Cellular Automata Model for Non-Structural Proteins Comparing
Transmissibility and Pathogenesis of SARS Covid (CoV-2, CoV) and MERS Covid
- URL: http://arxiv.org/abs/2212.00502v1
- Date: Fri, 25 Nov 2022 18:57:21 GMT
- Title: Cellular Automata Model for Non-Structural Proteins Comparing
Transmissibility and Pathogenesis of SARS Covid (CoV-2, CoV) and MERS Covid
- Authors: Raju Hazari and Parimal Pal Chaudhuri
- Abstract summary: Significantly higher transmissibility of SARS CoV-2 compared to SARS CoV (2003) can be attributed to mutations of structural proteins.
The key protein out of the 16 nsps, is the non-structural protein nsp1, also known as the leader protein.
- Score: 0.0
- License: http://creativecommons.org/licenses/by-nc-sa/4.0/
- Abstract: Significantly higher transmissibility of SARS CoV-2 (2019) compared to SARS
CoV (2003) can be attributed to mutations of structural proteins (Spike S,
Nucleocapsid N, Membrane M, and Envelope E) and the role played by
non-structural proteins (nsps) and accessory proteins (ORFs) for viral
replication, assembly and shedding. The non-structural proteins (nsps) avail
host protein synthesis machinery to initiate viral replication, along with
neutralization of host immune defense. The key protein out of the 16 nsps, is
the non-structural protein nsp1, also known as the leader protein. Nsp1 leads
the process of hijacking host resources by blocking host translation. This
paper concentrates on the analysis of nsps of SARS covid (CoV-2, CoV) and MERS
covid based on Cellular Automata enhanced Machine Learning (CAML) model
developed for study of biological strings. This computational model compares
deviation of structure - function of CoV-2 from that of CoV employing CAML
model parameters derived out of CA evolution of amino acid chains of nsps. This
comparative analysis points to - (i) higher transmissibility of CoV-2 compared
to CoV for major nsps, and (ii) deviation of MERS covid from SARS CoV in
respect of virulence and pathogenesis. A Machine Learning (ML) framework has
been designed to map the CAML model parameters to the physical domain features
reported in in-vitro/in-vivo/in-silico experimental studies. The ML framework
enables us to learn the permissible range of model parameters derived out of
mutational study of sixteen nsps of three viruses.
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