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COVID-19 antivirals and vaccines (Megathread)

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1 minute ago, CharonY said:

I vaguely remember such data but am not sure whether it was about viruses. I am going to have a look.

Would prepping rooms with an ozonator be any good for disinfecting rooms before admitting vulnerable people? I know it's not safe whilst in use.

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2 hours ago, StringJunky said:

Would prepping rooms with an ozonator be any good for disinfecting rooms before admitting vulnerable people? I know it's not safe whilst in use.

I am not sure, ozonation, UV treatment and disinfectant fogging are being used in certain biocontainment facilities, but I don't know whether they would work and/or may be harmful in patient care facilities. The latter are often more crowded than biological workspaces and patients are more vulnerable to ozone, for example. 

I know that fogging is not allowed but I don't think that there are recommendations regarding UV and ozone in patient care (to my knowledge).

Theoretically one could establish a protocol with thorough ozonation followed by quantitative ventilation or quenching to ensure safe levels. But again, I do not know if folks have tried or studied that.

 

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I was not thinking about patient treatment, either giving them sunburn or cooking them.

I was really thinking about decontamination, for instance whether to turn the washing machine temperature up or expose stuff to the strong sunlight we have at the moment.

And I was tryi g to fit into Hypervalent Iodine's one of three threads as requested.

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6 minutes ago, studiot said:

I was not thinking about patient treatment, either giving them sunburn or cooking them.

I was really thinking about decontamination, for instance whether to turn the washing machine temperature up or expose stuff to the strong sunlight we have at the moment.

And I was tryi g to fit into Hypervalent Iodine's one of three threads as requested.

Well, there are recommendations for decontamination of hospital bedding and clothing. Heat alone is seemingly insufficient for full decontamination based on above data, but a combination of heat/detergent/bleach might be. For sun light one might calculate the output for UVC and see whether that may be high enough, I suppose.

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1 hour ago, CharonY said:

I am not sure, ozonation, UV treatment and disinfectant fogging are being used in certain biocontainment facilities, but I don't know whether they would work and/or may be harmful in patient care facilities. The latter are often more crowded than biological workspaces and patients are more vulnerable to ozone, for example. 

I know that fogging is not allowed but I don't think that there are recommendations regarding UV and ozone in patient care (to my knowledge).

Theoretically one could establish a protocol with thorough ozonation followed by quantitative ventilation or quenching to ensure safe levels. But again, I do not know if folks have tried or studied that.

 

OK. Cheers.

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Posted (edited)

CAN LYSINE AND LYSINE ANALOUGES HAVE POTENTIAL ROLE IN PREVENTING VIRAL SPIKE PROTEIN AND ANGIOTENSIN CONVERTING ENZYME 2 (ACE2) ECTODOMAIN INTERACTION

A OBSERVATION

 

 

 

INTRODUCTION:

 

COVID-19 or SARS COV 2, is a beta coronavirus, with a positive sense single stranded RNA, responsible for the current 2020 Coronavirus pandemic in about 180+ countries, leading to more than a million cases , 50,000+ deaths.

The world scientific community has been quick to respond with valuable research papers, candidate drug trials and vaccine development programmes.

Many of the drugs, currently approved by the world FDAs have been able to cure the patients, but with prolonged treatment time and comparatively non responsive to patients with co morbidities, or to the complications arising from the infection ( cytokine storm, septic shock, renal failure, ARDS).

Such scenario is very clear in countries like Italy, Spain, and recently The USA.

 

CONTENTS:

1.       PATHOGENESIS OF RECEPTOR INTERACTION AND FUNCTION OF LYSINE

2.       MECHANISM OF LYSINE ANALOUGES.

3.       CONCLUSION

 

 

 

 

 

PATHOGENESIS OF RECEPTOR INTERACTON AND FUNCTION OF LYSINE

SARS COV 1 and SARS COV 2 have been found to target the same human ACE2 receptors as entry points to the cell. Human ACE2 is expressed  in Lungs , kidneys  and also in the CNS.

