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Since 2019, the antigens from Severe Acute Respiratory Syndrome Corona Virus 2 (SARS-CoV-2) have evolved from the initial D614 wild strain in the first epidemic wave, to D614G mutant in the second wave, to Delta mutant in the third wave, and to Omicron mutant in the fourth wave. Were the virulence and infectivity associated with different fragments in the Delta subtype of SARS-CoV-2? It is needed to analyze the sequences of the virus. The longest four glycine-free antigen fragments with tryptophan, longer or equal to 37 amino acids in length, were selected. The four fragment sequences in D614, D614G, N148, and I358 Omicron subtype were searched from the National Center of Biological Information website. The standard deviation (SD) of the molecular weight of the contained amino acids in the fragments was calculated to be the indicator of their antigen precession. The longest fragment was analyzed for the relationship between antigen precession and virus infectivity. On the other hand, 10 mutations in the Delta subtype were found in eight mutated fragments, and their antigen precession was used to analyze the correlation with virus virulence. The longest antigen fragments determined virus infectivity. Whole mutated fragments determined the virulence. Both were associated with different mutated fragments with varied antigen precession in the Delta subtype of SARS-CoV-2.
The Chinese University of Hong Kong, Hong Kong, China
Zhihong Li
Shantou University, Guangdong, China
Liping Li*
Shantou University, Guangdong, China
*Address all correspondence to: peijunzuo@hotmail.com and lpli@stu.edu.cn
1. Introduction
In December 2019, coronavirus disease (COVID-19), with the unmutated D614 antigen, was first reported in China [1]. The epidemic, originating in Wuhan, China, started on December 12, 2019, causing 2794 laboratory-confirmed infections, and by January 26, 2020, these infections had resulted in 80 deaths.
On March 1, 2020, only 9.9% of the analyzed 6244 global cases were the second generation strain of SARS-Cov-2, referred to as D614G, but this rapidly increased to 54% by March 10, 2020, causing D614G to become the dominant strain [2]. Based on the D614 to D614G mutation, D614G, the Delta subtype, was mutated before Omicron emerged, and there were 10 major mutated subtypes of SARS-CoV-2 [3]. These subtypes are shown in Table 1, and D614G is shown in bold. The SARS-Cov-2 B.1.617 lineage was found in India first [4] but quickly spread to other countries. The lineage includes three main subtypes: B1.617.1 (Kappa), B.1.617.2 (Delta), and B.617.3 (None-typed).
B.1.617.2 (Delta) first emerged in India in October 2020 [5]. As shown in Table 1, there were 10 common mutations, with some authors reporting five more noncommon, giving a total number of 15 mutations for Delta emerged before Omicron. The Omicron had at least 30 mutations.
The third generation of SARS-CoV-2 should be the Delta subtype. It is believed to have been transmitted faster than any other subtype, except for Omicron. Compared with the Alpha subtype (B.1.1.7), the sera collected from SARS-CoV-2 patients were fourfold less powerful against the Delta subtype [6]. Some authors considered that the antigenicity changes in the Delta subtype might not be sufficient against the current vaccines. In another paper the same team published, they compared the antigenicity with the H3N2 flu vaccine [7], suggesting that this may be the worst vaccine. But the truth was that most patients of the Delta subtype were immunized with the vaccine. We need to know why the vaccines did not work for the Delta subtype and also need to identify good vaccines.
The mutations occur and need to avoid the protective effects of vaccines. They also increased the limit of the detection. For example, the detection limit for the wild type D614 SARS-CoV-2 was 21.5 copies; for Omicron, it was 14.3 copies, but for the Delta subtype, it raised 32.0 copies [8]. The order for detection limitation was very similar to the order of virulence: Omicron was weakest, then D614, D614G, and Delta. Not all patients of SARS-CoV-2 reached the detection limit, with the positive ratio of patients being as low as 47.21% [9]. Therefore, it is important to find the mutation route of SARS-CoV-2.
