Virology test 1 review part 2 Flashcards

viral genetics

• NOT living organisms
• NOT cells
• NO nucleus, organelles, cytoplasm
• replicate ONLY inside living hosts cells
  • are complex nucleoprotein particles
  • are obligate intracellular parasites
• a quality that living matter has (autonomous replication) - which viruses do not have
• utilize host machinery to make components for production of viral particles
• "bad news" - nucleic acids (brain of virus)

RNA OR DNA

never both

• require getting in living cells to be able to replicate
• can be in plants, animals, bacteria (bacteriophages)
• have greatest genetic diversity in nature
• genome modification processes -> lead to inc. genome variability

• mutation
• recombination
• reassortment

natural selection act on the continuously changing genomes due to these 3, and = diversity + evol

some changes can be lethal -> not passed/die off

some changes provide better fit / survival -> fixed in genome

• errors in copying nucleic acid -> mutations
• some lethal, some good

• eventually eliminated
• OR
• fixed in genome - remain

whether a particular NONLETHAL mutation survives in the genotype, depends on whether the resulting change in the gene product is disadvantageous, neutral, or affords the mutant virus some selective advantage

genetically changed from wild type

original strain of a virus from which mutants are selected and to which mutants are compared

original version of a gene

a single or multiple mutations

• spontaneous
• induced (mutagens, carcinogens, etc.)
• engineered

• due to mistake in normal replication of viral nucleic acid
• accumulate in viral genomes + introduce variations in phenotypes subjected to selection during evol of virus
• DNA spontaneous mutation rate
  • 10^-8 to 10^-11
  • LOW
• RNA spontaneous mutation rate
  • 10^-3 to 10^-4
  • much more common, mutate more
  • due to lack of proofreading activity in RNA replication enzymes
  • ex: flu is RNA, new strains every year
  • majority pathogenic viruses are RNA bc variability/aggressiveness

• occur when wild type viruses are treated w/ mutagen/carcinogen
  1. chemical mutation
     • point mutation - single nucleotide altered
     • gross chromosomal mutations
       • change in #/structure chromosomes (not in viruses)
  2. physical mutagens
     • ionizing: X and gamma rays
     • nonionizing: UV rays

nucleotide

• phosphate
• pentose sugar
• nitrogenous base (ATCG)

revert to wild type w/ certain frequency

base pair change - change by 1 base in nucleotide

• transitions - purine -> purine or pyrimidine -> pyrimidine
• transversions - pur-> pyr or pyr -> pur

frameshift changes - generate nonfunctional product

• insertion/deletion or 1/2 bases
• cause shift -> codons all change (dont have same 3 bases in each as before)

• silent - no change in amino acid coding for (doesnt affect outcome)
• missense - change one aa for another
• nonsense- codon termination (UGA, UAA, UAG = stop codon). Transcription of gene stops. Serious mutaion

molec technique to induce nearly any mutation into viruses

• = expected changes
• know mutations want to produce
• steps before PCR was invented (review it)

genotype is NOT phenotype

1. null
2. temperature sensitive mutants (TS)
3. cold sensitive mutations
4. plague morphology mutations
5. host range mutation
6. genetic recombination between viruses

Phenotype is the observable expression of this genotype – a person's presentation

genotype - DNA sequence

• mutation completely inactivates the function of a gene
• any type of nucleic acid change can yield a null phenotype (ex: frameshift, point mutation, etc.)
• does not need to be due to large deletion
• null mutant is important to determine if gene is essential for a process

• conditional-lethal phenotype
• usually due to missense mutation -> create gene that results in protein product unable to maintain functional configuration at nonpermissive (high) temp
• leaky - retain some functional activity at the nonpermissive temperature
• useful in temperature shift experiments

• conditionally-lethal at low (nonpermissive) temp
• grow as well as wild type at high (permissive) temp

many times used as attenuation mutations for vaccines (cannot function/grow at low temps)

• altered morphology
  • large plaques release virus from host cell more rapidly than wild type
  • provide useful markers - mutants can illustrate processes like membrane fusion
• center of plaque - original bacteria that died
• large plaque - virus mutation killed everything rapidly
• can use as way to assess number of viruses

chat gpt:

In virology, the term "plaque" typically refers to a clear zone or localized area of cell death on a monolayer of host cells in a culture dish. This occurs when a virus infects and kills the host cells. Plaque assays are commonly used to estimate the concentration of infectious virus particles in a sample.

When we talk about mutations in the virus genome influencing plaque morphology, we mean that changes in the genetic material of the virus can lead to observable differences in the appearance of these clear zones

• conditionally lethal - selected in a number of viruses - can grow in human but not in certain animals, etc.
• can kill in humans that infect us, but not other things

when 2 diff viruses simultaneously infect same cell and exchange pieces of DNA/RNA btw them

• occurs when there is exchange btw new nucleic acid molecules = new nucleic acid molecule