First part of 206 Flashcards
HIV into Aids 3 phases
Acute, Chronic, AIDS
Acute phase
- retrovirus in immune cells with CD4
- Binds to CD4
- Fuses and releases DNA
- DNA splicing (into our DNA), transcription and translation of HIV mRNA
- Reassemble into new virions, bud into proteases, makes mature virus
Chronic phase
- dentritic cells capture virus
- present polypeptides to naive helper T cells
- Divide to produce activated helper T
- stimulate B cells to mature into plasma cells
- Make antibodies against virus
- Activate killer T cells to destroy infected host cells
- Recruit macrophages to destroy virions and infected host cells
AIDS
- Lots of immune cells trying to protect against HIV = More cells for HIV to infect!
- Compromised immune system so can’t fight off infections
How understanding evolution helps control HIV/AIDS
- need to stop viral reproduction w/o stopping regular cells
- Can stop: co-reception, fusion, reverse transcription or maturation
- Drug resistance evolves fast since reverse transcription=error prone
- New epitopes evolve faster than host
- viral pop gets more aggressive due to competition
- virus evolves new strains that can attach to diff co-receptors
- Can be controlled with 3 diff drugs taken CONSISTENTLY (just 80% of the time is the worst)
Patterns a unifying theory must explain (7)
- changes in traits w environmental changes
- results of artificial selection
- emerging infectious diseases
- vestigial organs
- homologous traits
- succession
- transitional forms
Evolution
Change in allele frequencies between generations
Natural selection
differences in lifetime reproductive success of individuals with different phenotypes
Evolution by natural selection 4 postulates
- Individuals within pop vary phenotypically
- phenotypic variation is at least partially heritable
- individuals vary in lifetime reproductive success
- Variation in survival/reproduction is nonrandom with respect to phenotype
What does natural selection and evolution act on
Natural selection acts on individuals and phenotypes/evolution occurs in populations and consists of changes in allele frequencies
What is standing variation
Multiple alleles at loci
3 types of quantitative analysis
- continuous
- discrete
- Meristic
Vp (variation of pop)=what
Vg+Ve+V(g x e)
heterozygosity = what
number of alleles/locus
Ve (phenotypic plasticity) example
- tanning in humans
V (g x e) (genetic variation in phenotypic plasticity) example
- how I burn easier than some people in the sun
V (g x e) generated 2 main ways
- Mutations
2. Recombination
Types of mutations (5)
- Point
- gene duplications
- chromosomal mutations
- chromosomal duplications
- epigenetic
3 statements of Hardy weinberg theory
- genotype and allele frequencies predicted from each other using binomial distributions
- Allele and genotype frequencices will not change between generations
- This is under certain assumptions
Formula of HW
(p+q)^2=p^2+2pq+q^2
5 HWE theorem assumptions + 1 new one
- No mutation
- Infinite population size
- Random mating
- No migration
- No selection
(No linkage)
Finite pop on genetic diversity
- sampling error
- genetic drift
- evolution but not adaptation due to drift
- smaller pop = hit harder by drift
- drift reduces genetic variation
- bottleneck
- founder effects
Bottleneck
severe short-term reduction in pop size
Founder effect
establishment of new population by small number of individuals
Effective population size
What individuals actually contributed to the next generation
size of “ideal” population that would have same amount of genetic drift as actual population (Ne)
Smaller than census size (Nc)
Important to predict heterozygosity
Used as null model to investigate how a pop deviates from ideal
