Summary: The presentation fully discusses the SARS-CoV-2 and COVID-19 topic, dealing with genomics, morphology, origin, disease pathogenesis, immunology, prophylaxis, and the current situation. Presentation transcription Good morning. I thank everyone and I am honored to be among you. In few minutes my purpose is to provide some clarifications, alleviate some doubts, and possibly even focus on some risks. I will be very concise; you are kindly asked to follow my talk while looking at the slides. You will be able to review them later, more conveniently. The things I am going to tell are probably well known to Colleagues, to whom I apologize immediately; I wanted to recall them all since the audience is large and the dissemination of information in recent years has not always been equable and excellent. Confusion, unfortunately, has produced suffering and damage; Julius Caesar says, in the Shakespeare's tragedy, that man fears most what he does not know. We want to clarify what we do know! In slide (7) I summarized the presentation; in broad strokes we will discuss SARS-CoV-2 and COVID-19, we will address aspects involving morphology, origin, pathogenesis, immunology, prophylaxis, and the current situation. The first set of slides (8-15) summarizes the morphology and genomic characterization of SARS-CoV-2. The slides serve to remove any possible doubt about the knowledge of v. The virus is well known and has been classified. We know exactly what it looks like, how big it is (10nm, RNA+), how its genome is made up, and how it functions. SARS-CoV-2 (sl.9) has been assigned to a particular subgenus – Sabercovirus - because of its feature, unique among "relatives,": the ability to use ALSO the Ace-2 receptor (everyone has heard of it) to entry host cells. Let us recall (sl. 9) the aspect concerning the coefficient of reproduction of the virus usually denoted by R0: as you see, the data are always official, it is calculated to be between 2 and 4 and I can add that it is a characteristic coefficient of reproduction, horizontal and for what we have been able to see in our observations of value 3. We know EXACTLY the ability/speed of mutation of SCV2 (10-4 nucleotide substitution site/year) so, no surprises there and its genetic composition; in case of doubt just sequence the virus! From its sequence we derive any capability of the virus and can trace its origin (sl. 16-20). Phylogenetically speaking, the coronavirus family is very old, 25-50 million years, and this has allowed it to adapt gradually to many animal hosts, producing two natural consequences: 1. a pro-gressive reduction in pathogenicity; 2. a high genetic sharing. In simple words it means that coronaviruses evolving have produced little serious and generally less and less lethal diseases in animals and eventually in humans and that, in the DNA of animals we can find relics of this ancient cohabitation. I remind you that notably about 8% of the human genome represents the remains of previous infections; much DNA in eukaryotes is derived from the horizontal spread of foreign genetic material, mainly carried by viruses (Mol. Biology. NL Craig et al. 2022, Oxford). Nature makes use of this tool for evolutionary purposes, and among its benefits we find the viral interference, that is the ability to be little or no susceptible to infections -one out of many resources in our natural complex immunity. Slides 16-21, which I devoted to the ORIGIN topic, recall some important studies and conclude with George GAO's very recent statement, "there's no evidence which animals were where the virus comes from" (Cit.). Comfortable with this? Slides 21-24 summarize pathogenicity. The talk opens by recalling that in SARS-CoV-2 it does not differ from that of any other virus and is the result of the genetics of the virus and the reactions of the host. Whatever symptoms and course one wants to deal with, it is not permissible, within reason, to be surprised by it. The various stages of infection are covered in slides 25-29. The virus inserts its genetic information, aimed at its replication, into the cell. Although, as we have said, it is endowed with the ability to make use of the ACE2 receptor, entry into the cell is also assured to it by other pathways, which I summarize in slide 25. In slides 27-30 the phenomenon of de-coherence is briefly addressed: reactions involving translation, transcription, synthesis and replication, within cells, take place according to a NON-classical mechanics (that is why it is called decoherent); it ensures much greater efficiency and speed. This involves any kind of "genetic material." There is also an ancillary extra probability of error (sl. 39). When things are done, the virus inserts a killer signal (black spot) into the cell: we call this process ubiquitination (sl. 31-33). The cell having fulfilled its task of replicating the virus despite itself, dies. Slide 35 summarizes the ways in which the virus stays, reproduces and spreads (spreads) in relation to host immunity. We have known these for some time, and they are summarized and adapted to the present case here, taken from an article of mine, published in 2020 (https://scidoc.org/articlepdfs/IJBRP/IJBRP-2332-3000-09-201.pdf ). This should be enough to enlighten the way where recurrence, relapse and "Long COVID" are dealt. Sl. 36-38 illustrate some aspects of possible immune reactions, a severe case of MISC is taken up, in a 15aa) girl, with lymphocytic atypia and, again (38) of the generality. On prophylaxis (sl. 39-40), the definition of immunization is shown, and it is worth remembering that the mere expression of any antibody titer is reductive: susceptibility and immunity (natural or acquired) are MUCH more. Sl. 36 RECALLS THE RISKS OF DEFICIENT, INACCURATE OR CONFUSING INFORMATION. I christened it "apocryphal." The sl.42 calls all of us to strict caution: let us not make use of impressions, inappropriate terminologies and superficial knowledge. A suspension of genetic material carried in nanoliposomes and administered