters. The fragments containing virus-specific sequences were detected by hybridization with 32P-DNA replicas of TBE genome RNA synthesized using reverse transcriptase. The presence of virus-specific sequences in DNA fragments from chronically infected cells proves the possibility of integration of DNA-replicas of TBE virus genome and genome of chronically infected cells.
...
PMID:[Incorporation of a DNA replica of the genome of the tick-borne encephalitis virus into cellular DNA]. 630 27

Sheep pulmonary carcinoma (SPC) has been shown to be associated in nature with a retrovirus, by electron microscopic, biochemical, and epidemiological criteria and by experimental transmission. In this study, a retrovirus has been isolated from SPC tumors which were experimentally induced by inoculation with a cell-free, reverse transcriptase containing fraction from a spontaneous field case of SPC, and propagated in culture. This novel virus was shown to be unrelated to murine, avian, and bovine leukemia viruses, to be exogenous to the ovine species, and to have only limited genetic relatedness to the lentiviridae (maedi-visna and caprine arthritis encephalitis virus).
...
PMID:Isolation and characterization of a novel retrovirus from sheep affected by pulmonary carcinoma. 632 72

Jaagsiekte, or ovine pulmonary adenomatosis, is caused by a recently discovered retrovirus. The virus cannot be cultivated in vitro at present, but a procedure is described for the isolation and purification of small amounts in the form of immune complexes with IgA from affected lungs. The virion was shown to possess a 70S RNA genome which can be transcribed by an endogenous reverse transcriptase. Nine size from 94 000 to 25 000 daltons, were found in purified preparations. Using neutralization of the viral reverse transcriptase and an enzyme immunoassay as criteria, no serological relationship could be demonstrated to representatives of type B, C and C oncoviruses, or to bovine leukemia virus, maedi-visna virus of sheep or caprine arthritis-encephalitis virus.
...
PMID:Isolation and preliminary characterization of the jaagsiekte retrovirus (JSRV). 667 94

We describe the first report of caprine arthritis-encephalitis virus (CAEV) isolation in Brazil. In December 1989 a four-year old anglonubian arthritic doe was submitted to euthanasia and its synovial membranes were cultured by explantation. This doe was positive for antibodies to the caprine arthritis-encephalitis virus (CAEV). The reverse transcriptase activity detected in culture supernatants, the characteristic cytopathic effect of lentivirus in these cultures, the detection of viral antigens in concentrated supernatants by the agar gel immunodiffusion test, and the results of the fluorescent antibody test and of Northern blot analyses are consistent with the isolation of the CAEV.
...
PMID:Caprine arthritis-encephalitis virus: isolation and identification in Rio Grande do Sul, Brazil. 751 Oct 15


1 2 3 4 5 6 7 8 9 10 Next >>

---