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45 Cards in this Set
- Front
- Back
- 3rd side (hint)
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what kind of RNA pols do all RNA (-) viruses use?
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a viral RNA pol that is contained within the virion itself.
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what is one general rule that all negRNA viruses use when replicating?
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copy to a pos RNA template for genome replication
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genus of rhabdovirus that causes rabies?
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lyssavirus
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what proteins are encoded in the rhabdovirus? what is their order in the genome?
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nucleocapsid (N), polymerase component (P), polymerase component (L), matrix (M), glycoprotein (G).
3'-c leader-N-P-M-G-L-5' |
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describe the general lifecycle of the rhabdovirus
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peplomer mediated attachment, viropexis, uncoating gets rid of the envelope but keeps the nucleocapsid on, L and P proteins make up the pol and interact with N (capsid) to expose genomic RNA (bubble effect) and start txn, first txn c leader RNA only, note each RNA segment after each gene has an E -end- I - intergenic- and S - start sequence, and then the rest of the genes are txned, but in a polar effect: N>P>M>G>L, all this is primary txn (txn of RNA genome). Leader RNA goes to nuc to inhibit cell DNA and RNA pols, all mRNAs except leader have a poly A tail and 5'MG cap, tsln occurs, G proteins go to plasma membrane, increasing N and P proteins cause the switch to replication, copy from + RNA template, strong promoter on this template, thus more neg genomic RNA made and it associates with the N protein ASAP, pool size of N is a regulatory switch to secondary txn (mRNA's txned from daughter (-) RNAs) geared toward N production and genome replication, capsids form, interact with M, budding and envelopement with G...
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cytopathology of rhabdoviruses?
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M protein destroys TFIIF (txn factor) of host cells, leader RNA inhibits RNA pol II and III as well as blocking cell DNA synth, this is cytocidal. cell protein synth is reduced, nucleocapsid make cytoplasmic inclusion bodies (negri bodies) in rabies. some members induce apoptosis by an unknown mechanism, inserted proteins can be a target for antibody and CD8 cells.
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describe the further classification of important paramyxoviridae as well as their pathologies and peplomer status.
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Subfam paramyxovirinae: Respirovirus with HN peplomer and are human parainfluenzavirus, Morbillivirus with an H peplomer causes measles, canine distemper, and rinderpest, rubulavirus with HN peplomer causes mumps and human parainfluenza, henipavirus has handra virus which causes CNS and resp disease and nipah virus. Subfamily Pneumovirinae contains pneumovirus with a G peplomer and has human respiratory syncytial virus, metapneumovirus is avian virus and new metapneumovirus of humans
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describe the structure of the paramyxovirus
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enveloped, HN attachment peplomer and F fushion peplomer. M protein. Helical capsid
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describe the general lifecycle of the paramyxovirus.
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attachment via cleavage of HN (neuraminidase) or H peplomer, fusion by F peplomer (needs cleavage too), uncoating (nucleocapsid is never completely uncoated), primary txn - P, L, C protein complex is the pol, stuttering causes txn of leader mRNA, and the 6 mRNAs for structural and non structural proteins. Polar effect NP>P/C>M>F>HN>L, all these mRNA's for proteins are capped and methylated. Bicistronic mRNAs (ex is measles that can translate same RNA to either P or C protein depending on frame) and RNA editing (measles RNA again can add a G to an mRNA to get a new frame and thus the V protein). Between each gene is the stop with oligo U's for poly A tail, intergenic sequence and the start codon for the next gene. Tsln occurs, HN and F go to plasma membrane, pool proteins build, switch to replication, daughter RNA can be txned again (secondary txn) or interact with M protein, envelopement and release, not that some peplomers are cleaved as it is released...
