Dr. P virology intro
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| cell tropism | Viral affinity for specific body tissues (tropism) is determined by
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| Cells can respond to viral infections in 3 ways | 1) No apparent change, (2) Death, and (3) Transformation
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| Systemic Spread | Apart from direct cell-to-cell contact, the virus may spread via the blood stream and the CNS.
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| Primary Replication | Virus's first replication site
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| Secondary replication | Virus second site of replication after systemic spread to this second site
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| Three modes of viral entry and replication | Primary, secondary, systemic
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| Why do retrovitroviruses not usually cause cell death? Why does this allow them to spread? | Retroviruses do not generally cause cell death, being released from the cell by budding rather than by cell lysis, and cause persistent infections.
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| What is true latency | True Latency - the virus remains completely latent following primary infection. Its genome may be integrated into the cellular genome or exists as episomes. Persistence - the virus replicates continuously in the body at a very low level
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| Most common type of viral damage to cell | Cell lysis
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| Types of genetic change | mutation, recombination
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| Tautomerism– | A base is changed by the repositioning of a hydrogen atom, altering the hydrogen bonding pattern of that base resulting in incorrect base pairing during replication.
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| Point mutation | POINT- often caused by chemicals or malfunction of DNA replication, exchange a single nucleotide for another.
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| Insertion | INSERTION- add one or more extra nucleotides into the DNA. They are usually caused by transposable elements, or errors during replication of repeating elements.
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| Deletion | DELETION- removal of one or more nucleotides from the DNA. Like insertions, these mutations can alter the reading frame of the gene. They are generally irreversible
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| Phenotype | PHENOTYPE: the observed properties of an organism
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| Conditional lethal phenotypic change | CONDITIONAL LETHAL - multiply under some conditions but not others - wild-type (wt) grows under both sets of conditions
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| What property do attenuated mutants have? | ATTENUATED MUTANTS milder (or no) symptoms vaccine development pathogenesis
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| Copy choice recombination | Copy choice a genetic recombination mechanism where the new DNA molecule comes about by replicating selected parts of each parental DNA molecule and by alternating between the two (maternal and paternal).
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| Helper virus | use when copies of a helper dependent viral vector lacks ability to replicate on its own. The helper virus is used to co-infect cells alongside the viral vector and provides the necessary enzymes for replication of the genome of the viral vector.
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| Phenotyping mixing | No changes in genome Possibly altered host range Possibly resistant to antibody neutralization
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| Mapping by recombination frequency- | The mathematical relationship expressing the frequency at which crossing over occurs between two chromosomal loci and the probability that two loci will become unlinked.
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| Mapping by marker rescue- | Repair of a mutational defect by recombination.
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| Recombinant vaccines | Insert the antigen into a virus with very low pathogenicity and this virus can be used as a vaccine, or the antigen can be filtered out and used as a subunit vaccine
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| Viral Replication | Recognition of target cell, attachment, penetration, Uncoating, macromolecular synthesis, assembly, budding of enveloped viruses, release
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| The binding of VAPs on the surface of virion to the receptors on the cell
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| Tropism | Tropism - the ability of a virus to replicate in particular cells or tissues.
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| is controlled partly by the route of infection but largely 1. By the interaction of a virus attachment protein (V.A.P.) with a specific receptor molecule on the surface of a cell, and has considerable effect on pathogenesis
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