scholarly journals The INDIA Mutations and B.1.617 Variant: Is There a Global "Strategy" for Mutations and Evolution of Variants of The SARS-CoV2 Genome?

2021 ◽  
Author(s):  
Jean-claude Perez
Keyword(s):  
Numerical Method ◽  
Fibonacci Numbers ◽  
Global Strategy ◽  
Messenger Rnas ◽  
Whole Genomes ◽  
Frequent Mutations

In this paper, we run for all INDIA mutations and variants a biomathematical numerical method for analysing mRNA nucleotides sequences based on UA/CG Fibonacci numbers proportions (Perez, 2021). In this study, we limit ourselves to the analysis of whole genomes, all coming from the mutations and variants of SARS-CoV2 sequenced in India in 2020 and 2021. We then demonstrate - both on actual genomes of patients and on variants combining the most frequent mutations to the SARS-CoV2 Wuhan genomes and then to the B.1.617 variant - that the numerical Fibonacci AU / CG metastructures increase considerably in all cases analyzed in ratios of up to 8 times. We can affirm that this property contributes to a greater stability and lifespan of messenger RNAs, therefore, possibly also to a greater INFECTUOSITY of these variant genomes.

scholarly journals The INDIA Mutations and B.1.617 Variant: Is There a Global "Strategy" for Mutations and Evolution of Variants of The SARS-CoV2 Genome?

2021 ◽  
Author(s):  
Jean-claude Perez
Keyword(s):  
Numerical Method ◽  
None None ◽  
Reference Genome ◽  
Fibonacci Numbers ◽  
Global Strategy ◽  
Messenger Rnas ◽  
Average Increase ◽  
Whole Genomes ◽  
Frequent Mutations

ABSTRACT. In this paper, we run for all INDIA mutations and variants a biomathematical numerical method for analysing mRNA nucleotides sequences based on UA/CG Fibonacci numbers proportions (Perez, 2021). In this study, we limit ourselves to the analysis of whole genomes, all coming from the mutations and variants of SARS-CoV2 sequenced in India in 2020 and 2021. We then demonstrate - both on actual genomes of patients and on variants combining the most frequent mutations to the SARS-CoV2 Wuhan genomes and then to the B.1.617 variant - that the numerical Fibonacci AU / CG metastructures increase considerably in all cases analyzed in ratios of up to 8 times. We can affirm that this property contributes to a greater stability and lifespan of messenger RNAs, therefore, possibly also to a greater INFECTUOSITY of these variant genomes. Out of a total of 108 genomes analyzed: - None ("NONE") of them contained a number of metastructures LOWER than those of the reference SARS-CoV2 Wuhan genome. - Eleven (11) among them contained the same number of metastructures as the reference genome. - 97 of them contained a GREATER number of metastructures than the reference genome, ie 89.81% of cases. The average increase in the number of metastructures for the 97 cases studied is 4.35 times the number of SARS-CoV2 UA/CG 17711 Fibonacci metastructures.

scholarly journals THE INDIA MUTATIONS AND B.1.617 DELTA VARIANTS: IS THERE A GLOBAL "STRATEGY" FOR MUTATIONS AND EVOLUTION OF VARIANTS OF THE SARS-COV2 GENOME?

2021 ◽  
Vol 9 (6) ◽  
pp. 418-459
Author(s):  
Jean Claude Perez
Keyword(s):  
None None ◽  
Exponential Growth ◽  
Reference Genome ◽  
Fibonacci Numbers ◽  
Global Strategy ◽  
Messenger Rnas ◽  
Average Increase ◽  
Whole Genomes ◽  
Frequent Mutations ◽  
Reference Strains

