Tell me, It is wrong on Infection?

The virus triggers cell division via the mitotic mechanism. The mitotic mechanism makes a copy of the original cell including the virus.

I’m no virologist (it’s been 25 years since I did undergrad microbiology), but that’s not my understanding of viruses that infect mammalian cells. My understanding is that viruses proliferate by subverting (hijacking, if you will) the machinery of the cell cycle but don’t actually stimulate the cell cycle. It’s the reverse – they stall, or at least slow, the cell cycle by associating with cell cycle components, like cyclins and cyclin-dependent kinases, and using them to drive the protein replication pathways in order to make new viral particles.

If we destroy the cells mitotic (MTOC) centers, the cell cannot divide and dies, killing the virus in the process.

Hmmm. Mitotic inhibitors are quite toxic and produce a variety of very unpleasant side-effects. They are used as anti-cancer drugs where the side-effects are not as bad as the alternative. Look up drugs like paclitaxel, docetaxel and vincristine. I don’t see them as a viable general anti-viral medication.
 
These links seem to be advertising puffery, for the makers of a supercomputer, which tell us nothing about the virus.
We need to understsnd term, Covid Camouflage for how virus avoid innate and humurol immune response and how host cells allow its entry into them. Simply, it is taken as a sugar nutrint by these instead of pathogen at least upto pre entry level into cells.
 
Look up drugs like paclitaxel, docetaxel and vincristine
I admit my limited knowledge, but I am very interested in the mechanics of cell division. It seems to me that might offer a possible path to inhibit the spread of a virus by inhibiting cell division.

In this case, I am thinking more along the lines of disrupting the centriole functions involved in the mitotic spindle which is responsible for transcription and separation of all cell contents in the process of cell division.

Inhibit the centriole and you inhibit cell division ??
If so, the host cell and its unwanted guest cannot multiply and both die??

It's really not an anti-virus procedure, but an anti-mitotic procedure, simply preventing cell from dividing altogether......:?
 
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Mitotic inhibitors are quite toxic and produce a variety of very unpleasant side-effects.
Ahh, yes, the cure is worse than the disease.
But allow me one more question before I'll sit back and just follow the conversation.

Am I correct in assuming that the tau protein is responsible for MT stabilization in the centrioles or centrosomes?
Tau protein is abundant in the central nervous system and involved in microtubule assembly and stabilization. It is predominantly associated with axonal microtubules and present at lower level in dendrites where it is engaged in signaling functions.
Dysfunction of tau protein may contribute to collapse of cytoskeleton, thereby causing improper anterograde and retrograde movement of motor proteins and their cargos on microtubules. These disturbances in intraneuronal signaling may compromise synaptic transmission as well as trophic support mechanisms in neurons.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3975420/

and this;

What is Centrosome?

Historically, the centrosome was also discovered by Edouardo van Beneden in 1883, and was named by Theodor Boveri in 1889.
  • The centrosome of a cell, is the organelle which acts as the primary microtubule organizing center of the cell.
  • It comprises of the centrioles along with a dense mass of protein known as the peri-centriolar material that surrounds it. It is an important regulator of the cell cycle.
  • In contrast to centrioles, centrosomes come into play during prophase of the cell cycle. It is found attached to the nuclear membrane, and is released at the end of prophase when the chromosomes start to align at the equator to begin the process of mitotic spindle formation.
  • After being released, they migrate to the poles of the cell. Each cell contains one centrosome, which replicates itself during the S phase of the cell cycle before mitosis.
  • After cell division and cytokinesis, each daughter cell receives one copy of the centrosome. Defects in centromeres can also lead to disease such as cancer, usually caused by an abnormal number of centrosomes. [/quote]
https://www.bioexplorer.net/centrosome-vs-centriole.html/

p.s. I hope this will not be considered Off Topic. Seems pertinent to me, but if I am wrong please accept my apologies..
 
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I admit my limited knowledge, but I am very interested in the mechanics of cell division. It seems to me that might offer a possible path to inhibit the spread of a virus by inhibiting cell division.

In this case, I am thinking more along the lines of disrupting the centriole functions involved in the mitotic spindle which is responsible for transcription and separation of all cell contents in the process of cell division.

