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VIRAL GENETICS
•
PATHOGENESIS
•
LIFE CYCLES
•
VACCINE DEVELOPMENT
•
DRUG RESISTANCE
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VIRAL GENETICS
“DNA chromosomes of eukaryotic host
organisms generally require geologic time
spans to evolve to the degree that their
RNA viruses can achieve in a single human
generation.”
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VIRAL GENETICS
•
VIRUSES GROW RAPIDLY
•
A SINGLE PARTICLE PRODUCES A LOT
OF PROGENY
•
DNA VIRUSES SEEM TO HAVE ACCESS
TO PROOF READING, RNA VIRUSES DO
NOT SEEM TO
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NATURE OF GENOMES
•
RNA or DNA
•
SEGMENTED OR NON-SEGMENTED
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GENETIC CHANGE
•
MUTATION
•
RECOMBINATION
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ORIGIN OF MUTATIONS
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SPONTANEOUS
–
tautomeric form of bases
–
polymerase errors
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Tautomeric forms of bases
most of time rarely
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ORIGIN OF MUTATIONS
•
SPONTANEOUS
–
tautomeric form of bases
–
polymerase errors
why do some viruses seem to alter very little, even though
one would expect high mutation rates?
mutation rates usually higher in RNA viruses (lack of proof
reading)
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ORIGIN OF MUTATIONS
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SPONTANEOUS
•
PHYSICALLY INDUCED
–
UV light , especially problem if no
access to repair
–
X-rays
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CHEMICALLY INDUCED
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TYPES OF MUTATION
•
POINT
•
INSERTION
•
DELETION
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PHENOTYPES
PHENOTYPE
–
the observed properties of an organism
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PHENOTYPIC CHANGES
•
CONDITIONAL LETHAL - multiply under
some conditions but not others - wild-type
(wt) grows under both sets of conditions
•
temperature-sensitive (ts) mutants do not grow at higher
temperature (altered protein)
•
host-range mutants do not grow in all the cell types that
the wt does
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PHENOTYPIC CHANGES
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PLAQUE SIZE
–
may show altered pathogenicity
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DRUG RESISTANCE
–
important in the development of antiviral agents
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ENZYME-DEFICIENT MUTANTS
–
some genes can be ‘optional’ in certain
circumstances
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PHENOTYPIC CHANGES
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“HOT MUTANTS”
–
grow better at elevated temperature than wt
–
less susceptible to host fever response
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ATTENUATED MUTANTS
–
milder (or no) symptoms
–
vaccine development
–
pathogenesis