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52 Cards in this Set
- Front
- Back
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Mimivirus size and 2 characteristics |
-over 400nm -both DNA and RNA -no division but assembled from preformed components -no protein translation apparatus (ribosomes), and no system for energy production (ATP) |
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Pandora and pithovirus characteristics |
-Pandora virus: GC rich, nuclear replication -pithovirus: pandoravirus-like, small AT-rich genome, fully cytoplasmic replication |
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General properties of viruses (genomes) |
-Viral genomes are either DNA or RNA (dsDNA, ssDNA, dsRNA, ssRNA) -some circular, most linear -all need to generate mRNA to be translated -ssRNA and dsDNA for DNA/RNA viruses |
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Viral Envelope |
-Enveloped viruses take some host membrane as they exit -some regular protein membranes are replaced by viral proteins -proteins form binding layer between envelope and capsid |
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Peplomers |
glycoproteins that remain exposed as spikes on outside of viral envelope, used for attachment and can be used to identify virus |
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Influenza peplomers |
-neuraminidase (for release of mature virions from host) and hemagglutinin (bind virions to RBCs and cause cells to clump) -hemagglutinin for virion attachment to hosts, most envelope proteins are glycoproteins -M matrix protein non-glycolsylated found in inner surface of membrane helps stabilize |
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Types of envelopes/naked viruses |
-helical nucleocapsid, icosahedral nucleocapsid, helical RNA-virus with bullet shaped envelope, rna retrovirus with icosohedral capsid -naked: adenovirus with fibers on capsid, papillome virus (warts) |
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Complex viruses, bacteriophages |
-complex viruses= virions composed several parts (parts w/ separate shapes/symmetry) -Bacteriophage= bacterial viruses, complicated structures, icosahedral heads and helical tails - |
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Complex virus example: Pox |
-one of largest animal viruses, complex internal structure, ovoid brick-shaped exterior, dsDNA contained in biconcave disk w/membrane |
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T-even phages |
-virions of T2,4,6 have binal symmetry, head like icosohedral, tail helical. -Tail has collar joining it to the head, a central hollow tube, a sheathsurrounding the tube, and a complex baseplate. In T-even phages, the baseplate is hexagonal and has a pin and a jointed tail fiber ateach corner |
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T1,5 and lamda phages T3,7 |
Sheathless tails, lack a baseplate and terminate in rudimentary tail fibers -T3,7 coliphages have short tails w/o tail fibers |
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Virus hosts |
-viruses only replicate in certain types of cells or organisms. Cell permissive to allow viral replication. Specificity of attachment is key. -Bacterial viruses easiest to grow -Animal can be cultivated, plant most difficult |
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In order for Viral replication |
virus must induce living host cell to synthesize all essential components to make more virions |
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Virus life cycle |
Receptor binding cell entry uncoating nucleic acid/protein synthesis assembly release |
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Virus growth curve |
Latent period (eclipse when no infectious particles, maturation) Burst size: number virions released, few to thousands, replication cycle 20-60min bacteriophages, 8-40hrs animal Burst time: time from phage absorption to release |
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Viral attachment/penetration |
-highly specific (requires complementary receptors on surface of host and virus) -host receptors carry out normal functions -Receptors include proteins, carbs, glycoproteins, lipids, lipoproteins, or complexes |
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Tropism of virus |
Virus attaches to specific receptors. For instance polio attached to receptors on gut, nasopharynx, spinal cord. Measles everywhere |
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HIV binding to T-helper cells |
HIV glycoprotein spikes GP-120 and GP-41 bind to CD4 receptor on T-cells and CCR-5 fusin. -2 RNA strands and enzymes in HIV. Enzymes are reverse transcriptase, protease and integrase |
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Permissive cell |
host cell that allows the complete replication cycle of a virus to occur. Changes to virus and host cell surfaces facilitate penetration |
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3 methods for viral entry and uncoating (entire genome or nucleocapsid depending on envelope or naked)
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1. fusion of envelope with host membrane nucleocapsid enters 2. endocytosis in vesicle, endosome aids in viral uncoating 3. injection of nucleic acids |