According to the studies published in (https://doi.org/10.1007/s00134-020-05985-9)

( Haibo Zhang1,3,6 , Josef M. Penninger4,5, Yimin Li3, Nanshan Zhong3 and Arthur S. Slutsky1,2,3*)

 

“There are many similarities of SARS-CoV-2 with the original SARS-CoV. Using computer modeling, Xu et al. [6] found that the spike proteins of SARS-CoV-2 and SARS-CoV have almost identical 3-D structures in the

receptor-binding domain that maintains van der Waals forces. SARS-CoV spike protein has a strong binding affinity to human ACE2, based on biochemical interaction studies and crystal structure analysis [7]. SARSCoV-2 and SARS-CoV spike proteins share 76.5% identity in amino acid sequences [6] and, importantly, the SARSCoV-2 and SARS-CoV spike proteins have a high degree of homology [6, 7]. Wan et al. [4] reported that residue 394 (glutamine) in the SARS-CoV-2 receptor-binding domain (RBD), corresponding to residue 479 in SARS-CoV, can be recognized by the critical lysine 31 on the human ACE2 receptor [8]. Further analysis even suggested that SARS-CoV-2 recognizes human ACE2 more efficiently than SARS-CoV increasing the ability of SARS-CoV-2 to transmit from person to person [4]. Thus, the SARS-CoV-2 spike protein was predicted to also have a strong binding affinity to human ACE2. This similarity with SARS-CoV is critical because ACE2 is a functional SARS-CoV receptor in vitro [9] and in vivo [10]. It is required for host cell entry and subsequent viral replication. Overexpression of human ACE2 enhanced disease severity in a mouse model of SARS-CoV infection, demonstrating that viral entry into cells is a critical step [11]; injecting SARS-CoV spike into mice worsened lung injury. Critically, this injury was attenuated by blocking the renin-angiotensin pathway and depended on ACE2 expression [12]. Thus, for SARS-CoV pathogenesis, ACE2 is not only the entry receptor of the virus but also protects from lung injury. We therefore previously suggested that in contrast to most other coronaviruses, SARS-CoV became highly lethal because the virus deregulates a lung protective pathway”

 

Going into a little bit more detail about the SARS COV2 residue 394 ( glutamine)on viral RBD and critical lysine 31 on ACE2 receptor,

The study emphasizes on the interaction  between  different residues of  viral  receptor binding domain and lysine residues of ACE 2 of both human and civet.

(.https://doi .org/10.1128/JVI.00127-20.)

(Yushun Wan,a Jian Shang,a Rachel Graham,b Ralph S. Baric,b Fang Lia)

“First, residue 493 in 2019-nCoV RBD (corresponding to residue 479 in SARS-CoV) is a glutamine (Fig. 1B and D). A previously designed SARS-CoV RBD is optimal for binding to human ACE2 (Fig. 1B and C)(26). According to the structure of this designed RBD, residue 479 is located near virus-binding hot spot Lys31 (i.e., hot spot 31) on human ACE2 (Fig. 1C). Hot spot 31 consists of a salt bridge between Lys31 and Glu35 buried in a hydrophobic environment. In civet SARS-CoV RBD (year 2002), residue 479 is a lysine, which imposes steric and electrostatic interference with hot spot 31. In human SARS-CoV RBD (year 2002), residue 479 becomes an asparagine. The K479N mutation removes the unfavorable interaction at the RBD-human ACE2 interface, enhances viral binding to human ACE2, and plays a critical role in the civet-to-human transmission of SARS-CoV (Fig. 1C)(24–26). Here, we constructed a structural model for the complex of 2019-nCoV RBD and human ACE2 (Fig. 1D). Importantly, Gln493 in 2019-nCoV RBD is compatible with hot spot 31, suggesting that 2019-nCoV is capable of recognizing human ACE2 and infecting human cells. Second, residue 501 in 2019-nCoV RBD (corresponding to residue 487 in SARS-CoV) is an asparagine (Fig. 1B and D). Based on our previous structural analysis, residue 487 in SARS-CoV is located near virus-binding hot spot Lys353 (i.e., hot spot 353) on human ACE2 (Fig. 1C)(26). Hot spot 353 consists of a salt bridge between Lys353 and Asp38 also buried in a hydrophobic environment. In civet SARS-CoV RBD (year 2002), residue 487 is a serine, which cannot provide favorable support for hot spot 353. In human SARS-CoV isolated in year 2002, residue 487 is a threonine, which strengthens the structural stability of hot spot 353. The S487T mutation adds the favorable interaction at the RBD-human ACE2 interface, enhances viral binding to human ACE2, and plays a critical role in the human-to-human transmission of SARS-CoV (24–26). In human SARS-CoV isolated in year 2003, residue 487 is a serine and there was no human-to human transmission for this SARS-CoV strain. “

 

 

INFERENCE

1.       The viral RBD residues are primarily recognizing lysine residues on the ACE2 receptors.

2.       There is involvement of breaking of salt bridges ( electrostatic and hydrogen bonds) between lysine residues and similar amino acids on the ACE 2 receptor.