In this paper, we run for all INDIA mutations and variants a biomathematical numerical method for analysing mRNA nucleotides sequences based on UA/CG Fibonacci numbers proportions (Perez, 2021). In this study, we limit ourselves to the analysis of whole genomes, all coming from the mutations and variants of SARS-CoV2 sequenced in India in 2020 and 2021. We then demonstrate - both on actual genomes of patients and on variants combining the most frequent mutations to the SARS-CoV2 Wuhan genomes and then to the B.1.617 variant - that the numerical Fibonacci AU / CG metastructures increase considerably in all cases analyzed in ratios of up to 8 times. We can affirm that this property contributes to a greater stability and lifespan of messenger RNAs, therefore, possibly also to a greater INFECTUOSITY of these variant genomes. Out of a total of 108 genomes analyzed: None ("NONE") of them contained a number of metastructures LOWER than those of the reference SARS-CoV2 Wuhan genome. Eleven (11) among them contained the same number of metastructures as the reference genome. 97 of them contained a GREATER number of metastructures than the reference genome, ie 89.81% of cases. The average increase in the number of metastructures for the 97 cases studied is 4.35 times the number of SARS-CoV2 UA/CG 17711 Fibonacci metastructures. Finally, we put a focus on B.1.617.2 crucial exponential growth Indian variant. Then, we demonstrate, by analyzing the main worldwide 19 variants, both at the level of spikes and of whole genomes, how and why these UA / CG metastuctures increase overall in the variants compared to the 2 reference strains SARS-CoV2 Wuhan and D614G. Then, we discuss the possible risk of ADE for vaccinated people. To complete this article, an ADDENDUM by Nobelprizewinner Luc Montagnier vas added at the end of this paper.

scholarly journals Systematic review of mutations associated with resistance to the new and repurposed Mycobacterium tuberculosis drugs bedaquiline, clofazimine, linezolid, delamanid and pretomanid

2020 ◽  
Author(s):  
Suha Kadura ◽  
Nicholas King ◽  
Maria Nakhoul ◽  
Hongya Zhu ◽  
Grant Theron ◽  
...  
Keyword(s):  
Systematic Review ◽  
Mycobacterium Tuberculosis ◽  
Resistance Mechanisms ◽  
Phenotypic Resistance ◽  
Resistance Evolution ◽  
Linezolid Resistance ◽  
Novel Drugs ◽  
Whole Genomes ◽  
Frequent Mutations ◽  
Repurposed Drugs

Abstract Background Improved genetic understanding of Mycobacterium tuberculosis (MTB) resistance to novel and repurposed anti-tubercular agents can aid the development of rapid molecular diagnostics. Methods Adhering to PRISMA guidelines, in March 2018, we performed a systematic review of studies implicating mutations in resistance through sequencing and phenotyping before and/or after spontaneous resistance evolution, as well as allelic exchange experiments. We focused on the novel drugs bedaquiline, delamanid, pretomanid and the repurposed drugs clofazimine and linezolid. A database of 1373 diverse control MTB whole genomes, isolated from patients not exposed to these drugs, was used to further assess genotype–phenotype associations. Results Of 2112 papers, 54 met the inclusion criteria. These studies characterized 277 mutations in the genes atpE, mmpR, pepQ, Rv1979c, fgd1, fbiABC and ddn and their association with resistance to one or more of the five drugs. The most frequent mutations for bedaquiline, clofazimine, linezolid, delamanid and pretomanid resistance were atpE A63P, mmpR frameshifts at nucleotides 192–198, rplC C154R, ddn W88* and ddn S11*, respectively. Frameshifts in the mmpR homopolymer region nucleotides 192–198 were identified in 52/1373 (4%) of the control isolates without prior exposure to bedaquiline or clofazimine. Of isolates resistant to one or more of the five drugs, 59/519 (11%) lacked a mutation explaining phenotypic resistance. Conclusions This systematic review supports the use of molecular methods for linezolid resistance detection. Resistance mechanisms involving non-essential genes show a diversity of mutations that will challenge molecular diagnosis of bedaquiline and nitroimidazole resistance. Combined phenotypic and genotypic surveillance is needed for these drugs in the short term.

scholarly journals SARS-CoV2 Variants and Vaccines mRNA Spikes Fibonacci Numerical UA/CG Metastructures

2021 ◽  
Author(s):  
Jean-Claude Perez
Keyword(s):  
Numerical Method ◽  
Mrna Stability ◽  
Fibonacci Numbers ◽  
The World ◽  
One Year ◽  
Almost All