Some scientists try to find the regulation or rule for Delta and Delta plus mutations [10]. The authors analyzed the frequencies of the mutations, and the data set was numerous.
Some scientists use “deep phylogenetic-based clustering analysis” to uncover new and shared mutations in SARS-CoV-2 variants due to directional and convergent evolution [11]. The phylogenetic clustering analysis needs at least three sequences.
Two main Receptor-Binding Domain (RBD) conformations have been described, standing-up and lying-down states, with high and low affinity to ACE2, respectively [12, 13]. The standing-up and lying-down states are also qualified data.
However, our approach is different from other authors. We analyzed the trends of the “precession” changing in the mutated fragments, and the data were quantified. Our “precession” method can be analyzed as less than two sequences.
In the four waves of SARS-CoV-2, there were four main subtypes: D614, D614G, Delta, and Omicron. What caused such step-by-step evolutions of these four subtypes? In our previous work, we found the antigens of the SARS-CoV-2 showed a preference to evolve from most “rough” status and in a dose-dependent manner [14]. In the first two waves of SARS-CoV-2, the status of D614, caused by the first wave, was “rough”; meanwhile, the status of D614G, caused by the second wave, was “precise”.
Besides D614G, did the other nine confirmed mutations in the Delta type follow the same trend as D614G, from “rough” to “precise”, after mutation? We analyzed data to confirm if this way was true in this paper.
This paper will try to find a regulation or a rule for the longest fragments, longer or equal to 37 amino acids in length if the mutants first happened in the position of “rough”, but not in other positions. If the infectivity is associated with the longest fragments. We will also examine if, after mutation, the “rough” status of mutants in the Delta type was changed to “precise” in the fragments of N148 (E156del, F157del, and R158G), T19R, G142D, L452R, T478K, D614G, P681R, and D950N. If the precession of the whole mutation is associated with the virulence.
At the website https://www.ncbi.nlm.nih.gov/, select Protein in All Databases. Put the access number to search the protein sequence of the subtype SARS-CoV-2.
The amino acid sequence of protein “QHD43416” containing D614, and the sequences of protein “7KDK_A”, “7V8A_B”, and “7V8A_C” containing D614G.
The amino acid sequences of proteins “7V8B_A”, “7V8A_B”, and “7V8A_C” contained the Delta subtypes, with mutations of N148 (E156del, F157del, and R158G), T19R, G142D, L452R, T478K, D614G, P681R, and D950N.
2.2 Alignment protein sequences of the subtype SARS-CoV-2
Input the protein sequences of SARS-CoV-2 original sequence, D614, the D614G mutants, and the Delta subtype and Submit.
In the alignment result of Clustal Omega, all “G” amino acids were shown in yellow (Figures 1–4).
Figure 1.
The amino acids of N148 and G142D. The amino acid sequence of protein “QHD43416” contained D614, “7KDK_A”, contained G614, “7V8B_A”, “7V8A_B”, “7V8A_C” contained Delta subtype were searched from NCBI. The amino acid sequences of D614, the G614 mutant, and Delta subtype were compared with the online software of Clustal Omega. In the alignment result of Clustal Omega, all “G” amino acids are marked by the yellow color. N148 and G142D were indicated by the arrows.
Figure 2.
The amino acids of I358, L452R, T478K, and D614. In the alignment result of Clustal Omega, all “G” amino acids were marked by the yellow color. I358, L452R, and D614 were indicated by the arrows. I358 was mutated in the Omicron subtype.
Figure 3.
The amino acids of P681R and F718. In the alignment result of Clustal Omega, all “G” amino acids were marked by the yellow color. P681R and F718 were indicated by the arrows.
Figure 4.
The amino acids of D950N. In the alignment result of Clustal Omega, all “G” amino acids were marked by the yellow color. D950N was indicated by the arrow.