Inhibit the centriole and you inhibit cell division ??
If so, the host cell and its unwanted guest cannot multiply and both die??

It's really not an anti-virus procedure, but an anti-mitotic procedure, simply preventing cell from dividing altogether......:?
I think, resisting a thief at entry door
I admit my limited knowledge, but I am very interested in the mechanics of cell division. It seems to me that might offer a possible path to inhibit the spread of a virus by inhibiting cell division.

In this case, I am thinking more along the lines of disrupting the centriole functions involved in the mitotic spindle which is responsible for transcription and separation of all cell contents in the process of cell division.

Inhibit the centriole and you inhibit cell division ??
If so, the host cell and its unwanted guest cannot multiply and both die??

It's really not an anti-virus procedure, but an anti-mitotic procedure, simply preventing cell from dividing altogether......:?
Btw, should we not first try to see if theif could possibly be resisted at entry gate level instead of dealing it after it entered house and taken control of that? Will it not be too muchdmuch complicated and less fruitful task?
 
I think, resisting a thief at entry door
Oh that would be excellent, if you know who is knocking on the door.
Btw, should we not first try to see if they could possibly be resisted at entry gate level instead of dealing it after it entered house and taken control of that? Will it not be too muchdmuch complicated and less fruitful task?
Sure, seems to me that would be the perfect defense. But how would one achieve that objective? Seems there are three possible defense strategies.

(a) Do we change the virus before it enters the cell, or (b) do we change the cell to make it impenetrable, or (c) do we prevent the cell from dividing before the virus becomes virulent after the cell has been invaded?

My understanding is that when we kill viruses or bacteria, eventually they will develop immunity or mutate into a more resistant strain. I believe Covid19 is mutating fairly regularly. Seems this is a tricky one.

There is an effort on the way which, rather than killing the organism, tries to make bacteria (and perhaps viruses) "deaf and dumb" so that they never become virulent. According to Bonnie Bassler this has worked on bacteria by introducing false chemical signals which render bacteria "deaf" or unable to "communicate", via "quorum sensing.

Earlier I posted about research showing that viruses also communicate and employ quorum sensing, so perhaps we might be able to render them deaf and dumb without altering the virus itself, but by introducing confusing "language". But that still requires a knowledge of the specific language the viruses use to communicate.

In this case I speculated that regardless of any adaptive mutation, perhaps we could just prevent the host cell from dividing (shutting down the power in the house, so to speak), thus effectively trapping the virus in the cell, until both cell and virus die. This would prevent the need for constantly trying to keep up with any mutations.

We do not need to kill anything, all we need is a universal method of shutting down mitosis.

I'll leave it here and just follow the thread as it develops. Thanks for your kind indulgence.
 
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Oh that would be excellent, if you know who is knocking on the door.
Sure, seems to me that would be the perfect defense. But how would one achieve that objective? Seems there are three possible defense strategies.

(a) Do we change the virus before it enters the cell, or (b) do we change the cell to make it impenetrable, or

My understanding is that when we kill viruses or bacteria, eventually they will develop immunity or mutate into a more resistant strain. I believe Covid19 is mutating fairly regularly. Seems this is a tricky one.

There is an effort on the way which, rather than killing the organism, tries to make bacteria (and perhaps viruses) "deaf and dumb" so that they never become virulent.

Above should be primary defense. Like weakening the theif and resisting it at entry gate.For it, please refer my previous posts. Rest all other should be secondary issues like handling a theif after it entered the house and taken hold of that.
 
Above should be primary defense. Like weakening the theif and resisting it at entry gate.For it, please refer my previous posts. Rest all other should be secondary issues like handling a theif after it entered the house and taken hold of that.
Er yes. Preventing infection is certainly a better option than curing it after-the-fact. Not really a burst of insight.

The take-away: wear your masks. That cuts down on the transmission rate and infection rate.
 
Er yes. Preventing infection is certainly a better option than curing it after-the-fact. Not really a burst of insight.

The take-away: wear your masks. That cuts down on the transmission rate and infection rate.
Sorry, that will be preventive measure not primary treatment. I meant primary treatment.
 
