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11 Cards in this Set

  • Front
  • Back
viruses
-Replicate independently of cell's chromosome
-Require living host in order to reproduce
-Obligate intracellular parasites (obligated to infect host cell in order to reproduce)
-Infect all cell types
-Acellular
-Contain DNA or RNA genome
-ss or ds RNA or DNA; linear, circular, segmented
-Most common types: ds DNA & ss RNA
-Extracellular form= virion (complete virus particle - nucleic acid surrounded by protein coat known as capsid)
-may have envelope
virus structure
-About size of ribosome (very tiny)
-Nucleocapsid (nucleic acid of DNA or RNA + protein coat)
-Non envelope= naked virus
-Proteins sticking out are spikes
-Envelope: outer, flexible membraneous layer
-Virus makes spikes or peplomers
-Hemagglutinin spike: helps with attachment to cell, agglutinates RBC, build wall around itself so immune cells cant get to it
-Roles of envelope: viral attachment to host cell, enzymatic activity (neuraminidase spike - released from host cell, help break down host cell so it can get out), Nucleic acid replication, Identifying virus
-Usually STEALS envelope from host cell (budding)
Capsid shapes
-Helical: Influenza is segmented, ss RNA, overall looks round but looking at capsid see helical
-TMV (subunits making it up are called protomers)
-Icosahedral: Uses fewest genes to enclose DNA/RNA, geometric/flat faces/edges, causes CNS rare disorder, protomers/capsomers (protein subunits of icosahedral capsids)
-Pintamers= group of 5; Hexamers= group of 6
-Complez: Several different shapes, Vaccina virus, T4 bacteriophage (sometimes binal symmetry b/c color, tail pins & fibers, capsid head are elongated icosadral)
Viral multiplication (steps)
1. Attachment: not random but very specific; Lot of bacterial viruses will recognize receptor as LPS
2. Entry: Some just inject (capsid attached to outside of cell, injects DNA into cell); enveloped animal viruses put whole virus into cell (endocytosis, fusion of envelope, punch hole)
3. Uncoating: have to get nucleic acid out; envelope virus - uncoating could happen right inside membrane, further into cytoplasm, travel to nucleus), When virus enters & now has naked nucleic acid, starts transcribing mRNA to make enzymes. Needs to totally take over host cell. Most nucleases will cut up DNA
4. Synthesis: of viral protiens & nucleic acids - next starts replicating its own nucleic acid
5. Assembly: start building new virus particles, package up nucleic acid (put in capsid 1st thing)
6. Release
Bacteriophages
-Viruses that infect bacteria
-Bacterial viruses cause 1/3 of all bacterial mortality
-Lots of them in ocean
Virulent (lytic) bacteriophages
-Begin multiplying immediately after entering host
-Lyses bacterial host cell for release
-Ex. T4
-Receptor is LPS
-Early mRNA is made. Enzymes needed to help
-New sigma factors help to recruit DNA polymerase of host cell so they can replicate their DNA. New sigma factors bind to host DNA polymerase to be used for viral DNA
-Late mRNA: code for things to actually build viral components (tail fibers, collar, tail pins, etc). Puts DNA into icosahedral heads; adds helical segment by self assembly

-Virulent means deadly
-Lytic bacteriophages lyse at the end
-Burst size= if you infect E. coli with T4 bacteriophage, burst size is 100. Most it can release is ~ 100 bacteriophages
Temperate (lysogenic) Bacteriophages
-Ex. lambda shape (flexible tail)
-Inject nucleic acid instead of going immediately
-DNA incorporates onto bacterial chromosome
-Now called prophage
-Chromosome replicates along with cell dividing
-Induction causes prophage to hop out of chromosome and go into lytic cycle
-CAN cause lyse of cell after induction (induction caused by DNA damage)
-Only time induction doesnt happen is if something else kills cell really quickly before it can do that or if theres mutation keeping it from leaving cell (cryptic - cell cant get out)
-Cell most likely going to die if its been infected
Lysogeny & how lytic cycle may be induced in lysogens
-Only in bacteria
-Integrase enzyme will recognize certain place on chromosome in bacteria, cut that DNA so prophage can go into it, then glues it back again (cut & paste enzyme)
-Always integrate between galactose & biotin operons (attachment site - always where lambda will go into chromosome)
-Operon= cluster of genes transcribed together
-Can use galactose as carb source
-Replicates with host genome
-Lysogen: infected bacterial host (bacterium with prophage integrated on chromsome)
-Appears normal
-Prophage may change phenotype of its host
-Phage may switch from lysogen to lytic cycle upon induction
-Prophage keeps it from being infected by other bacterium

-Induction of lytic cycle: temperate phage reproduction is initiated
-Results in switch to lytic cycle
-Triggered by drop in lambda repressor levels (usually caused by exposure to UV light or chemical mutagens damaging DNA)
-Advantage for virus
-Excisionase: binds integrase enzyme; cuts DNA & glues in prophage; enables integrase to reverse integration process (cut prophage back out & now can go into lytic cycle)
Effects of animal viruses on their hosts
-Acute: rapid onset & recovery; get virus that infects your host cells - damages them so you get symptoms & then you get better. Example flu or cold
-Latent: virion enters cell & nucleic acid stays in cell - stress induces symptoms; viral DNA hangin out not doing anything in cell until something induces it; Different from prophage b/c not integrated into chromosome; virus stops reproducing & remains dormant for some time; example HSV
-Chronic: doesn't kill host cell but releases viruses usually through budding; example HIV; many years with infection may take years to show up b/c released so slowly over time; virus almost always detectable; ex. hepatitis B
-Cancer: virus activates proto-oncogene or inserts oncogene; HPV linked to cervical cancer

-"persistent" infection= Latent & chronic
Replication process of HIV (retrovirus)
-Retrovirus: reverse transcriptase (RNA --> DNA); HIV; released by budding
-Virus particle segmented genome
-Peplomers help with attachment
-Uncoating at membrane. Virus attaches to T cell, envelope & capsid left behind, RNA goes into cell
-ss RNA in cell. 1 of those RNA genomes will become ds DNA. Make single stranded copy using reverse transcriptase (RNA --> DNA --> mRNA)
-- peplomers come from virus; membrane comes from host cell
-Transform host cell by bringing oncogene into cell
-Integrate viral genome into host chromosome
Role of viruses in causing cancer
-"Oncoviruses"
-Viruses either insert oncogene (causes cancer) into chromosome or they can turn on protooncogene (gene normally in our bodies but easily mutated into cancer)
-If virus incorporates into that gene it could make it into an oncogene
-Tumor= growth/lump of tissue resulting from neoplasia (abnormal cell growth)
-Metastasis: cells from malignant/cancerous tumors spread throughout body
-Cartinogenesis: multiplication of multiple genes
-Protooncogene --> oncogene is spontaneous mutation
-Most human viruses associated with cancer have ds DNA genomes