2.3 Select longest G-free antigen fragments longer or equal to 37 amino acids in length
In the original D614 subtype of SARS-CoV-2, QHD43416, select the G-free antigen fragments longer or equal to 37 amino acids. Such fragments do not contain any G, glycine. Normally, the non-G amino acid has the mutation potential to a smaller amino acid. Glycine is the smallest amino acid. The selected results are shown in Table 2.
Peptides
Amino acids
Mean of molecular weight
SD
Contains “W”
F718
43
125.3
20.69
N
I358
41
134.2 (Omicron)
31.66(3)
Y
N148
38
140.1 (Delta)
26.92(2)
Y
D614
37
129.3 (D614G)
25.23(1)
Y
Table 2.
The molecular weight and SD of D614, N148, I358, and another candidate of potential mutant peptide.
In the “W” contained fragments, among non-“G” peptides, the SD in D614, 25.23 is the smallest. This means the status is most “rough”. Most likely, the mutation will happen to here. This is already confirmed by the G614 mutation. The N148 was the mutant confirmed by the Delta subtype, and the I358 was also a mutant confirmed by the Omicron subtype. The order was the evolution from “rough” to “precise”. These antigens were also evolved to “precise” status.
2.4 Find whole mutation fragment in Delta subtype of SARS-CoV-2
In sequence of Delta subtype of SARS-CoV-2, “7V8B_A”, “7V8A_B”, and “7V8A_C”, find the mutations of N148 (E156del, F157del, R158G), T19R, G142D, L452R, T478K, D614G, P681R, and D950N. The fragments may contain G amino acid, but the least rough fragments were selected. The results are shown in Table 3. The mutations contain eight fragments and 10 site mutations in the Delta subtype. These eight fragments were compared and shown in Figure 5.
Peptides
Amino acids
Mean of molecular weight
SD
Contains “W”
T19
34
130.9
22.46
N
T19R
34
132.6
23.54↑
N
G142
17
144.9
32.31
Y
G142D
17
140.7
33.06↑
Y
N148
38
140.1
26.92
Y
E156del
36
136.5
28.65↑
Y
F157del
36
136.5
28.65↑
Y
R158G
36
136.5
28.65↑
Y
L452
28
143.9
25.86
N
L452R
28
145.4
26.35↑
N
T478
5
118.5
9.798
N
T478K
5
123.9
15.83↑
N
D614
37
129.3
25.23
Y
D614G
37
127.7
26.74↑
Y
P681
30
127.6
28.36
N
P681R
30
129.5
29.49↑
N
R682G
30
124.3
28.51↑
N
R683S
30
123.9
28.68↑
N
R685S
30
127.2
28.57↑
N
D950
24
128.6
18.64
N
D950N
24
128.6
18.64→
N
Table 3.
The molecular weight and SD of D614, N148, and confirmed mutant peptides in Delta subtype.
Beside 10 mutants N148 (E156del, F157del, R158G), T19R, G142D, L452R, T478K, D614G, P681R, D950N in Delta subtype, G682, S683, S685 were also mutants at least in “7V8B_A”, “7V8A_B”, “7V8A_C”. Twelve in 13 were mutated from “rough” status to “precise”; only 1, D950N, was not changed.
Figure 5.
Eight fragments containing 10 confirmed mutations from the Delta subtype were selected. These fragments were compared.
2.5 Calculate the precession of whole mutation fragment in Delta subtype of SARS-CoV-2
In each fragment, the molecular weight of contained amino acid were different. The mean and standard deviations (SD) of molecular weight were calculated using Excel. The results are shown in Tables 2 and 3. The standard deviations (SD) of molecular weight can indicate precession. The smaller the SD, the rougher the precession, and the easier it is to be recognized by the immune system. The fragment precession was calculated both before and after the mutation.