by injection is distributed to the body and acts in predictable and known ways. It produces effects and it is appropriate to dwell on this term: not adverse effects, simply effects. We talked about, so far, the functions of virus. Nanoliposomes do not "deliver to the cell" (it is written somewhere) the genetic material they contain. It (the genetic content), thanks to them, forcibly penetrates the cell, profiting from natural features of the membranes, and the mechanisms by which the fusion and entry into the interior (of virtually every cell that encounters the suspension) takes place are not a simple "delivery." Then, the genetic material that enters the cell is subjected to complex processing, in an environment, we have seen, that is decoherent, which, in many respects, can also involve the risk of errors (sl. 34 and 42). Errors that cannot be classified as “adverse events”: they simply are consequential events. Genetic material, processed within the cells, then must go out; there is no window or door through which this occurs. Almost exclusively, cell membrane rupture, then cell death, is required, with the release of even waste material, including foreign, useless, or harmful proteins, which inevitably trigger, at the sub-endothelial and tissue level, inflammatory reactions. Finally, any antihygienic genetic material produced will have to be carried into the body and presented to our immunocompetent cells: macrophages, lymphocytes, neutrophils... It will have to be exposed and, surely, everyone knows from general pathology that the antihygienic mosaic of which the body most frequently makes use is the erythrocyte membrane: it will be the erythrocytes that will carry the antigens that have been produced everywhere in the body. In conclusion we are talking (I have been extremely reductive) about a phenomenology quite different from that which characterizes the vaccines which, up to now, we have used. For that reason, I do not believe that we can make use, although I have seen that there is strong agreement in this regard, of the terminology that assigns the name of vaccine to products based on mRNA technology. The philosopher Lucretius (c. 99 BC – c. 55 BC) made use of sense neologisms when he had to translate Epicurus’ Greek terms into Latin words, and he did not have a suitable vocabulary; we have an excellent scientific terminology and I think we should be careful in assigning designations, not giving in to media or promotional suggestions. Epidemiology (sl. 43-44) offers a readable scenario and tools to analyze it and to answer any question. They are summarized in 13 points (45), and with them I conclude (46-47) spotting where we are and asking where we are going. I conclude (46-48), THANKING you for your kind attention (49). Giovanni Meledandri, Faculty Member Department of Human Sciences Guglielmo Marconi University of Rome 44, Via Plinio. 00192 Rome RM, Italy. email: g.meledandri@unimarconi
INTERDISCIPLINARY INSIGHTS FROM THE SARS-CoV-2 AND COVID-19
Meledandri G
2023-01-01
Abstract
Summary: The presentation fully discusses the SARS-CoV-2 and COVID-19 topic, dealing with genomics, morphology, origin, disease pathogenesis, immunology, prophylaxis, and the current situation. Presentation transcription Good morning. I thank everyone and I am honored to be among you. In few minutes my purpose is to provide some clarifications, alleviate some doubts, and possibly even focus on some risks. I will be very concise; you are kindly asked to follow my talk while looking at the slides. You will be able to review them later, more conveniently. The things I am going to tell are probably well known to Colleagues, to whom I apologize immediately; I wanted to recall them all since the audience is large and the dissemination of information in recent years has not always been equable and excellent. Confusion, unfortunately, has produced suffering and damage; Julius Caesar says, in the Shakespeare's tragedy, that man fears most what he does not know. We want to clarify what we do know! In slide (7) I summarized the presentation; in broad strokes we will discuss SARS-CoV-2 and COVID-19, we will address aspects involving morphology, origin, pathogenesis, immunology, prophylaxis, and the current situation. The first set of slides (8-15) summarizes the morphology and genomic characterization of SARS-CoV-2. The slides serve to remove any possible doubt about the knowledge of v. The virus is well known and has been classified. We know exactly what it looks like, how big it is (10nm, RNA+), how its genome is made up, and how it functions. SARS-CoV-2 (sl.9) has been assigned to a particular subgenus – Sabercovirus - because of its feature, unique among "relatives,": the ability to use ALSO the Ace-2 receptor (everyone has heard of it) to entry host cells. Let us recall (sl. 9) the aspect concerning the coefficient of reproduction of the virus usually denoted by R0: as you see, the data are always official, it is calculated to be between 2 and 4 and I can add that it is a characteristic coefficient of reproduction, horizontal and for what we have been able to see in our observations of value 3. We know EXACTLY the ability/speed of mutation of SCV2 (10-4 nucleotide substitution site/year) so, no surprises there and its genetic composition; in case of doubt just sequence the virus! From its sequence we derive any capability of the virus and can trace its origin (sl. 16-20). Phylogenetically speaking, the coronavirus family is very old, 25-50 million years, and this has allowed it to adapt gradually to many animal hosts, producing two natural consequences: 1. a pro-gressive reduction in pathogenicity; 2. a high genetic sharing. In simple words it means that coronaviruses evolving have produced little serious and generally less and less lethal diseases in animals and eventually in humans and that, in the DNA of animals we can find relics of this ancient cohabitation. I remind you that notably about 8% of the human genome represents the remains of previous infections; much