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)

Pretreatment of chick embryo fibroblasts (CEF) with low doses of homologous interferon (16 u/ml) drastically inhibits cell transformation by, and replication of Rous sarcoma virus (RSV). Treatment of chick cells with 16 u/ml of interferon before de novo infection with a transformation defective (td) mutant-RSV, also resulted in a reduction of extracellular virus particles. This was determined by infectivity titrations, virus associated reverse transcriptase (RT) activity and measurement of metabolically radioactively labelled virus particles. The viral proteins pr 180, pr 76, p 27, p 19 and p 12 were still synthesized in interferon-treated cells in an unaltered form, although at slightly reduced levels. No difference in the pattern of structural proteins could be detected between virus particles harvested from cells treated with interferon and from control cells. In contrast to de novo infected cells, concentrations of interferon as high as 200 u/ml had no influence on the reversible transformation of cloned fibroblasts infected with a temperature sensitive mutant of RSV. In addition, fibroblasts infected with td-SR-RSV-D before addition of interferon showed only a marginal effect on formation of infectious virus even after treatment with 200-500 u/ml of interferon. This was not caused by interferon-resistance of the td-SR-RSV-D infected cells since viral protein synthesis by superinfecting Vesicular stomatitis virus (VSV) was as sensitive to interferon as in cells not preinfected with retrovirus. Our results support the notion that exogenous infection of fibroblasts with avian retrovirus is inhibited by interferon during an early phase of the replication cycle.
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PMID:Interferon inhibits establishment of fibroblast infection with avian retroviruses. 618 Jan 4

Vesicular stomatitis virus of the New Jersey serotype (VSV-NJ) causes vesicular disease in cattle, pigs, and horses throughout the Americas. Vesicular disease is clinically indistinguishable from foot-and-mouth disease (FMD). Therefore, outbreaks of vesicular disease in FMD-free areas must be rapidly diagnosed by laboratory methods and affected farms must be quarantined until laboratory results confirm the absence of FMD. Diagnosis is currently performed in high-containment (biosafety level 3) laboratories by using complement fixation and virus isolation in tissue culture. We describe here an alternative method for the detection of VSV-NJ RNA in clinical samples. This method includes a rapid acid guanidine-phenol RNA extraction procedure coupled with a one-tube polymerase chain reaction (PCR) using reverse transcriptase. By using this test, we were able to detect the largest number of positive samples (53 of 58), followed by complement (48 of 58) and isolation in tissue culture (43 of 58). The primers chosen for this assay amplify a 642-nucleotide region of the phosphoprotein gene of VSV-NJ but not of VSV-IN. Sequencing of the PCR product enables genetic typing of virus isolates and epidemiological studies. Since no infectious materials are necessary to perform this test and any infectious virus in clinical samples is destroyed by acid guanidine-phenol treatment, diagnosis can be safely performed in regular diagnostic laboratories.
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PMID:Rapid detection of vesicular stomatitis virus New Jersey serotype in clinical samples by using polymerase chain reaction. 839 84

Horses were inoculated with Vesicular stomatitis New Jersey and Indiana viruses by routes simulating contact and vector transmission. Clinical signs, lesions, antibody development, viral shedding and persistence, and viremia were monitored. Horses were infected with both viruses by all routes as confirmed by seroconversion. Salivation, primary lesions at inoculation sites, and secondary oral lesions were the most common clinical findings. Viral shedding was most often from the oral cavity, followed by the nasal cavity; titers were highest from oral cavity samples. Virus was rarely isolated from the conjunctival sac and never from feces or blood. Development of neutralizing antibody coincided with cessation of lesion development and detection of virus by isolation. Circulating virus-specific IgM, IgG, IgA, and neutralizing antibodies developed in most animals postinoculation (PI) days 6 to 12, depending on the route of inoculation. At postmortem (PI days 12 to 15), lesions were healing, were not vesicular, and did not contain detectable virus by isolation, reverse transcriptase polymerase chain reaction, or immunohistochemistry. Numerous infiltrating lymphocytes and plasma cells suggested that lesion resolution was partially due to local immunity. Detection of viral RNA from tonsil and lymph nodes of head at necropsy suggests that these tissues play a role in the pathogenesis of the disease; molecular techniques targeting these tissues may be useful for confirming infection in resolving stages of disease. The routes of inoculation used in this study reflect the diversity of transmission routes that may occur during outbreaks and can be used to further study contact and vector transmission, vaccine development, and clarify pathogenesis of the disease in horses.
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PMID:Experimental vesicular stomatitis virus infection in horses: effect of route of inoculation and virus serotype. 1709 51