Download Unit 6c Viruses

Unit 6c Viruses
Structure of a virus
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To be a virus, you need:
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Genetic material (DNA or RNA)
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Protein coat (to enclose genetic material)
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Some are membrane-bound (helps them fuse
with host cell)
Viral Replication
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Viruses replicate rapidly within host cell and use
“component assembly model” to make many
viruses within one host cell
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Two main ways virus replicate within host cell
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Lytic Cycle (main mechanism)
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Lysogenic Cycle
Lytic Cycle
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Virus attaches to host cell → injects its genetic
information (DNA or RNA) into cell
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Genetic information goes into nucleus & is
replicated by host cell
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Some replicated DNA is transcribed into mRNA
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mRNA exits nucleus & is translated into protein
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Duplicated DNA & viral proteins form new viruses
within the cell → cell lyses (breaks open) → virus
is released & infects neighboring cells
Lysogenic Cycle
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Bacteriophage inject genetic material into host
bacteria, genetic material integrates into host
cell's DNA, bacteria continues to replicate DNA
and divide
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Essentially virus “hides out” in DNA of bacteria
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At some point, virus transfers to lytic cycle
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Ex: Cold sores (Herpes Simplex Virus or HSV-1)
Genetic Exchange b/n Viruses
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If two similar viruses happen to be in the same
cell during lytic cycle, exchange of genetic
material may occur
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Increases variation among viruses which can lead
to creation of new strains of virus
Lysogenic Cycle & Virulence of Bacteria
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When bacteriophage infect bacteria & enter
lysogenic cycle, they can change the virulence
of the bacteria
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Ex: Cholera (vibrio cholerae) bacteria by itself
is not toxic until it's infected by CTX phage
virus
RNA viruses (aka Retroviruses)
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Use RNA as genetic information
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Contain enzyme called reverse transcriptase
which takes RNA and makes it DNA, DNA enters
nucleus, etc...
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BAD NEWS – no proofreading in reverse
transcriptase and it is very error-prone
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High error rate → increase pathogenicity of virus
via genetic variation
Ex: HIV Virus
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“Large” retrovirus (60x smaller than rbc) with high
mutation rate
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HIV generates 1010 virions per day with
approximately 3x10-5 mutation rate per bp per
replication cycle
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BAD: Create vaccine → HIV mutates → vaccine no
longer works
Most treatment for HIV is based on targeting
reverse transcriptase
One good mutation...
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People with CCR5-delta32 mutation (deletion
of 36bp) are resistant to HIV
–
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Mutation causes helper T cells to have a
nonfunctional receptor protein that makes it
impossible for HIV to enter the cell
5-15% of Europeans vs. < 1% Africians and
Asians