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describe the cytopathic effects of paramyxovirus
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necrosis, intracytoplasmic and intranuclear (measles) inclusions. leader mRNAs may shut off host RNA and DNA synth. F peplomer can cause giant cells via syncytia
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describe the V protein of paramyxovirus
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measles V protein is an inhibitor of host antiviral response. Prevents IFN response thus the cell evades programmed cell death.
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diseases caused by filovirus?
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ebola and hemorrhagic fever
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describe the structure of the filoviridae.
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enveloped with very long filamentous shaped virions, peplomer is a trimer of glycoproteins, helical capsid, weird shaped virions like a U or a 6.
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what are the seven proteins of filoviridae?
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NP (capsid), L (RNA pol component), VP30 (associated with L), VP35 (associated with L), VP40 (matrix protein), VP24 (probly a matrix protein), GP (large homotrimer glycoprotein)
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replication scheme of filovirus?
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attachment, penetration, uncoating, replicate in cytoplasm, initial txn makes 7 monocistronic mRNAs, then synth of plus strand template, then synth of daughter DNA and then assembly and envelopement in the plasma membrane
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what does Ebola (filovirus) do differently than others?
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mRNA editing, PG gene can encode the big peplomer protein w/o editing or a nonstructural secreted glycoprotein via posttranscriptional editing (insert an A and result in frame shift)
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cytopathology of filovirus?
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intracytoplasmic inclusions from viral nucleocapsids, CPE and lysis
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what are the orthomyxovirus genera and which are important to humans?
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fluA, B, and C. B and C are human pathogens - C is no big deal, while A is animals (including avian) and humans
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what is the structure of the virion of orthomyxovirus?
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enveloped, M2 channel proteins in envelope, HA peplomer for attachment and penetration that must be cleaved, NA peplomer with neuraminidase activity, matrix, 8 nucleocapsids and genomic RNA molecules
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what are the proteins of FLU a?
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PB2 is part of RNA pol and cleaves 5'cap of cell mRNA's to be used as a primer as well as transcriptase activity. PB1 is a component of the RNA pol and contains transcriptase and replicase activity and binds cell mRNA caps to keep them in the nucleus, PA is part of the pol contains transcriptase and replicase activity, HA peplomer, NP capsid, NA peplomer, M1 matrix protein, M2 channel, NS1 inhibits cell mRNA splicing and poly A addition as well as binds PKR to block interferon response. NS2 mediates egress of capsids out of the nucleus.
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None
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what determines subtypes of influenza type A?
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the nature of the HA and the NA
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describe the attachment, penetration, and uncoating of orthomyxos?
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HA binds cell receptor and cleavage, viropexis, HA proteins causes internal fusion with endosome, H+ ions enter via M2, nucleocapsids then disociate from the M protein and go to the nucleus.
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how are H5N1 flu viruses (bird) infective?>
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our URT does not have the correct receptor but our lungs, type II pneumocytes and the alverolar macs, do. Thus a worse disease that is harder to regrow tissue and ios fatal, also its HA peplomer has multiple basic amino acids that make it more easily cleaved and thus more infectious
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describe orthomyxovirus txn.
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in the nucleus, 3 part RNA pol: PB1 binds 5' cap end of cell mRNAs (that viral NS1 protein has kept in the nucleus) and cleaves the cap end to use as a primer for viral txn, thus each viral mRNA is a hybrid of genomic RNA and 5' end of cellular RNA, also has a poly A tail. M1 mRNA is spliced to mRNA for M2. NS1 mRNA is spliced to NS2 mRNA thus from 8 RNAs we get 10 mRNAs.
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describe translation and protein processing in orthomyxos?
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peplomers to the ER/golgi for processing then to PM. P proteins return to the nucleus to associate with nucleocapsids, some M1 enter the nucleus and bind capsids and then the NS2 protein that mediates egress from the nucleus
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give an overview of neg RNA virus replication (in general for all the viruses).