3.       It can be said that the RBD of viral sipke protein acts as lysine receptor.

4.       The viral glutamine and asparagine residues are capable of breaking salt bridge bonds on the ACE2  receptor.

 

 

 

 

 

 

 

MECHANISM OF LYSINE ANALOUGES:

Lysine analogues such as Tranexemic acid , aminocaproic acid are antifibrinolytic agents.

Tranexamic acid is a synthetic derivative of the amino acid lysine and inhibits fibrinolysis by reversibly binding to lysine-binding sites on plasminogen, thereby preventing the cleavage of fibrin.

 

Now about the lysine residues on fibrin and binding of plasmin to the lysine residues:

. https://febs.onlinelibrary.wiley.com/doi/pdf/10.1016/0014-5793(85)81150-9

 

“Plasmin catalysed hydrolysis of fibrinogen results primarily in the formation of fibrinogen fragments with C-terminal lysine residues, since plasmin preferentially cleaves Lys-Xaa bonds of fibrinogen”

 

“the Cterminal lysine residues of fibrinogen fragments are essential for high-affinity binding of the fragments to plasminogen, then any protein or peptide with C-terminal lysine residue may bind plasminogen and be a modulator of enzyme systems that involve plasminogen.”

 

 

OBSERVATION:

1.       SIMILARITY OF THE CONTEXT OF MECHANISMS IN BOTH THE CASES

1.       BOTH SYSTEM REQUIRES LYSINE BINDING (PLASMINOGEN AND VIRAL SPIKE PROTEIN)

2.       BOTH  SYSTEM HAS SERINE PROTESE ASSISTNG THE MECHANISM ( UROKINASE  AND TMPRSS2 –TRANSMEMBRANE PROTEASE SERINE 2)(FOR REFERENCE-https://doi.org/10.1007/s00134-020-05985-9)

3.       BOTH SYSTEM REQUIRES BREAKING OF EXISTING LYSINE RESIDUE BONDS ( PEPTIDE AND SALT BRIDGES RESPECTIVELY)

HENCE THEORETICALLY,  IT CAN BE OBSERVED THAT LYSINE ANALOUGES ( TRANEXEMIC ACID, AMINOCAPROIC ACID) WHO ARE PROVEN ANTI FIBRINOLYTICS, CAN BE PUT TO TEST TO CHECK THE POTENTIAL ON PREVENTING THE INTERACTION BETWEEN VIRAL SPIKE PROTEIN AND ACE2 RECEPTOR.

 

 

ACKNOWLEDGEMENT: REFERENCE:  1. https://doi.org/10.1007/s00134-020-05985-9

2.       .https://doi .org/10.1128/JVI.00127-20.

3.       . https://febs.onlinelibrary.wiley.com/doi/pdf/10.1016/0014-5793(85)81150-9

 

PLEASE GIVE YOUR VALUABLE OPINION

 

Edited by Strange
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1 hour ago, RAJDEEP said:

ACKNOWLEDGEMENT: REFERENCE:  1. https://doi.org/10.1007/s00134-020-05985-9

2.       .https://doi .org/10.1128/JVI.00127-20.

3.       . https://febs.onlinelibrary.wiley.com/doi/pdf/10.1016/0014-5793(85)81150-9

!

Moderator Note

Please do not post copyrighted articles. It is unnecessary when you have provided links to the sources.

Also, please make it clearer what you are quoting from elsewhere and what parts are your contribution. It is impossible to have a discussion, otherwise.

 

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Ok, thank you

The inference , content, and observation are my contribution.

The pathogenesis and mechanism of lysine analouges are quoted from studies.

Thank you for informing me

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There was a short but heartening article on tonight's 10 O'Clock local News .

The University of Bristol has developed a new class of totally artificial vaccine and has one ready for trial against Covid-19.

