UNIT 3 DAY 4 - THE COVID VIRUS KEEPS EVOLVING Flashcards

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1
Q

coronavirus

A

covered with spikes

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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
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3
Q

antibiotics

A
  • kill bacteria, don’t work against viruses
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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
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5
Q

coughing and sneezing

A

expel virus-laden droplets

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6
Q

virus transmission occurs by 2 routes

A
  1. relatively large airborne droplets falling within 5 seconds and contaminating surfaces
  2. tiny aerosols remain airborne for hours, accumulate in poorly ventilated spaces (IMPORTANT)
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7
Q

factors affecting airborne transmission

A
  1. distance –> droplets travel less than 6 feet, aerosols disperse over distance, concentrating diminishing exponentially with distance
  2. duration
  3. ventilation
  4. intensity of inhalation and/or exhalation
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8
Q

soap

A
  • destroys virus as soap molecules wedge themselves into the lipid membrame
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9
Q

viral envelope

A

protein encapsulates genetic material

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10
Q

spike protein

A

used by virus to gain entry to human cells –> attaches to ACE-2

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11
Q

ACE-2

A

attaches protein early

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12
Q

endocytosis

A

human cells ingests virus

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13
Q

exocytosis

A

virus carried by golgi bodies out of cell

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14
Q

hijacks

A

takes DNA and mutates it

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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
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16
Q

endoplasmic reticulum

A
  • network of membrane inside a cell through which proteins and other molecules move
  • ribosomes attach to endoplasmic reticulum
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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
  1. transmissibility –> capacity to infect people
  2. virulence –> severity of symptoms
  3. 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
Q

Why did Lenski expect to see a significant change in the 12 populations?

A
  • 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
Q

Lenski’s first finding

A
  • diminishing returns to mutations over time –> bacteria made many of their most reproductively advantageous moves early on
27
Q

Lenski’s first finding explanation

A
  • 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
Q

How does Lenski’s thoughts differ from Darwin and Fisher?

A
  • 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
Q

Lenski’s 2nd finding

A
  • 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
Q

Lenski’s 3rd finding

A
  • rare mutations have potential to explode in growth
    –> large jumps are proceeded by small gradual mutations that set the stage for bigger changes
31
Q

lineages

A
  • 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
Q

SARS-CoV-2

A
  • 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
Q

COVID vaccines

A
  • developed and deployed vaccines in real time
34
Q

immunised

A
  • exert selective pressure for virus to find new, more efficient replication strategies
35
Q

Fear there will be a 2nd mutate moment

A
  • viruses are able to circumvent our vaccines
  • prospect of a variant that is vastly more contagious or deadly
36
Q

why do viruses evolve?

A
  • 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
Q

what is Dr. Burtoni’s three potential futures for the coronavirus?

A
  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
Q

What is the key difference between Lenski’s experiment and the situation in which the SARS-CoV-2 is evolving?

A
  • 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
Q

How can “peak fitness” differ in different environments?

A
  • highest number of cases per day depends on many factors: population size, vaccination rates, climates
40
Q

Why did Beta and Gamma variants evolve in areas with high levels of prior infection, whereas the delta variant evolved in India?

A
  • 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
Q

how could the virus evolve in ways that allow it to escape our immune response?

A
  • 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
Q

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?

A
  • 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