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Dr. P virology intro

cell tropism Viral affinity for specific body tissues (tropism) is determined by
Cells can respond to viral infections in 3 ways 1) No apparent change, (2) Death, and (3) Transformation
Systemic Spread Apart from direct cell-to-cell contact, the virus may spread via the blood stream and the CNS.
Primary Replication Virus's first replication site
Secondary replication Virus second site of replication after systemic spread to this second site
Three modes of viral entry and replication Primary, secondary, systemic
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.
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
Most common type of viral damage to cell Cell lysis
Types of genetic change mutation, recombination
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.
Point mutation POINT- often caused by chemicals or malfunction of DNA replication, exchange a single nucleotide for another.
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.
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
Phenotype PHENOTYPE: the observed properties of an organism
Conditional lethal phenotypic change CONDITIONAL LETHAL - multiply under some conditions but not others - wild-type (wt) grows under both sets of conditions
What property do attenuated mutants have? ATTENUATED MUTANTS milder (or no) symptoms vaccine development pathogenesis
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).
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.
Phenotyping mixing No changes in genome Possibly altered host range Possibly resistant to antibody neutralization
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.
Mapping by marker rescue- Repair of a mutational defect by recombination.
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
Viral Replication Recognition of target cell, attachment, penetration, Uncoating, macromolecular synthesis, assembly, budding of enveloped viruses, release
The binding of VAPs on the surface of virion to the receptors on the cell
Tropism Tropism - the ability of a virus to replicate in particular cells or tissues.
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
Created by: VCOM2013