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Endocytosis entry of viruses |
1. enters through endocytosis and then increased acidity allows nucleocapsid to escape (w/ enveloped, can also enter through fusion) 2. or nucleic acid is extruded from endosome (w/ capsid) |
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Uncoating? |
uncoating may be done by host or viral enzymes. Bacteriophages do not need uncoating because nucleic acid is injected |
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Conformational changes of HIV entry |
1.HIV gp120 binds to CD4, initial conformation change. then bind to coreceptors (chemokine) CCR5 and CXCR4 2. co-receptor interaction triggers fusion viral/cell membranes (initiated by HIV-1 fusion peptide located in gp41) 3. Fusion/entry HIV genome RNA and proteins at cell surface w/ neutral pH. Once inside cell RNA transcribed by reverse transcriptase into DNA 4. HIV pre-integration complex transported to nucleus targeted cell for integration into cell DNA to initiate chronic infection |
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Conformational changes for influenza entry |
1. binds via hemaglutinin 1 (HA1) to terminal sialic acid on glycoproteins or glycolipids 2. Virus internalized by receptor mediated endocytosis into low pH endosome, triggers conformational change that exposes viral fusion peptide located at HA2 3. genomic ribonucleoprotein complex transported to nucleus to initiate transcription/replication viral genome |
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Bacteriophage T4 |
- virus of E.coli, complex penetration system a) virions attach by tail fibers that interact with polysaccarides on E.coli envelope b) tail fibers retract and tail core contacts cell wall c) lysozyme-like enzyme forms small hole in peptidoglycan d) tail sheath contracts and viral DNA passes into cytoplasm |
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Outer receptors involved in T4 |
techoic acid, LPS, OMPs, flagella, OMPA-LPS porins (OMPF) |
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Host defense mechanisms |
- there are immune mechanisms and RNA interference (RNAi) -Prokaryotes have CRISPR, restriction modification system |
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Prokaryote restriction modification system |
DNA destruction system, only effective against double stranded DNA viruses (ssDNA and RNA unaffected). Restriction enzymes (endonucleases) cleave DNA at specific sequences -modification of host's DNA at sequences prevents from cleaving own DNA |
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Phage adaptations (RBP) |
1) can evolve to target new receptor binding proteins (like when host receptors modified) through genes encoding for Receptor Binding Proteins or tail fibers. ex. mutation in protein J of coliphage lamda enables RBP to bind to new receptor Ompf and LamB |
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Phage adaptations (masked receptors) |
surface molecules (ex. capsule or exopolyssacharide EPS) at receptor can prevent access so virus uses depolymerase it can degrade these substances |
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Phage adaptations (Stochastic expression RBPs) |
bacteria express phage receptors in stochastic manor, through phase variation or physiological regulation like response to growth phase, phages can modify RBPs to interact with surface component expressed at that times. Uses mutation in gene encoding major tropism determinant (Mtd) for Bordetella spp phages, by proteolytic cleavage of tail fibers for Lactococcus lacis TP901-1 and tuc2009, or duplication His box in coliphage T4 tails |
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Viral defense against bacterial restriction enzymes |
1) chemical modification viral DNA (T-even glycosylate DNA and some methylate DNA). mod after genomic replication by proteins encoded by virus 2)can produce proteins that inhibit restriction system (T3/T7) 3) encode restriction system to destroy host DNA 4) some bacteria have multiple defense systems |
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Viral molecular mimicry |
to prevent destruction by restriction enzymes, molecular mimicry of antirestriction proteins, 24 base pairs of B-form DNA, protein forms dimer that resembles bent DNA that occurs when restenzymes find target, so dimer binds to type 1 rest enzymes and prevents their effect |
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How Phages get around CRISPR |
-ICP1 phage of Vibrio Cholera uses its own Crispr/cas system, when Cholera mutated phage also mutated -Maybe could use to fight C. difficile (severe diarrhea) so treat with something other than fecal transplants -ICP1 has six cas genes and CR1/CR2 crispr loci -Coevolutionary arms race between bacteria and phages |
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Viral genome examples DNA |
ssDNA, dsDNA (linear and circular) -poxviridae (smallpox) helical complex - enveloped herpesviridae -naked adenoviridae (tonsillitis) |
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RNA viral genome |
