Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0155339 (Brown)
 12,436 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The cDNA derived from the Newcastle disease virus (NDV) hemagglutinin-neuraminidase (HN) gene was inserted into a replication-competent Schmidt-Ruppin Rous sarcoma virus-derived vector. Chick embryo cells transfected with this vector expressed HN-sized protein which could be precipitated with anti-HN antibody. These cells adsorbed avian red blood cells and the cell surfaces exhibited neuraminidase activity while cells transfected with an antisense version of the gene were negative for hemadsorption and neuraminidase. The cells transfected with the retroviral vector containing the HN gene were resistant to infection by NDV and influenza virus, viruses which bind to sialic acid containing receptors, but sensitive to vesicular stomatitis virus (VSV). Cells transfected with the antisense version of the HN gene were sensitive to NDV, influenza virus, and VSV infection. Thus the HN protein-expressing cells are likely resistant to NDV and influenza virus due to the destruction of the cellular receptors by the neuraminidase of the HN protein. The expression of the influenza virus HA protein using the same retrovirus vector has been reported previously (L. A. Hunt, D. W. Brown, H. L. Robinson, C. W. Naeve, and R. G. Webster, 1988, J. Virol. 62, 3014-3019). Cells infected with this vector were sensitive to infection with influenza virus, NDV, and VSV. Thus expression of a viral surface protein does not necessarily confer resistance of the cell to the homologous virus.
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PMID:Avian cells expressing the Newcastle disease virus hemagglutinin-neuraminidase protein are resistant to Newcastle disease virus infection. 254 25

The DNA as isolated from duck fibroblasts transformed by a duck-adapted Prague strain of Rous sarcoma virus and used for transfection. Transformed recipient BLEF and DEF cultures exhibited considerable morphological variability. The virus designated daPR-RSV-C morphf was obtained from the culture with fusiform transformation and cloned. The virus retained the ability to induce fusiform transformation, even after 20 passages on chicken fibroblasts. There was a good correlation between focus forming activity of the virus and its tumorigenicity in chickens. The frequency of morphf mutation to another phenotype was less than 10(-3) in cloned virus. Foreign avian embryonic cells transformed by this virus clone had a similar morphological appearance as transformed chicken cells. The clone also retained two additional non-conditional markers - subgroup C specificity and the ability to replicate efficiently in duck cells ("duck adaptation"). Freshly obtained cloned virus was found not to contain a transformation-defective mutant. Such a mutant occurred in the second passage of the virus of DEF where the mutant was isolated. Inoculation of the td mutant into Brown Leghorn embryos gave rise to a sarcoma in one of the 36 examined chickens. However, no transforming virus was detected in the sarcoma. SDS-polyacrylamide gel electrophoresis showed that cloned daPR-RSV-C morphf contained only genomic RNA; its molecular weight 3.08 X 10(6) daltons corresponded to the molecular weight of a non-defective PR-RSV-C used as control.
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PMID:Characterization of a mutant of the Prague strain of Rous sarcoma virus inducing fusiform transformation of avian fibroblasts in vitro. 628 73