DNA in eukaryotes is derived from the horizontal spread of foreign genetic material, mainly carried by viruses (Mol. Biology. NL Craig et al. 2022, Oxford). Nature makes use of this tool for evolutionary purposes, and among its benefits we find the viral interference, that is the ability to be little or no susceptible to infections -one out of many resources in our natural complex immunity. Slides 16-21, which I devoted to the ORIGIN topic, recall some important studies and conclude with George GAO's very recent statement, "there's no evidence which animals were where the virus comes from" (Cit.). Comfortable with this? Slides 21-24 summarize pathogenicity. The talk opens by recalling that in SARS-CoV-2 it does not differ from that of any other virus and is the result of the genetics of the virus and the reactions of the host. Whatever symptoms and course one wants to deal with, it is not permissible, within reason, to be surprised by it. The various stages of infection are covered in slides 25-29. The virus inserts its genetic information, aimed at its replication, into the cell. Although, as we have said, it is endowed with the ability to make use of the ACE2 receptor, entry into the cell is also assured to it by other pathways, which I summarize in slide 25. In slides 27-30 the phenomenon of de-coherence is briefly addressed: reactions involving translation, transcription, synthesis and replication, within cells, take place according to a NON-classical mechanics (that is why it is called decoherent); it ensures much greater efficiency and speed. This involves any kind of "genetic material." There is also an ancillary extra probability of error (sl. 39). When things are done, the virus inserts a killer signal (black spot) into the cell: we call this process ubiquitination (sl. 31-33). The cell having fulfilled its task of replicating the virus despite itself, dies. Slide 35 summarizes the ways in which the virus stays, reproduces and spreads (spreads) in relation to host immunity. We have known these for some time, and they are summarized and adapted to the present case here, taken from an article of mine, published in 2020 (https://scidoc.org/articlepdfs/IJBRP/IJBRP-2332-3000-09-201.pdf ). This should be enough to enlighten the way where recurrence, relapse and "Long COVID" are dealt. Sl. 36-38 illustrate some aspects of possible immune reactions, a severe case of MISC is taken up, in a 15aa) girl, with lymphocytic atypia and, again (38) of the generality. On prophylaxis (sl. 39-40), the definition of immunization is shown, and it is worth remembering that the mere expression of any antibody titer is reductive: susceptibility and immunity (natural or acquired) are MUCH more. Sl. 36 RECALLS THE RISKS OF DEFICIENT, INACCURATE OR CONFUSING INFORMATION. I christened it "apocryphal." The sl.42 calls all of us to strict caution: let us not make use of impressions, inappropriate terminologies and superficial knowledge. A suspension of genetic material carried in nanoliposomes and administered by injection is distributed to the body and acts in predictable and known ways. It produces effects and it is appropriate to dwell on this term: not adverse effects, simply effects. We talked about, so far, the functions of virus. Nanoliposomes do not "deliver to the cell" (it is written somewhere) the genetic material they contain. It (the genetic content), thanks to them, forcibly penetrates the cell, profiting from natural features of the membranes, and the mechanisms by which the fusion and entry into the interior (of virtually every cell that encounters the suspension) takes place are not a simple "delivery." Then, the genetic material that enters the cell is subjected to complex processing, in an environment, we have seen, that is decoherent, which, in many respects, can also involve the risk of errors (sl. 34 and 42). Errors that cannot be classified as “adverse events”: they simply are consequential events. Genetic material, processed within the cells, then must go out; there is no window or door through which this occurs. Almost exclusively, cell membrane rupture, then cell death, is required, with the release of even waste material, including foreign, useless, or harmful proteins, which inevitably trigger, at the sub-endothelial and tissue level, inflammatory reactions. Finally, any antihygienic genetic material produced will have to be carried into the body and presented to our immunocompetent cells: macrophages, lymphocytes, neutrophils... It will have to be exposed and, surely, everyone knows from general pathology that the antihygienic mosaic of which the body most frequently makes use is the erythrocyte membrane: it will be the erythrocytes that will carry the antigens that have been produced everywhere in the body. In conclusion we are talking (I have been extremely reductive) about a phenomenology quite different from that which characterizes the vaccines which, up to now, we have used. For that reason, I do not believe that we can make use, although I have seen that there is strong agreement in this regard, of the terminology that assigns the name of vaccine to products based on mRNA technology. The philosopher Lucretius (c. 99 BC – c. 55 BC) made use of sense neologisms when he had to translate Epicurus’ Greek terms into Latin words, and he did not have a suitable vocabulary; we have an excellent scientific terminology and I think we should be careful in assigning designations, not giving in to media or promotional suggestions. Epidemiology (sl. 43-44) offers a readable scenario and tools to analyze it and to answer any question. They are summarized in 13 points (45), and with them I conclude (46-47) spotting where we are and asking where we are going. I conclude (46-48), THANKING you for your kind attention (49). Giovanni Meledandri, Faculty Member Department of Human Sciences Guglielmo Marconi University of Rome 44, Via Plinio. 00192 Rome RM, Italy. email: g.meledandri@unimarconiI documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.