The explanation given was that they have developed a suitable base molecule to attach fragments of the covid virus to, in order to fool/stimulate the body's defneces into producing the necessary antibodies.

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Data from some compassionate uses of treatments are starting to come up. I do not the time to follow them closely, but the antiviral Remdesivir seems to show beneficial effects in a small cohort of 61 patients. The important bit here is that among the cohort were folks with stronger symptoms with 57% being on ventilators, and 8% even being on ECMO (in comparison hydroxycholoroquine, showed no beneficial effect for patients  with such advanced symptoms). In 68% of the patients improvement in oxygen-support were detected. However, a controlled trial will be necessary to ascertain that these improvements are indeed due to the drug.

The antiviral used for HIV/AIDS treatment (LPV/r) did not seem to show any benefits or at best very weak ones.

For favipiravir one recently published study seems to be on hold, so no idea what the issue is there. But from another weak benefits were reported.

 

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8 minutes ago, CharonY said:

Data from some compassionate uses of treatments are starting to come up. I do not the time to follow them closely, but the antiviral Remdesivir seems to show beneficial effects in a small cohort of 61 patients. The important bit here is that among the cohort were folks with stronger symptoms with 57% being on ventilators, and 8% even being on ECMO (in comparison hydroxycholoroquine, showed no beneficial effect for patients  with such advanced symptoms). In 68% of the patients improvement in oxygen-support were detected. However, a controlled trial will be necessary to ascertain that these improvements are indeed due to the drug.

The antiviral used for HIV/AIDS treatment (LPV/r) did not seem to show any benefits or at best very weak ones.

For favipiravir one recently published study seems to be on hold, so no idea what the issue is there. But from another weak benefits were reported.

 

Just read Japan is offering Favipiravir to countries for testing.

Quote

Japan to offer anti-flu Avigan drug to 20 virus-hit nations for free

Japan plans to provide the anti-flu drug Avigan for free to 20 countries hoping to use it to treat coronavirus patients, Foreign Minister Toshimitsu Motegi said Tuesday.

The 20 countries receiving the drug, which is currently undergoing clinical tests, include Bulgaria, the Czech Republic, Indonesia, Iran, Myanmar, Saudi Arabia and Turkey, with an additional 30 countries showing interest, according to Motegi.

Japan will provide the United Nations Office for Project Services with a $1 million grant to buy and distribute the drug, also known as Favipiravir, which is developed by a subsidiary of Fujifilm Holdings Corp.

“We will work with interested countries to expand clinical research on Avigan internationally,” the foreign minister told a news conference.

Researchers at Wuhan University and other institutions in China have said the drug was effective on coronavirus patients, especially for those with mild symptoms of COVID-19.

https://www.japantimes.co.jp/news/2020/04/07/national/science-health/coronavirus-japan-avigan-20-nations-free/

 

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Yes there were two studies I have seen, one showing modest effects, but again only in cases with mild symptoms (making it harder to assess whether it is useful, especially based on small cohorts), whereas the other one got a note that it is being on hold, not sure why yet.

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24 minutes ago, CharonY said:

Yes there were two studies I have seen, one showing modest effects, but again only in cases with mild symptoms (making it harder to assess whether it is useful, especially based on small cohorts), whereas the other one got a note that it is being on hold, not sure why yet.

I read some lung specialists are diverging from intubation, wondering if it's causing more harm than good, and trying to establish what's actually happening in the alveoli. They are trying clot busters and blood thinners to try and keep their patients alive. It looks like research is happening in the field in the raw. It must be very taxing for them.

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Here is what I could read and understand about vaccines.

The vaccine will depend on the mutation rate of the surface antigen (Spike protein). Protein S gathers in trimers on the surface of virions and plays a key role in the entry of the virus into its target cell. After the advanced protein binds to the human cell receptor, the viral membrane fuses with the human cell membrane, allowing the genome of the virus to enter human cells.

We now detect three distinct variants of covid-19. Type A, B and C. I do not know if these mutations come from the S or L strains. Chinese researchers have also identified 149 minor variants among the 103 genomes analyzed. Indeed RNA viruses mutate much more easily and more quickly than DNA viruses, because with each replication, nucleic acids are poorly copied.

My question is: The result of the mutation of the surface antigen is therefore more likely to degrade, than to succeed in a new link mechanism and membranes fusion, since they replicate poorly?
 

I would even say that the virus is doomed to its loss.

