19903592
Description
Flashcards by Katherine Havighorst, updated more than 1 year ago
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Created by Katherine Havighorst
over 4 years ago
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| Question | Answer |
| What is the definition of a virus? | An infective agent that typically consists of a nucleic acid molecule in a protein coat; is too small to be seen by light microscopy, and is able to multiply only within the living cells of a host |
| Describe the structure of a virion | -capsid-coated genome (aka "nucleocapsid") -lipid envelope -tegument layer between envelope and nucleocapsid -proteins |
| Why are all cells not alike for a specific virus? | -crypt cells continually dividing (in S phase(, neuronal cells are fully differentiated and can't divide -different cell types have different metabolic activity -different cell types have different functions |
| What are the basic characteristics of viruses? | -small (*mostly) -nonvisible with light microscopy (*mostly) -DNA or RNA genomes (in vertebrates; mostly RNA) |
| What is the symmetry of viruses? | -filamentous viruses: helical symmetry -isometric viruses: icosohedral symmetry |
| What host cell components do viruses need? | -enzymatic machinery -ribosomes -tRNA -membranes -enzymes for synthesizing NT/AA/CHO/ATP/etc |
| What are Koch's Postulates? | 1. The microorganism must be found in abundance in all organisms suffering from the disease, but should not be found in healthy organisms 2. The microorganism must be isolated from a diseased organism and grown in pure culture 3. The cultured microorganism should cause disease when introduced into a healthy organism 4. The microorganism must be reisolated from the inoculated, diseased experimental host and identified as being identical to the original specific causative agent |
| How are viral genomes arranged? | DNA: circular and linear RNA: linear and segmented |
| What do viral genomes encode? | Proteins and regulatory signals for -viral genome replication -virion assembly and packaging -regulation of viral gene expression -modulation of host defenses -viral cell-to-cell transmission |
| Explain why virions are "metastable" | They are both stable and unstable -stable: most protect genome -unstable: most come apart on infection |
| Why do viruses exhibit cubic and/or helical symmetry? | Genetic Economy -multiple identical protein subunits require symmetry Greater Stability -symmetrical arrangement maximizes protein contact |
| What is the "Red Queen Hypothesis"? | Infectious agents and their hosts co-evolve,: as one changes, the other adapts to said change |
| What are the effects of a cytocidal infection? | -Morphologic changes in cells; inhibition of protein, RNA and DNA synthesis; cell death -Virions produced |
| What are the effects of a persistent, productive infection? | -Little metabolic disturbance; cells continue to divide, loss of special functions may occur in differentiated cells -Virions produced |
| What are the effects of a persistent, non-productive infection? | -Nil -No virion produced, virus may be induced by co-cultivation / irradiation / chemical mutagens |
| What are the effects of a transformation infection? | -Alteration in cell morphology; cells can be passaged indefinitely; may produce tumors when transplanted to experimental animals -No virions produced as they are oncogenic DNA viruses |
| List the stages of the virus replication cycle | 1. Enter cell and translocate to the site of replication 2. Replicate genome and produce mRNA 3. Generate viral proteins 4. Assemble progeny virus and emerge from cell 5. Evade host defenses 6. Disperse and persist in the host |
| Describe mechanisms of cell injury by viruses | -Infection by cytolytic viruses (cytopathic effects) -Inhibition of host protein and RNA synthesis -Syncytium formation by enveloped viruses -Induction of apoptosis |
| How do viruses induce apoptosis in host cells? | -blebbing of plasma membrane -condensation of chromatin around nuclear membrane -cell shrinks, condenses, and breaks into membrane bound apoptotic bodies -membrane alterations initiate phagocytosis and removal without inflammation |
| What are the 3 components of virus entry? | Attachment Penetration Uncoating |
| Give the characteristics of a dsDNA genome | Small genomes: use cell enzymes for transcription and DNA replication Intermediate genomes: encode their own DNA replication machinery, use host cell RNA Polymerase 2/3 Large genomes: encode all their own mechanics |
| Give the characteristics of an ssDNA genome | -Genome replication by host DNA replication system -Uses cellular RNA Poly.2 to make mRNA Examples: Circovirus & Parvovirus |
| Give the charactersitics of ss(+)RNA genomes | -Genome is mRNA TRANSLATED IMMEDIATELY AFTER INFECTION -Encodes viral RNA-dependent RNA polymerase **produces polyprotein** |
| Give the characteristics of ss(-)RNA genomes | -Genome is segmented/non-seg RNA *CELLS CANNOT COPY - STRAND RNA* -encodes RNA-dependent RNA polymerase in virion *replicate in cytoplasm* |