mostly single stranded. - positive sense genomes are ready for translation -negative sense have to be converted -segmented where genes exist on separate pieces of RNA |
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Production of viral nucleic acids and protein |
-generation of mRNA occurs first -viral genome as template for viral mRNA -in some RNA, viral RNA serves as mRNA -some cases transcription enzymes are contained in virion -RNA (+/-, ds) require specific RNA dependent RNA polymerase because cell needs DNA template to make RNA -RNA depedent RNA polymerase (RNA replicase) |
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DNA viruses class I, VII, II |
-class I classical semiconservative, dsDNA + -class VII transcription followed by reverse transcription, dsDNA + -Class II classical conservative and discard - strand, ssDNA, must synthesize dsDNA intermediate -DsDNA intermediate also used to generate the viral genome – one becomes genome,other stand is discarded. SsDNA has +strand DNA -Viral mRNA is expressed in preference to host mRNA |
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Production viral Nucleic acid and protein: mRNA |
-mRNA + configuration, it's compliment - -positive RNA virus: ssRNA same orientation mRNA -negative: ssRNA with complimentary to mRNA -retroviruses: animal viruses responsible for cancer/acquired immunodeficiency (incoming RNA +, but not mRNA. need reverse transcriptase. have ssRNA but replicate through dsDNA intermediate |
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Genome replication of class III, IV, V, VI |
Class III: makes ssRNA + and transcribes from this for ssRNA- partner Class IV: make ssRNA- which transcribed for ssRNA+, used directly as mRNA Class V: make ssRNA + and transcribe this to ssRNA- Class VI: make ssRNA+ by transcription of -dsNA |
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RNA viruses specific RNA-dependent RNA polymerase |
all RNA require specific RNA-dependent RNA polymerase -ssRNA complementary to mRNA=- -Cell polymerases only make RNA from DNA template so mRNA of +RNA viruses encodes virus specific RNA-dep-RNA-poly called RNA replicase. |
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For -RNA viruses |
mRNA must be synthesized first, so must carry some enzyme w/ and inject. Complementary + made, then used as mRNA and to make more -strands |
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for +RNA viruses |
Encode virus RNA replicase (poly) the poly makes complementary (-) then uses as template for more + which can be used as mRNA or packaged for new virions -usually molar excess 10:1 or 100:1 +/- -can be enveloped or naked but all produce capsid proteins for binding to viral DNA (capsid, nucleocapsid, nucleoproteins) |
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Retrovirus genome replication |
have ssRNA in virions, replicate through dsDNA intermediate. Copy RNA into DNA via reverse transcription. Bring in reverse transcriptase. dsDNA is template for mRNA |
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RNA vs DNA virions |
-RNA virions smaller than DNA, so RNA more dependent on using host proteins, target nucleolus (subnuclear structure) -DNA/retro target nuclear structures as replicate in nucleus. Primary site replication of +RNA and most -RNA is cytoplasm |
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Why +RNA need access to nucleolus |
-viral proteins must transit through nuclear-pores to enter/exit nucleus, if viral proteins that are required for cytoplasmic functions (RNA synth and encapsidation) are sequestered in nucleolus/nucleus then progeny affected -capsid and RNA-binding proteins shown to localize to nucleolus in infected cells or when overexpressed |
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Virus nucleic acid/protein production in eukaryotes |
DNA enter nucleus where replicated/assembled. DNA also transcribed to RNA to translation for virus proteins. uses host nucleotides -RNA replicated/assembled in cytoplasm |
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Viral proteins |
-timing/amount regulated, under control of virus -production follows synthesis of mRNA -Early proteins synth soon after infection, necessary for replication of virus NA. usually catalytic, synth in smaller amounts -late proteins: synth later, proteins for virus coat, structure, larger amounts |
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Assembly of virus |
-late proteins important bacteriophages in stages, some assembled in nucleus, some in cyto, may be seen as paracrystalline |
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Mimivirus replication |
releases a large number complex virions through amoebal lysis. takes place in autonomous giant assembly center. Assembly/filling capsids in replication center before to cytoplasm. Enter phagocyticly, release DNA cyto, viral morphogenesis in giant cytoplasmic virus factory |
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Mimivirus factory |
3 zones: inner replication center, intermediate assembly zone, peripheral zone where acquire fibrils |
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Virus release |
nonenveloped viruses lyse host cell Enveloped use budding from host, ex. influenza |