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txn via the endogenous RNA pol is first, "stutters" to make all the genes in the genome and adds cap and poly A tail to them. Then viral proteins are made and one of them causes the switch (usually capsid protein) to copy the RNA genome to the pos template that has no cap or polyA tail, this template has promoter sequences that are very important, thus lotsa neg DNA made and then its packaged and released.
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# of flu A Subtypes? Flu B? FluC?
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135, 1 and 1
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M2 channel protein is a target of what drug?
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amantidine
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describe antigenic shift.
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change in subtye of type A flu, thus change in HA peplomer, it is a re-assortment of pieces of RNA of an animal virus and a human virus. Creates pandemics like bird flu
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describe antigenic drift.
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due to mutations from RNA pol in Flu A and B, which are abundunt, changes HA protein, why we need new vaccines every year, can lead to epidemics
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what is influenza failsafe to get all 8 RNAs in the capsid?
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it can package more, up to 13, it only needs 8 to be infective
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cytopathology of orthomyxos?
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cytocidal, NA digests URT mucous, M2 integrates into cell membranes and allows leakage. PB1 destroys cellmRNAs as it steals caps. NS1 traps cell mRNA in nucleus and retards splicing and inactivates interferon, PB1 gene also has alternate ORF in some flu A strains that encodes small F2 protein that alter mitochondria and cause apoptosis
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describe the structure of reoviruses.
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double layered icos, no envelope, 10 - 12 dsRNA molecules of genome
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general lifecycle of reoviruses?
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attach, penetrate by viropexis, partial uncoating, primary txn of core via viral RNA pol that takes (-) RNA from dsRNA and makes mRNA with cap but no tail, tsln, proteins made then they trap their father mRNAs and form immature particle, mRNA is copied to form dsRNA genome, this is CONSERVATIVE replication, secondary txn via original neg RNAs copied to late viral mRNAs that lack cap and tail. late proteins made, then virus matures and exits.
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if late txn of reovirus makes mRNA without caps, how does tsln occur?
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virus knocks out all cellular mRNA caps as well and these transcripts have a caplike structure that the ribosomes bind to, so only these late mRNAs are translated
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affects of reovirus on host cells?
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cytocidal, cytoplasmic inclusions, cell cytoskeleton altered, sigma 1 protein blocks cell DNA synth and induces apoptosis, inhibits cell protein synth, at times cap dependent tsln is blocked,
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if two strains/serotypes of reovirus infect a cell, what can happen?
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reassortment where the daughter viruses have RNA from both strains.
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two important reovirus genera?
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rotavirus: major infantile diarrhea; coltivirus: colorado tick fever, tick is vector
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structure of bunyavirus?
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envelope, 3 helical capsids
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what are some important genera of bunya?
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bunya: encephalitis, phlebo: sandfly fever; nairo: hemorrhagic fever; hantavirus
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describe the basic bunyavirus lifecycle.
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viropexis, does the normal (-)RNA virus replication dance and then envelopes with peplomers at the golgi, vessicle takes it to bud out of the plasma membrane
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describe the three RNA molecules in bunya and the proteins they encode.
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L,M and S. L contains the L protein which is the pol, capper, and has other enzyme functions. M makes the peplomer protein that is then cleaved to G1 and G2. S gives rise to cpasid protein (N) and smaller Nns proteins
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describe the abisense replication that is done by SOME of the bunyaviruses.
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only S RNA segment will do this, its genomic RNA has both + and - parts. Early txn makes an mRNA of the negative part to make N protein, then template is made. Now the negative template part (originally + in the genome), undergoes late txn to make mRNAs for that, get the Ns proteins, then the template is used to make genomic mRNA
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describe the structure of arenavirus.
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enveloped, 2 helical capsids with L and S RNA, each are ambisense, also has ribosomes trapped in the virion
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pathogens of arenavirus?
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LCMV causes lymphocytic choriomeningits while junin, machupo, guanartio, sabia, whitewater, arroyo, and lassafever all cause hemmorrhagic fever.
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