UNIT 3 DAY 4 - THE COVID VIRUS KEEPS EVOLVING Flashcards
1
Q
coronavirus
A
covered with spikes
2
Q
virus process
A
- virus enter through nose, sometimes through eyes and mouth
- once inside, virus invades cells in nasal cavity and trachea –> can travel deeper into lungs
- virus enters, attaches to cells in airway that produces proteins called ACE-2
- virus infects cell –> fuses its oily membrane to cell membrane –> once inside, coronavirus releases snippet of genetic material (RNA)
- infected cell reads RNA, begin to make proteins, keeping immune system at bay, assemble new copies
3
Q
antibiotics
A
- kill bacteria, don’t work against viruses
4
Q
infection progresses
A
- new spikes and other proteins form new copies of coronavirus –> carried to outer-edge of cell
- each infected cell releases millions of copies of virus before cells dies
5
Q
coughing and sneezing
A
expel virus-laden droplets
6
Q
virus transmission occurs by 2 routes
A
- relatively large airborne droplets falling within 5 seconds and contaminating surfaces
- tiny aerosols remain airborne for hours, accumulate in poorly ventilated spaces (IMPORTANT)
7
Q
factors affecting airborne transmission
A
- distance –> droplets travel less than 6 feet, aerosols disperse over distance, concentrating diminishing exponentially with distance
- duration
- ventilation
- intensity of inhalation and/or exhalation
8
Q
soap
A
- destroys virus as soap molecules wedge themselves into the lipid membrame
9
Q
viral envelope
A
protein encapsulates genetic material
10
Q
spike protein
A
used by virus to gain entry to human cells –> attaches to ACE-2
11
Q
ACE-2
A
attaches protein early
12
Q
endocytosis
A
human cells ingests virus
13
Q
exocytosis
A
virus carried by golgi bodies out of cell
14
Q
hijacks
A
takes DNA and mutates it
15
Q
mRNA
A
- single-stranded RNA involved in protein synthesis
- role = carry protein information from DNA In nucleus to cytoplasm
- translation of mRNA into protein places of ribosomes
16
Q
endoplasmic reticulum
A
- network of membrane inside a cell through which proteins and other molecules move
- ribosomes attach to endoplasmic reticulum
17
Q
apoptosis
A
- cell death
- stress of viral production on endoplasmic reticulum leads to apoptosis
18
Q
why did SARS-CoV-2 evolve
A
- it acquired mutations, fast replication, slight genetic change and huge populations
19
Q
mutations
A
- mutations accumulate, work together to elicit changes and enhanced traits
- one mutation, might not increase transmissibility of virus alone
20
Q
characteristics of disease-causing virus
A
- transmissibility –> capacity to infect people
- virulence –> severity of symptoms
- immune escape –> ability to invade immune protections
21
Q
can viruses become VERY contagious and VERY deadly?
A
- no, as they would burn themselves out
22
Q
commensal bacteria
A
- not harmful, may be beneficial
23
Q
Lenksi experiment
A
- population of E. Coli into 12 flasks (37 degrees c), feed on water, glucose and other nutrients
- when bacteria replicated (each day) –> transferred some drops of food mixture into new flaks
24
Q
Evolution experiment
A
- how quickly, effectively, creatively and consistently microorganisms improve their reproductive fitness
- evolutionary biologists defined fitness as reproductive success: the number of offsprings that survive/number of grandchildren
- since bacteria don’t have children (they just divide), Lenski measures fitness and how fast one of his evolved population divides and multiplies in direct competition with its start-of-the-experiment ancestor
25
Why did Lenski expect to see a significant change in the 12 populations?
- by forcing his 12 populations to subsist only on glucose, instead of the rich mix of nutrients they find in their usual environment (the human intestine)
- Lenski had placed them in a state of maladaption (trait more harmful than helpful) relative to their intestine-living ancestor
-He wanted to see how quickly they would evolve to be better at coping with their new environment
26
Lenski's first finding
- diminishing returns to mutations over time --> bacteria made many of their most reproductively advantageous moves early on
27
Lenski's first finding explanation
- if a population starts out poorly adapted, mutations of relatively large effects can be advantageous early on
- mutations of large effects that help more than they hurt will be extremely rare
- huge size and short generation time of bacteria populations means that huge numbers of mutations will be generated, increasing the odds that a beneficial mutation of large effect eventually appears
- population rapidly increases in fitness due to the initial accumulation of mutations of large effects
- increases in fitness more slowly, as only mutations of small effects are viable
28
How does Lenski's thoughts differ from Darwin and Fisher?
