Chapter 13 The Genetics of Viruses and Prokaryotes

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Transcript Chapter 13 The Genetics of Viruses and Prokaryotes

Chapter 13
The Genetics of Viruses and
Prokaryotes
Biology 101
Tri-County Technical College
Pendleton, SC
Viral Components
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Are obligate intracellular parasites
Outside living host cell exist as individual
particles called VIRIONS
Have central core of either DNA or RNA but
never both
Surrounded by CAPSID composed of
capsomeres (one or more proteins)
Components, cont.
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Animal viruses may have ENVELOPE
derived from host cell’s plasma membrane
Virions lack cell wall and ribosomes of
bacteria
Therefore, they are unaffected by antibiotics
VIROIDS are infectious genetic material
Describing Viruses
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Can be described by whether the genome is
DNA or RNA
Whether the nucleic acid is single-stranded or
double-stranded
Whether the shape of the virion is simple or
complex crystal
Whether the virion is surrounded by a
membrane (envelope)
Obligate Intracellular Parasites
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Viruses NOT classified as “living”
Whole viruses NEVER arise directly from
preexisting viruses
Develop and reproduce ONLY within cells of
specific hosts
Cells of animals, plants, fungi, protists, and
prokaryotes (both bacteria and archaea)
serve as hosts
Parasite, cont.
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Use host’s synthetic machinery to reproduce
themselves
Usually destroy host cell in process
How quickly is extremely variable depending
on replication cycle utilized
Host cell releases progeny viruses which
then infect new hosts
Replication Cycles
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Virus that infects bacteria called
bacteriophage (phage for short)
Virus that reproduces only via LYTIC cycle is
called a VIRULENT virus
Once phage has injected its nucleic acid into
host, that nucleic acid takes over host cell’s
machinery
Viral genome contains promoter sequence
that attracts host RNA polymerase
Cycles, cont.
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EARLY GENES code for proteins that shut
down host transcription, stimulate viral
genome replication, and stimulate LATE
GENE transcription
Nuclease enzymes digest host’s
chromosomes, providing nucleotides for
synthesis of viral genomes
In late stage, viral late genes code for
proteins of viral capsid and for those that lyse
host cell to release new viriions
Lytic Cycle Visual
Cycles, III
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LYSOGENIC virus called TEMPERATE virus
Lysogenic bacteria contain noninfective entity
called a PROPHAGE
Prophage can remain inactive within host
genome through many cell divisions
Cell becomes stressed or damaged,
prophage released from inactive state and
lytic cycle proceeds
Enveloped Cycle(s)
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**Influenza virus’s glycoproteins (on capsid)
bind to receptors on host cell’s plasma
membrane
Virus enters cells by endocytosis
Viral and vesicle membranes fuse, capsid
breaks down, and viral RNA is released
Viral RNA makes mRNA via viral RNAdependent polymerase
Enveloped cycles, cont.
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Viral mRNA is translated into viral proteins
(capsid and envelope)
Virion is assembled
Envelope glycoproteins made on host ER
and transported to cell membrane via Golgi
apparatus
New viruses assemble by budding and are
released from cell
Influenza Visual
Enveloped III
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HIV is a retrovirus (reverse transcriptase)
Attaches to host cell at membrane protein
CD4
Viral envelope fuses with host’s plasma
membrane, capdis breaks down, and viral
RNA released into cell
Viral RNA uses reverse transcriptase to make
complementary DNA (cDNA)
Enveloped IV
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Viral RNA degrades
Second DNA strand is synthesized
cDNA enters nucleus and is integrated into
host chromosome forming PROVIRUS
Upon activation, proviral DNA transcribed into
viral RNA which is exported to cytoplasm
In cytoplasm, viral RNA translated into
proteins using host ribosomes
Enveloped V
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Viral proteins, new capsids, RNA, and
envelopes are assembled
Assembled virus buds from plasma
membrane
Spend some quality time on Overheads 13. 4
(influenza) and 13.5 (HIV)
Enough said
HIV Visual
Lytic vs Lysogenic
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In animal cells, lytic and lysogenic cycles
cause differing pathologies
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lytic infections of plasma cells by the Epstein-Barr virus
(EBV) occur in mononucleosis
latent infections of B cells by EBV predispose the person
to lymphoma
lytic infections by human papilloma virus (HPV) cause
genital warts
latent infections by some strains of HPV lead to cervical
cancer
Vectors and more…
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VECTOR is an agent like an insect that
carries a pathogen affecting another species
Can also refer to plasmid or virus that carries
an inserted piece of DNA into bacterium for
cloning purposes in recombinant DNA
technology
Viruses that infect plants must pass through
cell wall as well as PM
Vectors, cont.
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Insect vector penetrates cell wall with its
proboscis allowing virions to move from
insect to plant
HORIZONTAL transmission refers to spread
from plant to plant
VERTICAL transmission refers to spread
from parent to offspring
Can be either vegetative or sexual
reproduction
The good and the bad…
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Phages using lytic cycle destroy their hosts
so might be useful in treating bacterial
infections
D’Herelle used phages to control infection of
chickens by Salmonella gallinarium
Phage protected group did not get the
bacterial disease
Also used phage treatment successfully with
plague-causing bacteria and with infectious
cholera
Prions
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“Proteinaceious infective particle”
Are simply abnormal proteins
Transmissible spongiform encephalopathies
(TSEs)
Include scrapie, mad cow disease, and kuru
Prions
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molecules of a normal body protein that have changed
their three-dimensional configuration
PrPC
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The normal protein
is called PrPc (for cellular)
is a glycoprotein normally found at the cell surface inserted in
the plasma membrane
has its secondary structure dominated by alpha helices
is easily soluble
is easily digested by proteases
is encoded by a gene designated (in humans) PRNP located
on our chromosome 20
Prions, cont.
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PrPSC
The abnormal, disease-producing protein
is called PrPSC (for scrapie)
has the same amino acid sequence as the normal protein; that is,
their primary structures are identical but
its secondary structure is dominated by beta conformation
is insoluble in all but the strongest solvents
is highly resistant to digestion by proteases
When PrPSC comes in contact with PrPC, it converts the PrPC
into more of itself (even in the test tube).
These molecules bind to each other forming aggregates
It is not yet clear if these aggregates are themselves the cause of
the cell damage or are simply a side effect of the underlying
disease process