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Elucidation of the mechanisms of pathogenesis underlying the
diseases caused by viruses and bacteria has fascinated scientists
for many years in two ways. Firstly, these pathogenic agents
represent relatively sim ple biological systems for the study of
basic biological processes such as replication, gene regulation,
genetic variability and host-pathogen interactions. Secondly,
process in this field is valuable in a practi cal sence, since it
can help in the control of these diseases. The avail ability of new
genetic and immunological techniques, especially recom binant DNA
methods and monoclonal antibody technology, has provided powerful
tools for unravelling the genetic, biochemical and immunologi cal
basis of viral and microbial pathogenesis. Molecular cloning has
allowed the isolation of single genes or groups of genes related to
phenotypes which appear to be immunologically important for
pathogene sis. The specific elimination of such genes from the
complex genomes of the pathogens can now be achieved with similar
genetic techniques. These genetic studies have provided additional
information on the role played by specific phenotypic traits in
pathogenesis, especially when combined with relevant animal model
systems. Furthermore, the struc tural analysis of important
virulence factors and surface antigens may allow the prediction of
antigenic domains suitable for the development of new vaccines. The
38th Mosbacher Colloquium focuses on the molecular basis of viral
and microbial pathogenesis. The virology part begins with the well
studied plant viroids. The unusual structure of their genome, as
well as knowledge about their replication and pathogenicity, are
presented.
The fact that none of the known DNA polymerases is able to initiate
DNA chains but only to elongate from a free 3' -OH group raises the
problem of how replication is initiated, both at the replication
origin and on Okazaki frag ments. It was first shown by A. KORNBERG
et al. that a general mechanism to initiate replication is through
the formation of an RNA primer catalyzed by RNA polymerases or by a
new class of enzymes, the primases (KORNBERG 1980). This mechanism,
which can be used in the case of circular DNA molecules or linear
DNAs that circularize or form concatemers, cannot be used at the
ends of linear DNAs since the RNA primer is removed from the DNA
chain, and there is no way of filling the gap resulting at the 5'
-ends of the newly synthesized DNA chain. In some cases linear DNA
molecules contain a palin dromic nucleotide sequence at the 3' -end
that allows the formation of a hairpin structure which provides the
needed free 3'-OH group for elongation. This mechanism, first
proposed by CAVALIER-SMITH (1974) for eukaryotic DNA repli cation,
was shown to take place in several systems (KORNBERG 1980, 1982).
Another mechanism to initiate replication consists in the specific
nicking of one of the strands of a circular double-stranded DNA,
producing a 3'-OH group available for elongation (KORNBERG 1980)."
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