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25 Cards in this Set

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  • Back
general properties of retrovirus?
vRNA to vDNA, integration, after integration it depends on species what it will do, most do not kill the host cell except lentivirus (HIV), the provirus behaves like cell genes, may be passed in germline and is transcribed by cellular RNA pol. Some are transformers to oncogenes with individual properties
what is characteristic of all simple retrpviruses with oncogenes except rous sarcoma?
they are all replication defective (once they integrate they cannot replicate) except for rous sarcoma
structure of simple retrovirus (include genes and proteins)?
enveloped with SU and TM peplomers, complex capsid we do not understand, virion contains several viral enzymes: RT, Rnase, IN, and protease; tRNA is primer of minus DNA strand synth; three genes which are GAG, POL, and ENV. Genemoe: 5'cap-R-U5-pB-GAG-POL-ENV-ppt-U3-R-polAtail 3', pB is primer binding site for tRNA, pp is poly purine sequence for primers and DNA strand synth, GAG makes MAtrix, CApsid, NucleoProtein, and PRotease; POL makes RT, RNase, and H-IN(integrase); ENV makes SU - surface and TM - transmembrane glycoproteins
what cells do retroviruses enter?
only dividing cells
genera of simple retroviruses?
alpha, beta, and gamma
what component of the genome is essential for later packaging and where is it located?
psi - in between pB and GAG
what is missing from the genome of replication defective simple retroviruses with an oncogene?
GAG, POL, or ENV are replaced with vONC, note RS has all the genes and adds vONC to the genome
what do the complex retrovirus genomes have that are different from the simples?
additional genes like REX and TAX
describe the morphology of the retroviruses.
A types are precursors to B types, are seen in the cytoplasm, and are doughnut like (cheerio); B types bud out from A types at the plasma membrane and they have an ecentric core; C types do not have a central core and you do not see the precursor for the virion, it buds at the membrane; D type is simillar to L type with less prominent peplomers; L type has a toroid like inner structure (space capsule) and no cytoplasmic precursor - similar to C type.
describe provirus synthesis.
cell tRNA binds to primer area near U5, RT binds tRNA and copies in 5 to 3 direction (short DNA made, no genes on it) and stops at the R5 then does a molecular jump to the other genomic RNA to the R3 sequence and copies forming a DNA with identical ends (has U5 and U3 in each end), RNAse digests all the RNA except for small polypurine which serves as a primer that binds the newlymade DNA (which is neg DNA) at the second primer and now the RT becomes a DNA pol and makes the + DNA with a molecular jump again simillar to the first one, but onto the other end of the same template DNA. Now we have dsDNA with U3, R, and U5 at each end (LTR's) (look at pic).
T/F RT is a monomer.
F it is a dimer
what does the provirus look like (gene wise)
where are the cis elements on the LTR and what is their purpose??
on U3, they sense many viral and/or cellular transactivators that tell the provirus to undergo txn or not to undergo txn… environmental sensers
what is the primer for -DNA synth? + DNA?
what are the fates of the simple retrovirus primary RNA transcript (from the provirus in the nucleus)?
becomes one of the diploids in the daughter genome and gets a tRNA added. Tslned to GAG, tslned to GAG-POL via frameshift, spliced for ENV, spliced to vONC in viruses that have it
how often is the GAG-POL combo protein made?
one out of 20 mRNAs will have the frameshift
what is the vSRC gene?
a tyrosine kinase
when does protease activity of the GAG and GAG-POL complete?
not until after the virus buds out and is released from the cell in some cases.
how can recombination occur in retroviruses?
2 ways, copy choice model is during RT, the growing minus strand switches from one RNA to another virus's RNA and they are co-packaged. Strand displacement-assimilation model is during RT via + strand synth by making the molecular jump to a previously co packaged RNA... problem in AIDs bc all the peplomer proteins which are antigenic switch around...
outcomes of retroviral infection?
produce virions - may kill cell. Transform via vONC. Transform by activating a cONC. Transorm via TAX. Transform and replicate (rous sarcoma), mutagenesis of cell gene due to integration. Transduction of cell gene like a c onc or a vonc
how can replicant competent retroviruses cause cell transformation?
it is either a Rous sarcoma virus or the virus integrates near a CONC and the U3 enhancer portion of the LTR causes over expression of the nearby cellular CONC
what are the types of proteins that V ONC can encode?
tyrosine kinase, receptor for growth factor, growth factor itself, GTP binding protein, nuclear DNA binding protein, steroid hormone receptor, transcription factor, serine or threonine protein kinase, adaptor protein that activatess signal transduction pathways
what retroviruses are rapid transformers?
ones that have vONC or vSRC
what viruses cause leukemia/lymphoma but have extra genes including TAX?
deltaretrovirus genome
how do retroviruses with vONC replicate and proliferate if they are replication deficient?
by complementation, if the cell gets infected with another virus, it can use that viruses proteins to spread