This may be of interest;
Virology question of the week: What matters more, multiplicity of infection or virus concentration?
6 MAY 2014
cultured_cells.jpg
This week’s question comes from a graduate student studying virology, who writes:
My professor recently said that really, the MOI doesn’t matter in a culture, it is the concentration of viral particles in the media that matters. Ie: if you have 10 million cells or one cell, but you are infecting the plate with 5mL of 100 million viral particles/mL, then the amount of virus interacting with each cell is not different in either scenario (pretending that it isn’t nearly impossible for that single cell to survive in culture alone). I argued with him, saying that the cytotoxicity to the single cell would certainly be increased. He then said that a student hadn’t argued with him about that in his 15 years of teaching and I promptly decided to get some evidence before I continued the discussion.....more..
https://www.virology.ws/2014/05/06/...iplicity-of-infection-or-virus-concentration/
 
Sorry, it is too technical for me to understand.
It seems to have something to do with "viral load".
Viral load refers to the amount of virus in an infected person’s blood. This is expressed as the number of viral particles in each milliliter of blood. Higher viral load can have different implications for different viruses but typically means the infection is progressing.
Viral load and how it is measured
Viral load tests measure the quantity of genetic material, commonly RNA, of a virus present in the blood. Several tests are typically done over an extended period, with initial measurements serving as the baseline and subsequent measurements compared to this.
Viral load measurements can differ daily, and therefore long-term trends are used to evaluate disease progression.
There are three main tests used to measure viral load. These are reverse transcription-polymerase chain reaction (RT-PCR) tests, branched DNA (bDNA) tests, and nucleic acid sequence-based amplification (NASBA) tests. These tests report viral load results differently, which means it is crucial to be consistent in the test used throughout the monitoring.[/quote] https://www.news-medical.net/health/What-is-Viral-Load.aspx
 
It seems to have something to do with "viral load". Viral load and how it is measured There are three main tests used to measure viral load. These are reverse transcription-polymerase chain reaction (RT-PCR) tests, branched DNA (bDNA) tests, and nucleic acid sequence-based amplification (NASBA) tests. These tests report viral load results differently, which means it is crucial to be consistent in the test used throughout the monitoring.
https://www.news-medical.net/health/What-is-Viral-Load.aspx[/QUOTE]
Thanks. Do these tests give negative test report if viral load is less?
 
Viral load is a very important measure of severity of virus infection. It can also be a measure of patient's immune response or of treatmentitreatment effective or not. However, it need to be understood, how low viral load can be possible esp after few days of initial exposure because virus should be able to make many copies quickly after it infected the cells?
 
Hello,
I am discussing Adsorption linked with possible molecular presence in higher dilutions. However one more idea striked to me and just casually mentioning here. Probably it may also be relevent for this topic subject.
"Adsorption in virusesEdit
Adsorption is the first step in the viral life cycle. The next steps are penetration, uncoating, synthesis (transcription if needed, and translation), and release" from wiki link on adsorption.

There sre some factors affecting adsorption. They are surface area, temperature, pressure, (pH ?) Etc.
My concern now here is that, can these factors effecting adsorption be linked to increase or decrease in getting and spread of Covid 19 infection? Bit important for seasonal and body's environmental variations. Pls contribute.
 
Hello,
I am discussing Adsorption linked with possible molecular presence in higher dilutions. However one more idea striked to me and just casually mentioning here. Probably it may also be relevent for this topic subject.
"Adsorption in virusesEdit
Adsorption is the first step in the viral life cycle. The next steps are penetration, uncoating, synthesis (transcription if needed, and translation), and release" from wiki link on adsorption.

There sre some factors affecting adsorption. They are surface area, temperature, pressure, (pH ?) Etc.
My concern now here is that, can these factors effecting adsorption be linked to increase or decrease in getting and spread of Covid 19 infection? Bit important for seasonal and body's environmental variations. Pls contribute.
Fuck off.
 
Related Things at basic, gross and universal levels look relatively different at these levels but can still have some dependency on each other.

An English article still has its dependency of english language alphabets.
 
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