In this paper, we suggest a biomathematical numerical method analysing mRNA nucleotides sequences based on UA/CG Fibonacci numbers proportions. This method is used to evaluate then compare the spike genes related to the main SARS-CoV2 VARIANTS circulating presently within the world. The 8 main results proposed to be reproduced by peers are: 1/ SARS-CoV2 genome and spike evolution in one year 2020-2021. 2/ SARS-CoV2 Origins. 3/ Comparing 11 reference variants spikes. 4/ analysing 32 CAL.20C california variant patients spikes. 5/ Toward a meta mRNA Fibonacci gene end message code. 6/ analysing S501 UK, S484 South Afrika and 2 mutations IINDIA variants. 7/ Suggesting a possible variants spike mRNA palindrome symmetry metastructure improving mRNA stability then infectuosity. 8/ Analysing Fibonacci Metastructures in the mRNA coding for the vaccines PFITZER and MODERNA. Particularly, we suggest the following conjecture at mRNA folding level: CONJECTURE of SARS-CoV2 VARIANTS: The growth of long Fibonacci structures in the shape of podiums for almost all of the variants studied (UK, California, South Afrika, India, etc.) suggests the probable folding of the Spike mRNA in the form of a hairpin, which can strengthen the cohesion and the lifespan of this mRNA. Finally, we show that this kind of Fibonacci matastructures disapears TOTALLY analysing the published mRNA sequences of PFITZER and MODERNA vaccines.

scholarly journals SARS-CoV2 Variants and Vaccines mRNA Spikes Fibonacci Numerical UA/CG Metastructures

2021 ◽  
Author(s):  
Jean-Claude Perez
Keyword(s):  
Numerical Method ◽  
Mrna Stability ◽  
Fibonacci Numbers ◽  
Human Host ◽  
The World ◽  
One Year ◽  
Almost All

In this paper, we suggest a biomathematical numerical method analysing mRNA nucleotides sequences based on UA/CG Fibonacci numbers proportions. This method is used to evaluate then compare the spike genes related to the main SARS-CoV2 VARIANTS circulating presently within the world. The 8 main results proposed to be reproduced by peers are: 1/ SARS-CoV2 genome and spike evolution in one year 2020-2021. 2/ SARS-CoV2 Origins. 3/ Comparing 11 reference variants spikes. 4/ analysing 32 CAL.20C california variant patients spikes. 5/ Toward a meta mRNA Fibonacci gene end message code. 6/ analysing S501 UK, S484 South Afrika and 2 mutations IINDIA variants. 7/ Suggesting a possible variants spike mRNA palindrome symmetry metastructure improving mRNA stability then infectuosity. 8/ Analysing Fibonacci Metastructures in the mRNA coding for the vaccines PFITZER and MODERNA. Particularly, we suggest the following conjecture at mRNA folding level: CONJECTURE of SARS-CoV2 VARIANTS: The growth of long Fibonacci structures in the shape of podiums for almost all of the variants studied (UK, California, South Afrika, India, etc.) suggests the probable folding of the Spike mRNA in the form of a hairpin, which can strengthen the cohesion and the lifespan of this mRNA. Finally, we show that this kind of Fibonacci matastructures disapears TOTALLY analysing the published mRNA sequences of PFIZER and MODERNA vaccines. Finally, we show that this kind of Fibonacci matastructures disapears TOTALLY analysing the published mRNA sequences of PFIZER and MODERNA vaccines. One fact is certain, the 2 mRNAs of the Moderna and Pfizer vaccines will result in a low functionality of the spike vaccine because by doping these sequences in CG rich, their designers, in search of greater STABILITY of these RNAs will have built, according to us , sequences which, as soon as they are inserted into the human host, will seek to mutate, like SARS-CoV2 variants, towards CG ==> UA forms in order to improve, paradoxically, their STABILITY and probably also their LIFETIME..

Wuhan nCoV-2019 SARS Coronaviruses Genomics Fractal Metastructures Evolution and Origins

2020 ◽  
Author(s):  
Jean-Claude Perez
Keyword(s):  
Fibonacci Numbers ◽  
Adaptation Strategy ◽  
Formal Proof ◽  
Global Strategy ◽  
Whole Numbers ◽  
Johannes Kepler ◽  
Synthetic Genome ◽  
Entire Sequence ◽  
Different Strains ◽  
Artificial Origin