- Both Darwin and Fisher imagined that evolution by natural selection proceeds in numerous tiny steps
- Fisher reasoned that only mutations of tiny effect could yield improvements without damaging side effects
- If Darwin and Fisher are right, a population encountering a new environment, to which it is poorly adapted, would evolve
29
Lenski's 2nd finding
- bacteria never stopped getting fitter
- 70,000 generations in and still finding new ways to improve
- at the start, there will be mutations with large effects but as generations pass, the effects will be smaller
30
Lenski's 3rd finding
- rare mutations have potential to explode in growth
--> large jumps are proceeded by small gradual mutations that set the stage for bigger changes
31
lineages
- most lineages have gone extinct but 2 persist in the present:
--> Cit+ = specialises on eating citrate
--> Cit- = can't eat citrate and is better at eating glucose
32
SARS-CoV-2
- 1 citrate moment: when it evolved the ability to leap into humans
- since then, virus accumulated innumerable mutations, allow to generate copies of itself more efficiently --> alters how it binds to our cells
33
COVID vaccines
- developed and deployed vaccines in real time
34
immunised
- exert selective pressure for virus to find new, more efficient replication strategies
35
Fear there will be a 2nd mutate moment
- viruses are able to circumvent our vaccines
- prospect of a variant that is vastly more contagious or deadly
36
why do viruses evolve?
- viruses evolved to fit environment strains from different locations move apart at thriving in that specific locations --> changing environment for virus to exceed --> strong selection pressure
37
what is Dr. Burtoni's three potential futures for the coronavirus?
1. virus can't evolve its way around vaccines
2. virus partially evade our vaccine-generated immune defences --> became less infectious or lethal
3. virus could accumulate mutations that allow it to circumvent immunity without suffering a major reduction in transmissibility of lethality
38
What is the key difference between Lenski's experiment and the situation in which the SARS-CoV-2 is evolving?
- most fundamental difference between Lenski's experiment and our reality
- Lenski's environment kept constant, COVID Is ever changing as vaccines develop, behaviour changes
39
How can "peak fitness" differ in different environments?
- highest number of cases per day depends on many factors: population size, vaccination rates, climates
40
Why did Beta and Gamma variants evolve in areas with high levels of prior infection, whereas the delta variant evolved in India?
- beta and gamma variants evolve in high levels of prior infection --> settled on mutations that offered them gains of immune escape but not transmissibility
- delta variant --> emerged in India, low vaccination rates, goal was to spread as fast and as far as possible, somewhat more immune-evasive and lethal
40
how could the virus evolve in ways that allow it to escape our immune response?
- virus alters the way it enters the body so antibodies can prevent it
- coronavirus = generalist ... can bind to many receptor sites, capacity for innovative mutations, many mutations at once, BUT human immune system complex, very effective against previously encountered pathogens
- convergent evolution --> many variants share similar mutations despite evolving separately
41
On the flip side of the virus's ability to evolve is our immune system's ability to respond: What lesson does human immunity to H1N1 and SARS-CoV-1 offer for being optimistic about our immune system's ability to respond to continually evolving SARS-CoV-2?
- In 2009, when the H1N1 influenza strain emerged, it had a curious feature: it caused more severe illness in younger people than older people
- It turned out that many older people had likely been exposed to relative of the strain decades ago-and that their immune systems, remembering that fight, were prepared for the next one
-The blood of COVID-19 survivors has the potential to neutralise the 2003 strain
-The vaccines appear to generate huge numbers of antibodies that work against SARS-CoV-1 in those who have also been infected with COVID-19
-Same antibodies bind to both of them
-Scientist don't think that their will every be a variant that completely escapes our immune systems
