By H. L. Sänger, B. Haas (auth.), Professor Dr. Rudolf Rott, Professor Dr. Werner Goebel (eds.)
Elucidation of the mechanisms of pathogenesis underlying the ailments attributable to viruses and micro organism has involved scientists for a few years in methods. first of all, those pathogenic brokers characterize fairly sim ple organic structures for the examine of easy organic methods equivalent to replication, gene law, genetic variability and host-pathogen interactions. Secondly, procedure during this box is effective in a practi cal sence, because it may help within the keep an eye on of those illnesses. The avail skill of recent genetic and immunological suggestions, in particular recom binant DNA equipment and monoclonal antibody know-how, has supplied robust instruments for unravelling the genetic, biochemical and immunologi cal foundation of viral and microbial pathogenesis. Molecular cloning has allowed the isolation of unmarried genes or teams of genes concerning phenotypes which seem to be immunologically vital for pathogene sis. the explicit removal of such genes from the advanced genomes of the pathogens can now be accomplished with comparable genetic strategies. those genetic experiences have supplied additional info at the function performed via particular phenotypic characteristics in pathogenesis, specially whilst mixed with appropriate animal version platforms. additionally, the struc tural research of vital virulence components and floor antigens may possibly enable the prediction of antigenic domain names appropriate for the advance of recent vaccines. The thirty eighth Mosbacher Colloquium makes a speciality of the molecular foundation of viral and microbial pathogenesis. The virology half starts with the good studied plant viroids. the weird constitution in their genome, in addition to wisdom approximately their replication and pathogenicity, are presented.
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It is not yet clear whether this 42 Table 1. Multiplication of reassortants between fowl plague virus (F) and A/chicken/ Germany "N"/49 (N) in lungs and brains after intranasal inoculation of 2-day-old mice. With exception of the first virus (virus N) the genes PB2, HA, NA and M of the reassortants are derived from fowl plague virus. If the PB1- or/and PA-gene is derived from virus N, the reassortants are neurotropic for mice. If in addition the NS-gene is derived from virus N, the virus titer found in the brain increases even further.
In: Palese P, Kingsbury DW (eds) Genetics of influenza virus. Springer Berlin Heidelberg New York, pp 21-69 Lazarowitz SG, Choppin PW (1975) Enhancement of the infectivity of influenza A and B viruses by proteolytic cleavage of the hemagglutinin polypeptide. Virology 68: 440-454 Lazarowitz SG, Goldberg AR, Choppin PW (1973) Proteolytic cleavage by plasmin of the HA polypeptide of influenza virus. Host cell activation of serum plasminogen. Virology 56:172-180 Lopez S, Arias CF, Mendez E, Espejo RT (1986) Conservation in rotaviruses of the protein region containing the two sites associated with trypsin enhancement of infectivity.
Klenk 1, M. Tashiro 2 , W. Garten 1, and R. Rott 2 Introduction Many viruses possess a lipid-containing envelope which is a simple biological membrane surrounding the viral genome and accessory proteins. Among the general features of membrane structure shared by all of these viruses are glycoproteins that span the lipid ~layer and usually appear as protrusions or spikes at the surface of the virus particles. Viral glycoproteins have found wide interest as models for structure and biosynthesis of membrane proteins.