3.1 The longest G-free peptide with Tryptophan (W) longer or equal to 37 amino acids in length
3.1.1 The antigen fragment D614 in the original strain, led the first wave of epidemic
As shown in Table 2, the D614 peptide has a mean molecular weight of 129.3, and the standard deviation (SD) for the individual molecular weight of its amino acids is 25.23. This peptide contains the biggest amino acid, tryptophan (W, molecular weight, 204.2262). In the “W” contained fragments, the SD of D614, 25.23 was the smallest among the G-free peptides. This means that the status is the “roughest” and that this location is the most likely place for a mutation. This site has already been confirmed to have the D614G mutation.
As shown in Figure 2, the candidates of mutant peptides are the arrowed fragments. The first is D614, TNTSNQVAVLYQDVNCTEVPVAIHADQLTPTWRVYST, 37 amino acids in length. This G-free fragment contains the D614 amino acid in the original strain in Wuhan, China, on December 12, 2019, which led to the first wave of the epidemic. The precession of this fragment is 25.23, shown in Table 2.
3.1.2 The antigen fragment D614G in the Italian strain led to the second wave of epidemic
The D614 has already been confirmed as a mutated peptide. It mutated to D614G on March 10, 2020, first emerged in Italy, and led to the second wave of the epidemic. The precession of this fragment is increased to 26.74, shown in Table 3. This D614G mutation remains no change in D614G, Delta, and Omicron subtype. D614G has 37 amino acids, the molecular weight is 127.7, the SD is 26.74, and it contains “W”.
3.1.3 The antigen fragment N148 in the Indian strain, led the third wave of epidemic
The other longer G-free peptide is N148, 38 amino acids in length, VYYHKNNKSWMESEFRVYSSANNCTFEYVSQPFLMDLE, as shown in Figure 1. This fragment has also already been confirmed as a mutated peptide in the Delta variant. It mutated in October 2020, in India and led to the third wave of epidemic. The precession of this fragment is 26.92 before mutation, larger than the precession of D614 and D614G, shown in Table 2. Its precession increased to 28.65 after the mutations on the same base as the D614G mutant (E156del, F157del, and R158G), shown in Table 3. N148 has 38 amino acids, the molecular weight is 140.1, the SD is 26.92, and it contains “W”.
3.1.4 The antigen fragment I358 in the south African strain led the fourth wave of epidemic
Another identified peptide is I358, 41 amino acids in length, EVFNATRFASVYAWNRKRISNCVADYSVLYNSASFSTFKCY, as shown in Figure 2. I358 mutation confirmed by the Omicron subtype. The order of evolution was from “rough” to “precise”, and these antigens were also shown to evolve to “precise” status.
The fragment was mutated on November 23, 2021, in South Africa, led to a fourth epidemic. The precession of this fragment is 31.66 before mutation, larger than the precession of D614, D614G, and Delta, as shown in Tables 2 and 3. The precession increased also. We will show the data in another paper. This peptide was also confirmed as an Omicron mutant. I358 has 41 amino acids, the molecular weight is 134.2, the SD is 31.66, and it contains “W”.
3.2 The longest G-free peptide without Tryptophan, W
The longest G-free peptide without tryptophan, W, is F718, 43 amino acids in length, AENSVAYSNNSIAIPTNFTISVTTEILPVSMTKTSVDCTMYIC, as shown in Figure 3. F718 has 43 amino acids, the molecular weight is 125.3, the SD is 20.69, and it does not contain “W”.
3.3 Whole mutated fragments in Delta subtypes D614G, N148 (E156del, F157del, and R158G), T19R, G142D, L452R, T478K, P681R, and D950N
Ten confirmed mutations observed in the Delta subtype are listed in Table 1. They are T19R, G142D, E156del, F157del, R158G, L452R, T478K, D614G, P681R, and D950N (Figure 4). Their molecular weights and SDs are shown in Table 3. The data shown in green indicates the parameters of the antigens before mutation. All mutated antigens, after evolution, are shown in yellow. Their SDs were shown to have increased in nine of the confirmed mutations. Only 1 SD showed no change, but no SD was shown to have decreased.
