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The evolution of SARS/ SARS-CoV-2 against drugs and vaccines which harms…
The evolution of SARS/ SARS-CoV-2 against drugs and vaccines which harms the human body
Mutation of SARS
Changing the properties/ proteins of SARS
Old strains of antibodies produced not affecting vaccines make because of mutations
Spike protein in RBD enhanced to enter human cells easier
Article #1 The coronavirus is mutating-does it matter? -Ewen Callaway $
At the 614th amino acid position
Acid aspartate
D was replaced by Glycine altering a sinlge nucleotide
29,903 letter RND code
called the D614G mutation
increased frequency of this mutation
"more transmissable form"
neutralizes antibodies that bind to virus
antibody being neutralized makes it non-infectious though it is
CD4+ cells and C8+ cells response are inhibited due to mutations
Article #3 Genetic Analysis Tracks SARS-CoV-2 Mutations in Human Hosts -
Bridget M. Kuehn
Positive aspects of constant mutation in SARS
Deletion
Article #13 - Considering mutational meltdown as a potential SARS-CoV-2 treatment by Jenson at el.,
Mutational meltdown
defined as when a population becomes extinct due to accumulation of deleterious mutations
Natural selection not being able to purge if the mutatinal pressure is too large dabble a little in ns
Article #12 - Two sides of the same coin- A population genetics perspective on lethal mutagenesis and mutational meltdown - Matuszewski et al.,
Slowed down spread
drug used to increase threshold and make virus mutate more
snowball effect in loss of population
Why is it so easy for viruses to mutate?
Article #2 Mechanisms of viral mutation by Sanjuan et al.,
based on ability to generate de novo diversity in short period of time
RNA virus mutate faster because of single strand compared to DNA with double
Fast mutation Makes drugs and vaccine useless
You can obtain vaccine or drug and virus mutates against it
Memory T cells being detoured by new strain
Human host provides great environment
Hard to detect by immune system once inside of host cell
Replicates inside of human cells
Article #15 Mechanism of host receptor adaptation by severe acute repiratory syndrome coronavirus by Wu, Peng, et al,.
Virus adapts to host
easy entry of spikes
two easy virus binding RBD, hot spot of ACE2
cACE2
hACE2
Easily trasnmitted to humans
Article #14 COVID : a new challenge for human being by Yang and Wang 2020
Respiratory droplets
articles contaminated with droplets
Thousands of mutations already based virus being under selective pressure
Repeat of Article #1
12,000 mutations in SARS-CoV-2 genome
Two single-letter mutation per month
selective pressure acts on mutation rates
can depend virus and host dependant processes
Repeat of article #2
Extreme replication rates
Article #7 Composition of human-specific slow codons and slow di-codons in SARS-CoV and 2019-nCoV are lower than other coronaviruses suggesting a faster protein synthesis rate of SARS-CoV and 2019-nCoV by Yang et al.,
syndrome-related coronavirus (SARS-CoV) may be much faster than other coronaviruses infect humans.
Article #8 Composition of human-specific slow codons and slow di-codons in SARS-CoV and 2019-nCoV are lower than other coronaviruses suggesting a faster protein synthesis rate of SARS-CoV and 2019-nCoV by YANG et al,.
viruses with high protein synthesis rates (as a consequence, replication rates) have great advantages to increase transmissibility.
the have a higher chance of successful infection even the initial when infection dose is low.
Natural selection
Article #5 Tracking Changes in SARS-CoV-2 Spike: Evidence that D614G Increases Infectivity of the COVID-19 Virus by Kober at el.,
D and G Type: G viruses were chosen by SARS for better spiking coat, whiles D fell back
Polybasic furin cleavage site
determines viral infectivity and host range
junction of spikes S1 and S2
Article #4 The proximal origin of SARS-CoV-2 by Andersen et al.,
O-linked glycans
Aritcle #6 Global aspects of viral glycosylation by Bagdonaite et al.,
Several viruses utilize mucin-like domains as glycan shields involved immunoevasion SARS maybe one of them
unclear but testing to see if it could create a "mucin-like" domain that shields epitopes key residues on spike protein
Usage of ACE2
Article #9 Angiotension- converting emzyme 2 is a functional receptor for the SARS cornavirus - Wenhui li et al.,
entry receptor
hallmark of its cross-species transmissibilty
Rbd associated with binding of S protein with ACE2
Article #10 A 193-Amino acid fragment pf the SARS cornavirus S protein efficiently binds angiotensin-converting emzyme 2
binding affinity of RBD with ACE2
RBD exhibits protuberant in-ward motion towards the human ACE2 binding interface which may be crucial for molecular interaction