Wuhan nCoV-2019 SARS Coronaviruses Genomics Fractal Metastructures Evolution and Origins “Where there is matter, there is geometry.” Johannes Kepler Jean-claude PEREZ, PhD Maths § Computer Science Bordeaux University, RETIRED interdisciplinary researcher (IBM Emeritus, IBM European Research Center on Artificial Intelligence), 7 avenue de terre-rouge F33127 Martignas Bordeaux metropole France, phone 33 0781181112 [email protected] ABSTRACT : The main result of this updated release is the formal proof that 2019-nCoV coronavirus is partially a SYNTHETIC genome. We proof the CONCENTRATION in a small région of wuhan New genome of 3 different régions from HIV1 ENVELOPPE GENE. In this article, we demonstrate that there is a kind of global human hosts adaptation strategy of SARS viruses as well as a strategy of global evolution of the genomes of the different strains of SARS which have emerged, mainly in China, between years 2003 first SARS genomes and the last 2020 nCoV-2019 Wuhan seafood market pneumonia virus isolate Wuhan-Hu-1, complete genome. This global strategy, this temporal link, is materialized in our demonstration by highlighting stationary numerical waves controlling the entire sequence of their genomes. Curiously, these digital waves characterizing the 9 SARS genomes studied here are characteristic whole numbers: the "Fibonacci numbers", omnipresent in the forms of Nature, and which our research for several decades has shown strong links with the proportions of nucleotides in DNA. Here we demonstrate that the complexity and fractal multiplicity of these Fibonacci numerical waves increases over the years of the emergence of new sArs strains. We suggest that this increase in the overall organization of the SARS genomes over the years reflects a better adaptation of SARS genomes to the human host. The question of a link with pathogenicity remains open. However, we believe that this overall strategy for the evolution of the SARS genomes ensures greater unity, consistency and integrity of the genome. Finally, we ask ourselves the question of a possible artificial origin of this genome, in particular because of the presence of fragments of HIV1 retrovirus. KEYWORDS : SARS, Wuhan nCoV-2019, Fibonacci numbers, Fractal genome, Numerical stationary periodic waves, HIV1, synthetic genomes.

scholarly journals WUHAN COVID-19 SYNTHETIC ORIGINS AND EVOLUTION

2020 ◽  
Vol 8 (2) ◽  
pp. 285-324 ◽  
Author(s):  
Jean-Claude PEREZ
Keyword(s):  
Fibonacci Numbers ◽  
Small Region ◽  
Adaptation Strategy ◽  
Formal Proof ◽  
Global Strategy ◽  
Whole Numbers ◽  
Synthetic Genome ◽  
Entire Sequence ◽  
Different Strains ◽  
Artificial Origin

The main result of this updated release is the formal proof that 2019-nCoV coronavirus is partially a SYNTHETIC genome. We proof the CONCENTRATION in a small région of wuhan New genome (300bp) of 3 different régions from HIV1 ENVELOPPE gene and 3 others from HIV2 and SIV (ENV and POL RT). All this is remarkable and bears the mark of a desire for organization of a human nature: LOGIC, SYMETRIES. In this article, we demonstrate also that there is a kind of global human hosts adaptation strategy of SARS viruses as well as a strategy of global evolution of the genomes of the different strains of SARS which have emerged, mainly in China, between years 2003 first SARS genomes and the last 2019 COVID-19 Wuhan seafood market pneumonia virus isolate Wuhan-Hu-1, complete genome. This global strategy, this temporal link, is materialized in our demonstration by highlighting stationary numerical waves controlling the entire sequence of their genomes. Curiously, these digital waves characterizing the 9 SARS genomes studied here are characteristic whole numbers: the "Fibonacci numbers", omnipresent in the forms of Nature, and which our research for several decades has shown strong links with the proportions of nucleotides in DNA. Here we demonstrate that the complexity and fractal multiplicity of these Fibonacci numerical waves increases over the years of the emergence of new SARS strains. We suggest that this increase in the overall organization of the SARS genomes over the years reflects a better adaptation of SARS genomes to the human host. The question of a link with pathogenicity remains open. However, we believe that this overall strategy for the evolution of the SARS genomes ensures greater unity, consistency and integrity of the genome. Finally, we ask ourselves the question of a possible artificial origin of this genome, in particular because of the presence of fragments of HIV1, HIV2 and SIV retroviruses.

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