Beside 10 mutants N148 (E156del, F157del, R158G), T19R, G142D, L452R, T478K, D614G, P681R, and D950N in the Delta subtype, G682, S683, and S685 were also mutants, at least in “7V8B_A”, “7V8A_B”, and “7V8A_C”. Twelve of the 13 were mutated from “rough” status to “precise”; only one mutant, D950N, showed no change. At least 92.31% of the antigens had evolved from “rough” to “precise”, and only 7.69% showed no change.
4.1 The longest fragments of G-free and with W antigen longer or equal than 37 amino acid
4.1.1 First wave of COVID-19 caused by D614
COVID-19 was broken out in Wuhan, China, on December 12, 2019. The original strain was D614.
From the sequence of D614, the four longest fragments of G-free and with W antigen longer or equal to 37 amino acids was found. They were D614, N148, and I358.
Before COVID-19 went mutated, the D614, N148, and I358 existed independent from any mutation.
For proteins or antigens, the SD of the molecular weight can work as an indicator of its “fineness”. The bigger the SD, the more the “fineness” or the more “precise” the protein or antigen is. In contrast, the smaller the SD, the “rougher” the protein or antigen is.
4.1.2 Second wave was caused by a mutation of D614 to D614G
The SD for D614 is 25.23. It is the smallest SD among the four longest antigens. It was mutated first on March 10, 2020. The mutated strain was D614G. The spike protein of SARS-CoV-2 contains about 1000 amino acids, and the D614 antigen contains only 37 amino acids. If this antigen mutated by chance, the possibility is only 3.7%, less than 5%, a small possibility. This mutation was not by chance, then by what?
The relationship between antigen and antibody is very similar to locker and key. A precision key can open any low-precision locker. The precision antibody should recognize and capture any low precession antibody. A precession key is a little smaller than the original key; otherwise, it cannot enter the space of the original locker. The D614G is a little smaller than D614 because G is the smallest amino acid.
Why did the mutation occur at D614 but not in the longer fragments, N148 or I358?
The virus would like to stay in the human body as long as possible. It would not to mutate the highest pressure status because the human body can generate the highest precision antibody to capture and neutralize it. If this were to happen, the virus could survive only 14 days in a single human body. The virus can stay in the human population for 3 months with the spread time.
The best way for the virus is to mutate to the next immediate degree. The D614G mutation proved this, and the precession was promoted from 25.23 to 26.74.
Therefore, the structure of D614G is the result of evolution, a more “precise” or complex status.
The human body has to generate more precession antibodies to recognize it.
The longest antigen, D614, worked as a factor to escape from the immune system; this is a factor to increase the infectivity of the virus.
4.1.3 Third wave was caused by mutation from D614G to Delta
The precession of D614G was promoted from 25.23 to 26.74. Which fragments will be mutated in the next immediate step?
The SD for N148 is 26.92 and the SD for I358 is 31.66. The virus would like to mutate the immediately next precision antigen, N148.
The third wave was caused by Delta subtype in October 2020 in India. N148 did mutate to a new antigen with three site mutations, E156del, F157del, and R158G, in this time and in the right order. The final precession was improved from 26.92 to 28.65. The size of the antigen was also decreased.
N148 is an antigen with 38 amino acids. If the mutation is mutated by chance, the single-site mutation rate is 3.8%, and if the three-site mutation happened in the N148 fragment, the mutation rate is 5.487 × 10−5. It is an extremely small possibility and not mutated by chance. It did mutate after the second wave of D614G, also 10 months after the first wave broke out in Wuhan, China,
The possibility of D614 mutated D614G, then mutated to Delta is lower than 2.03 × 10−6.
The longest antigens D614 and N148, worked as a factor to escape from the immune system; this is a factor to increase the infectivity of the virus.
4.1.4 Fourth wave was caused by mutation from Delta to Omicron
The precession of Delta was promoted from 26.92 to 28.65. Which fragments will be mutated in the next immediate step?
The SD for I358 is 31.66. This is the last choice for the virus to mutate in this antigen.
It did mutate on November 23, 2021, in the Omicron strain, leading to the fourth wave in South Africa.
