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Di truyen hoc virus

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1
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.”
3
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

SPONTANEOUS

tautomeric form of bases

polymerase errors

7
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

SPONTANEOUS

PHYSICALLY INDUCED

UV light , especially problem if no
access to repair

X-rays

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

PLAQUE SIZE

may show altered pathogenicity

DRUG RESISTANCE

important in the development of antiviral agents

ENZYME-DEFICIENT MUTANTS

some genes can be ‘optional’ in certain
circumstances
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PHENOTYPIC CHANGES

“HOT MUTANTS”

grow better at elevated temperature than wt

less susceptible to host fever response

ATTENUATED MUTANTS

milder (or no) symptoms

vaccine development

pathogenesis

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