But I have also just seen that the purpose of mutating the virus is to overcome the resistance of the human immune system.

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21 hours ago, StringJunky said:

I read some lung specialists are diverging from intubation, wondering if it's causing more harm than good, and trying to establish what's actually happening in the alveoli. They are trying clot busters and blood thinners to try and keep their patients alive. It looks like research is happening in the field in the raw. It must be very taxing for them.

No doubt, trying things on the fly and in the middle of an emergency is not something take lightly. There will be an urgent need for mental health care.

16 hours ago, Kartazion said:

Indeed RNA viruses mutate much more easily and more quickly than DNA viruses, because with each replication, nucleic acids are poorly copied.

That is not the reason per se, as obviously in both RNA and DNA viruses the genetic material needs to be amplified and both can incorporate errors. There are a few mechanisms, such as polymerases, exoribonucleases  and other enzymes that may proofreading functions and thereby reduce mutations. Coronaviruses have such functions and therefore have a lower mutation rate compared to other RNA viruses and put them in the upper range of DNA viruses (~10^-7 - 10^-6 for SARS-CoV, I believe similar for SARS-CoV-2).

16 hours ago, Kartazion said:

My question is: The result of the mutation of the surface antigen is therefore more likely to degrade, than to succeed in a new link mechanism and membranes fusion, since they replicate poorly?

The mutations are not necessarily in the spike protein, if that is what you are asking. Mutations are going to accumulate in areas that do not inhibit the ability of the virus to propagate. In fact, some of the mutations observed are "silent" meaning that the codon changes, but as a whole still codes for the same amino acid (this includes mutations in the spike and nucleocapsid genes). These mutations are unlikely to result in significant phenotypic differences. 

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As I have advised previously about this subject, I'm no expert or deemed to have any professional understanding of this subject, but a research medical journal I read advised back in 2017 about corona virus and trials that were being carried out back then. You start to get to a point that you hear people on the TV in the medical world with a lifetime of experience trying to advise you things that they are being told to keep their mouths shut about. Two doctors on the TV recently tried to speak out about this virus and one doctor was told to shut up and could not say what he wanted, and the other doctor had contracted the virus and since has past away. Recent information I've read had this to say about the corona-virus going back as far as 2017;

 Ivermectin

Lab tests performed by Australian researchers showed that this anti-parasitic drug stopped the coronavirus growing in cell cultures within 48 hours. This widely available drug has already been shown to be effective against other viruses including HIV, dengue, flu and Zika. 

Ivermectin is already approved by drug regulators and is widely available although it would have to be trialled in patients before becoming an accepted therapy.  

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1 hour ago, CharonY said:

The mutations are not necessarily in the spike protein, if that is what you are asking. Mutations are going to accumulate in areas that do not inhibit the ability of the virus to propagate. In fact, some of the mutations observed are "silent" meaning that the codon changes, but as a whole still codes for the same amino acid (this includes mutations in the spike and nucleocapsid genes). These mutations are unlikely to result in significant phenotypic differences. 

Thanks a lot for your answers.

I concluded that these mutations, as numerous as they are, only very rarely result in a change in phenotype and viral function. In other words, the vaccine worked today will again be effective in 3 or 6 months.

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After SARS folks started working on therapeutics and vaccines. However, quite a few studies were ended or stopped once it became clear that SARS appeared to be fairly contained, so research funding stopped or was severely reduced. The clinicals are the expensive bit so often if money is lacking, they do not continue.

The good news is that current therapeutics in pipelines are often based on previous data collected on SARS-CoV or other coronaviruses. Otherwise the start would be much slower.

Just now, Kartazion said:

I concluded that these mutations, as numerous as they are, only very rarely result in a change in phenotype and viral function. In other words, the vaccine worked today will again be effective in 3 or 6 months.

It depends on what is being the antigen. Often folks concentrate on essential proteins such as the spike protein as if that one changes significantly, the virus may have a harder time to infect. These essential proteins are therefore often conserved (which means that the amino acid sequenece of the proteins is going to change less than non-conserved proteins).

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1 hour ago, Casio said:

Recent information I've read had this to say about the corona-virus going back as far as 2017; 

It was in 1930 in the United States that the first disease caused by a coronavirus was observed in poultry. It was in 1965 that the first coronavirus infecting humans (strain B814) was discovered.