The SD and the incubation time are shown to work in a dose-dependent manner. Such an effect is statistically significant, suggesting the order of evolution is correct and consistent with history. The D614G mutation happened first, the Delta subtype second, and the Omicron subtype third.
The I358 contains 41 amino acids. If the mutation happened by chance, the possibility was lower than 4.1% and a low possibility. It did not mutate by chance and mutated by the precession improvement. The possibility of D614 mutating to D614G, then mutating to Delta, then to Omicron is lower than 8.323 × 10−8.
Although the antigen precession did not predict the epidemic of the Alpha, Beta, and Gama subtypes, the failure of the prediction did prove it is true. The Alpha, Beta, and Gama subtypes did not form the major wave in the world. There were no cases in China for the three subtypes. The antigen precession can only predict the major epidemic.
The longest antigens, D614, N148, and I 358, worked as a factor to escape from the immune system; this is a factor to increase the infectivity of the virus.
4.2 The longest fragments of G-free and without W antigen longer or equal to 37 amino acid
The F718 fragment has an SD of 20.69, which is even smaller than 25.23. Why did this “rough” fragment not mutate? The possible reason might be the distribution of the amino acids as it did not contain any of the biggest amino acids, tryptophan (W). If any peptide did not contain “W”, it might not tend to be mutated in the first order.
To exclude the non-“W” fragments as potential candidates for evolution is a concern of statistical bias and could interfere with the SD calculations.
Tryptophan has its own biochemical functions, one being that it can be translated from a “stop codon”. It is reported that the Thymine-Guanine-Adenine (TGA, stop) codon in Spiroplasma is for tryptophan instead of a stop signal in other species [15].
Tryptophan may play an important role in the infectivity. It needed to be studied further.
4.3 Whole mutated fragments determine the virulence
In the 10 mutants of the Delta subtype, nine of them evolved from a “rough” to a “precise” status, with only one showing no change.
The 10 mutation was in eight antigens; these antigens were aligned, and the result was shown in Figure 5.
Let us ask why the detection limit for the wild type D614 SARS-CoV-2 was 21.5 copies; for Omicron, it was 14.3 copies, but for the Delta subtype, it raised to 32.0 copies [8].
The Delta subtype is the most difficult to detect, and this is to say the virus is most difficult to stay in the upper respiratory tract; instead, it is easy to deep in the lungs. The virus must have a loading amount to reach the detection limit. The increased loading virus caused more virulence. Most of the patients need oxygen. The need required oxygen was so huge that the news was reported about it in India in October 2020.
The possible reason for the increased virulence might be due to the Antibody Enhanced Effects (ADE). The previously generated low precession antibody will help the high precession antigen of Delta subtype enter the human body and cause inflammation.
At least 92.31% of the whole antigens had evolved from “rough” to “precise”, and only 7.69% showed no change. The whole antigen mutation in the Delta subtype determined the virulence of the virus.
4.3.2 The whole mutation antigens in Omicron subtype were at least 30 site mutations
The limit of the detection for the wild type D614 SARS-CoV-2 was 21.5 copies; for Omicron, it was 14.3 copies, but for the Delta subtype, it raised to 32.0 copies [8].
Omicron is easy to detect; this is to say the virus is easy to stay in the mouth but not easily deep in the lungs. Less virus loading will be found in the assays to reach the detection limit. And the less-loading virus caused weak virulence. The virulence should be weak in the Omicron strain. The virulence of Omicron was so weak, that many patients did not need any treatment.
Whole mutations antigen fragment in Omicron was over 30, but for most of them, the antigen precessions were decreased. If the majority of precessions were decreased, the whole precession would be displayed decreased, and the virulence of the virus would also decrease.
The previous high precession antibody will avoid the ADE when it meets the low antigen in the Omicron subtype.
The whole antigen mutation in the Omicron subtype determined the virulence of the virus.