| What is the life cycle of a retrovirus? | 1. Reverse transcription makes dsDNA copies of the RNA genome 2. DNA copy is *randomly inserted* into the host genome |
| What is the life cycle of a hepadnavirus? | 1. Viral cores with gapped dsDNA micgrate to the nucleus 2. dsDNA genome is repaired and ligated into a circle 3. Repaired genome transcribed by host cell into RNA 4. In cytoplasm, reverse transcription occurs to make dsDNA 5. Cycle repeats OR progeny enters ER to yield viral particles |
| What is directional release? | -Major determinant of infection pattern Apical release: back where they started "outside" the host (local/limited infection) Basolateral release: moving away from defenses of the luminal surface (systemic spread) |
| What is the principle of viral evolution? | No goal but survival |
| What are the limits of viral evolution? | -Viral populations frequently maintain stable master or consensus sequenes despite opportunities for extreme variation -Nature of particle constrains the quantity of nucleic acid that can be packaged -All genomes are nucleic acid; solutions for replication are limited -Viral replication requires host cell machinery; therefore have to be compatible -Viruses modulate a wide spectrum of host defenses |
| What causes antigenic drift? | Point mutations |
| What causes antigenic shift? | Viral reassortment |
| What is the "Quasispecies Concept"? | -Dynamic distribution of nonidentical but related replicons: quasispecies -Diversity allows rapid adaptation to dynamic environments (evolve resistance to vaccines and antivirals) |
| Why are most infection inapparent/of no consequence? | -virions fail to find a cell to infect -virions are destroyed or inactivated upon entering the host -many infections are limited to a cell or two at the site of infection -even if an immune response is launched, there are no clinical symptoms -viral replication/transmission can still occur during inapparent infections |
| What are the responses of the intrinsic defense system? | Autophagy Apoptosis RNA interference |
| What are the responses of the Innate immune response? | -Pathogen Pattern Recognition Receptors -Cytokines/Interferons -Local sentinel cells -Complement -Natural killer cells |
| What is autophagy? | -A natural, regulated cellular mechanism that disassembles unnecessary or dysfunctional compenets |
| What are examples of PRRs? | Toll-like receptors Rig-like receptors Cytoplasmic DNA receptors Complement NK cells |
| What is the common name of IFNa? | Leukocyte interferon |
| What is the common name of IFNb? | Fibroblast interferon |
| Name common ISGs and their effects | IFITM: block cytosolic entry MxA: block transcriptoin IFIT: bind RNA and inhibit translation |
| Why is the IFN system crucial for antiviral defense? | -a defective IFN response reduces the host's ability to contain infection, and leads to increased illness and death |
| What are local sentinel cells? | dendritic cells and macrophages (professional antigen presenting cells) |
| How do NK cells recognize virus-infected cells? | -recognize altered self -requires a two-receptor binding (to infection associated ligand and MHC 1) *virus infected cells are less likely to have MHC1 on their surface, therefore cannot double bind and NK cells will target* |
| How does the complement cascade activate inflammation? | C3a, C4a, and C5a bind to endothelial cells and lymphocytes |
| How does the complement cascade activate opsonization? | C3b and C1q bind virions, which phagocytic cells with C receptors engulf and destroy |
| How does the complement cascade induce cell lysis? | Membrane disruption/lysis is triggered by C6, C7, C8, and C9 forming MAC |
| What are the components of the cell-mediated immune response? | IFNy CTLs NK MO |
| What are the components of the humoral immune response? | igA igG igM Complement |
| What are the mechanisms of virus neutralization? | -blocked attachement -blocked endocytosis -blocked uncoating -intracellular neutralization -aggregation of virions |
| How do viral proteins modulate NK cell actions? | -inhibition by virl protein with homology to cellular MHC1 proteins -inhibition of expression of HLA/B, increase in HLA-E -release of virus-encoded cytokine binding proteins block NK cell activation or reduce amounts of activating ligand on cell surface -inhibition of NK cell stimiulating cytokines -Virions block inhibitory NK cell receptor or infect/kill the cell |
| How do viruses inhibit humoral immunity? | -inhibition of soluble complement factors (viral homologues of C4BP, CD46, CD55) -inhibition of MAC formation (viral CF59 homologue, incorporation of host proteins into virion) -inhibition of IgG Fc-dependent functions (viral IgG Fc receptors) |
| How do viruses interfere with MHC? | -interfere with MHC upregulation -targeting MHC and releated molecules for proteasome or endosome degradation -binding and/or retention of MHC in cellular compartments -interference with class 2 processing -inhibition of TAP-peptide binding or transportto ER -general inhibition -MHC homologues and/or effects on NK cell mediated lysis |
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