22 minutes ago, CharonY said:

It depends on what is being the antigen. Often folks concentrate on essential proteins such as the spike protein as if that one changes significantly, the virus may have a harder time to infect. These essential proteins are therefore often conserved (which means that the amino acid sequenece of the proteins is going to change less than non-conserved proteins).

Act with the synthetic antigen to identify the virus in all its aspects? Will the immune response be effective in causing the production of special proteins for covid-19?

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1 hour ago, Kartazion said:

Act with the synthetic antigen to identify the virus in all its aspects? Will the immune response be effective in causing the production of special proteins for covid-19?

I am not sure what you mean here. Perhaps some clarifications (in case that is the issue). An antigen is basically any substance to which antibodies can bind to. Once antibodies bind to the foreign substance they can eliminated following a number of pathways. 

An artificial antigen would essentially be the same protein (or parts of it, technically you just need a good epitope) but synthesized in vitro, rather than taking a virus and take fragments of it. However, the structure and sequence would identical to the real thing (for the biding site) in order to work.

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1 hour ago, CharonY said:

I am not sure what you mean here.

I meant to say making a synthetic antigen and injecting it into the patient so that his immune defense evolves.
I see that it is very technical. Thank you again.

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2 hours ago, Kartazion said:

I meant to say making a synthetic antigen and injecting it into the patient so that his immune defense evolves.
I see that it is very technical. Thank you again.

No, evolution in the technical sense does not apply here (evolution is a process describing gene pool changes within a population over generations). The adaptive response needs the target from the virus (or something identical you synthesize using the genetic code of the virus) .

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23 hours ago, CharonY said:

No, evolution in the technical sense does not apply here (evolution is a process describing gene pool changes within a population over generations).

I had omitted that the term evolution was a specific stage reserved for the discipline of biology. I meant a database of immune memory that would be expanded and completed. I then discovered a strange organ because of its location in the body. The thymus.

23 hours ago, CharonY said:

The adaptive response needs the target from the virus (or something identical you synthesize using the genetic code of the virus) .

Here's what I could figure out. When the antigen is detected by the human body, it then produces lymphocytes ; B cells for antibodies, and T cells that destroy the infected cells.
So why can't the immune system eradicate covid-19 in just a few moments? It's overwhelmed by the virus? Because the vaccine is giving the body time to prepare a sufficient number of antibodies?

I hope I'm not off topic.

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16 hours ago, Kartazion said:

Here's what I could figure out. When the antigen is detected by the human body, it then produces lymphocytes ; B cells for antibodies, and T cells that destroy the infected cells.

It is quite a bit more complex than that but it would require a lengthier explanation. Simply put is that while adaptive (as well as innate) responses can clear infections, obviously. However, at the same time pathogens have mechanisms that can delay or evade responses. Viruses replicate intracellularly, so once they managed to get into cells, they can remain hidden until the cells produces viral particles. There are also various strategies that keep those particles hidden from the host for longer. Simply speaking, if there are only few particles around who are not slipping into cells yet the immune system can clear them. But it is essentially a race between how well the virus hides and replicates vs the immune system finding viruses and infected cells.

 

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1 hour ago, CharonY said:

Viruses replicate intracellularly, so once they managed to get into cells, they can remain hidden until the cells produces viral particles. There are also various strategies that keep those particles hidden from the host for longer. Simply speaking, if there are only few particles around who are not slipping into cells yet the immune system can clear them.

This means that covid-19 can make a viral rebound and be reactivated in the case of a person who is already a carrier. 
The vaccine won't provide a solution if the virus is hiding. The vaccine will only be effective if the person has never had the virus, right?
 

I found this in addition to info:

Quote

The coronavirus genes has as many as 29 proteins, which perform a range of tasks from copying coronaviruses to suppressing the body's immune responses.

Protein NSP10 (Genetic Camouflage)
Human cells have antiviral proteins that find viral RNA and shred it. This protein works with NSP16 to camouflage the virus’s genes so that they don’t get attacked. 

Protein NSP15 (Cleaning Up) 
Researchers suspect that this protein chops up leftover virus RNA as a way to hide from the infected cell’s antiviral defenses.

Protein NSP16 (More Camouflage)
NSP16 works with NSP10 to help the virus’s genes hide from proteins that chop up viral RNA. 

 

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