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Titlebook: Mechanisms of Viral Pathogenesis; From Gene to Pathoge A. Kohn,P. Fuchs Conference proceedings 1984 Martinus Nijhoff Publishing, Boston 198

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Control Elements for the Expression of DNA Tumor Viruses a possible involvement of host specific factors. In an effort to define critical nucleotides we have constructed and analyzed mutants containing multiple nucleotide exchanges within the SV40 72 bp repeat. Our results define nucleotides essential for the enhancer function. We furthermore determined
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Pathogenicity of Vesicular Stomatitis Virus is Potentially Mediated by Wild-Type Leader RNA which Inas did other exogenous synthetic and natural RNAs. The wild-type leader RNA contains TAATA-like and consensus-like sequences, which could potentially inhibit the functions of RNA polymerase II and III, whereas similar sequences are absent in the nonpathogenic DI leader.
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Structural Feature of Picornavirus RNA Involved in Pathogenesis: A Very High Affinity Binding Site fNA protects eIF-2 against inactivation by dsRNA, apparently because it competes more effectively than dsRNA for eIF-2, while cellular mRNA competes less effectively. Our results suggest the following scenario for picorna virus- infected cells: (1) A strong picorna virus RNA template outcompetes cell
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Molecular Approach to Virulence: Isolation and Characterization of Avirulent Mutants of Rabies Virusade the lens..Various parameters of the immune response arising after intramuscular inoculation of CVS or Av01 have also been measured. The major difference is that interferon production and natural killer activity of splenocytes last for 2 or 3 days instead of few hours in the case of Av01 inoculat
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On The Role of Viral Envelope Proteins in Pathogenesismbrane fusion reaction has been characterized using intact cells and liposomes as target membranes, and both intact virus and membranes reconstituted with purified F protein as the fusogenic agents. Requirements for fusion have been determined, including a conformational change in the F protein upon
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Genetic Diversity of Bunyaviruses and Mechanisms of Genetic Variationh are the nucleocapsid protein N and the two surface glycoproteins G1 and G2. A minor large molecular weight protein designated L is sometimes observed, and this protein is presumed to be the virion transcriptase. The maturation of bunyaviruses occurs at smooth membrane vesicles, predominantly in membranes associated with the Golgi apparatus.
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