4.3.3 Zero mutated antigen in D614 original wild subtype
The distribution rate of wild type in the up respiratory tract should be between Delta and Omicron. The distribution rate in the lung should also be between Delta type and Omicron type. The loading virus could be between the two. The virulence should be between those two types also.
Zero mutated D614 wild strain should have the basic virulence.
4.3.4 Whole mutated antigen in D614G subtype
This whole mutation was the same as the longest fragment mutation because it had only one mutation. The infectivity, for sure, was increased. There was a report that the D614G patients had a higher rate of entering the intensive care unit (ICU) than D614 patients [2].
To sum up, just like D614 mutated to D614G, the Delta subtype of SARS-CoV-2 started to conduct its evolution in “rough” status fragments. The final goal for evolution was the “precise” status.
The mutations in the Omicron types of SARS-CoV-2 also follow such rules, and we would like to discuss this in other papers.
According to our hypothesis, the “common precise” with high precession antigens of the SARS-CoV-2 could be designed in silicon, developed in a laboratory, and confirmed in animal models.
Such “common precise” antigens could be used to develop “common precise” antibodies. If the “common precise” antibodies were used in the antigen test, all the various antigens with lower or the same precise degrees could be detected. One antibody could detect numerous lower precession antigens, even the antigens not mutated yet now, but will be mutated in the next 3 years.
The evolution of antigens from “rough” status to “precise”, has two meanings. The first meaning is that, like a trip, the departure site starts first from the most “rough” antigen and last from the most “precise” antigen. The longest fragments did this work to determine virus infectivity. The second meaning is that the “rough” antigen’s evolution destination to “precise” antigens. The whole mutation antigens did this work to determine the virulence. This paper did focus on both topics. Beside for forecast mutation, understanding such rules of evolution can also help the development of reagents for detecting both “rough” and “precise” antigens, or even help with the development of the vaccines against SARS-CoV-2, as well as other infectious diseases. And finally, this information could help to control of the Covid-19, other epidemic infectious diseases, and tumors.
The longest antigen fragments determined virus infectivity. Whole mutated fragments determined the virulence. Both were associated with different mutated fragments with varied antigen precession in the Delta subtype of SARS-CoV-2.
This work was supported by project NTF21021, Research Starting Funding from Shantou University, and project 220513116490768, Medical Health Issue in Technical Plan from Shantou Science Technical Bureau.
Peijun Zuo searched for the information, performed the analysis, and wrote the paper. Professor Dr. Liping Li provided the key advice. Longlong Zuo and Zhihong Li did an interpretation of the data.
This is not a traditional epidemiological study to find the relation between protein molecules and the epidemic disease caused by the protein mutation. It did not contain any samples from humans and animals. A research ethics approval is not applicable.
Question: Were the virulence and infectivity associated with different fragments in the Delta subtype of SARS-CoV-2? Findings: The longest antigen fragments determined virus infectivity. Whole mutated fragments determined the virulence mutated from “rough” status to “precise”, with only one in ten showing no change. Meaning: In a SARS-CoV-2 pandemic, the SD of the molecular weight of amino acids, the indicator of “precession”, may be used to forecast the coming mutations. The longest D614 fragment, N148 fragment, and I358 fragment determined the infectivity. The whole mutations determined the virulence.
Abbreviations
A
alanine
C
cysteine
COVID-19
coronavirus disease 2019
D
aspartate
E
glutamate
F
phenylalanine
G
glycine
H
histidine
I
isoleucine
K
lysine
L
leucine
M
methionine
N
asparagine
P
proline
Q
glutamine
R
arginine
S
serine
SARS-CoV-2
Severe Acute Respiratory Syndrome Corona Virus 2
SD
standard deviation
T
threonine
W
tryptophan
V
valine
Y
tyrosine
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Written By
Peijun Zuo, Longlong Zuo, Zhihong Li and Liping Li
Submitted: 25 August 2023Reviewed: 25 August 2023Published: 04 October 2023
Open access peer-reviewed chapter
