Tell me, It is wrong on Infection?

Maybe for a couple of hours as the cells begin to die. When decay sets in, that is from a different competing virus or bacteria. btw. Some viruses use bacteria to procreate.
6a878ab37cb0147d81037d5044741ca9.jpg


How long HIV virus survive in a Dead Human body www.thebody.com/article/long-hiv-virus-survive...

Okay, anyhow that will be survival not infection.
 
Not until a quorum is reached. That's the beauty. We can prevent the bacteria or viruses from reaching a quorumb by chemical language. We need to learn the language !

But the cure; no virulence, no procreation and the virus dies by natural selection without acquiring immunity.
Yes now I read about quorum sensing.. Something like it was also mentioned in BBC link, I quoted previously. However, if we can stop its replication, we can cure. But how to achieve it in case of COVID?
 
That's what we do with cancerous cells, no? Not very gentle on the host.

If you mean there is no "intent' you're right. Intent is not required. Its a chemical process. The communication is via chemistry. All we need to do is to confound the language and the virus remains benign.

tileshop.fcgi



Abiogenesis does not require motive or intent. It's a mathematical electro-chemical function . The virus is a transitional organism. Actually, it is thought that the virus devolved from a common ancestor with the bacteria, which was able to copy itself.

Btw, does it suggest that there will be no receptor mediated fusion if pH is low or high than neutral and no endocytotic fusion if pH is
neutral or high?
 
Btw, does it suggest that there will be no receptor mediated fusion if pH is low or high than neutral and no endocytotic fusion if pH is
neutral or high?
I have no clue. The main thing is that a virus is a chemical organism.
virusa3.jpg

In order to replicate, the virus depends on the host cell's chemical machinery. Note that these steps may differ slightly depending on the type of host cell that the virus is attacking.
Viruses lie around our environment all of the time just waiting for a host cell to come along. They can enter us through the eyes, nose, mouth or breaks in the skin (see How the Immune System Works for details). Once inside, they find a host cell to infect. For example, cold and flu viruses will attack cells that line the respiratory or digestive tracts. The human immunodeficiency virus (HIV), which causes AIDS, attacks the T-cells of the immune system.

Regardless of the type of host cell, viruses follow the same basic steps to replicate:
  1. A virus particle attaches to a host cell.
  2. The particle releases its genetic instructions into the host cell.
  3. The injected genetic material recruits the host cell's enzymes.
  4. The enzymes make parts for more new virus particles.
  5. The new particles assemble the parts into new viruses.
  6. The new particles break free from the host cell.
    All viruses have some type of protein on the outside coat or envelope that "feels" or "recognizes" the proper host cell(s). This protein attaches the virus to the membrane of the host cell. Some enveloped viruses can dissolve right through the cell membrane of the host because both the virus envelope and the cell membrane are made of lipids.
    Those viruses that do not enter the cell must inject their contents (genetic instructions, enzymes) into the host cell. Those viruses that dissolve into a cell simply release their contents once inside the host. In either case, the results are the same.
    https://science.howstuffworks.com/life/cellular-microscopic/virus-human2.htm
 
Yes now I read about quorum sensing.. Something like it was also mentioned in BBC link, I quoted previously. However, if we can stop its replication, we can cure. But how to achieve it in case of COVID?
Find a false key that will prevent the virus from attaching itself. It's just chemistry.
 
I have no clue. The main thing is that a virus is a chemical organism.
virusa3.jpg

In order to replicate, the virus depends on the host cell's chemical machinery. Note that these steps may differ slightly depending on the type of host cell that the virus is attacking.


Regardless of the type of host cell, viruses follow the same basic steps to replicate:
  1. A virus particle attaches to a host cell.
  2. The particle releases its genetic instructions into the host cell.
  3. The injected genetic material recruits the host cell's enzymes.
  4. The enzymes make parts for more new virus particles.
  5. The new particles assemble the parts into new viruses.
  6. The new particles break free from the host cell. https://science.howstuffworks.com/life/cellular-microscopic/virus-human2.htm
"Those viruses that do not enter the cell must inject their contents (genetic instructions, enzymes) into the host cell. Those viruses that dissolve into a cell simply release their contents once inside the host. In either case, the results are the same"

From your quote. How it can be possible, when those virus do not enter the cells?
 
"Those viruses that do not enter the cell must inject their contents (genetic instructions, enzymes) into the host cell. Those viruses that dissolve into a cell simply release their contents once inside the host. In either case, the results are the same"
From your quote. How it can be possible, when those virus do not enter the cells?
I showed illustration how viruses do enter cells or inject their DNA into the cell. Either way it is the cell that does the mitotic work. It treats the virus' DNA as its own. Sometimes the virus DNA attaches to the host's DNA and natural selection eventually sorts it out for detrimental or beneficial traits. Or it remains dormant.

The thing is, world-wide nature performs an incredible number of chemical experiments at the same time.
Hazen estimates that the earth has performed some 3 trillion, quadrillion, quadrillion, quadrillion chemical experiments during it's life time. None of this is intentionally ordered, it's all probabilistic. Some chemical reactions are inevitable, some are rare but given enough time and available variety of minerals every possible chemical reaction will eventually happen and natural selection sorts it for beneficial survival traits.

When you get right down to it, life is a chemical process. We are able to affect a little bit of it mainly because it is physical. No mystery or magic. All we need is knowledge. This is really small nano-scale stuff. Can't use regular lab equipment. This requires very sophisticated equipment.
 
I showed illustration how viruses do enter cells or inject their DNA into the cell. Either way...
Yes, you have shown two types. I think, it is only injected or Receptor mediated entry(ACE2) of genetic material in case of COVID. Pls tell about attachment by adsorption.
Anyway, for Virus to be active, fusion is first need and it can be pH and receptor dependent. Moreover priming if S protien will also be required for attachment to cell and for internalization of genetic material. If so, how these routes are targeted either by anti virals or by vaccine or by changing pH related physiology?
 
Yes, you have shown two types. I think, it is only injected or Receptor mediated entry(ACE2) of genetic material in case of COVID. Pls tell about attachment by adsorption.
From what I can tell, it is as if many viruses grow a sort of velcro type grappling hooks. Don't forget the size of viruses. They are so small that allows them entry or attachment in spaces so small, we cannot see with a regular microscope. Once they succeed in attachment, the programmed chemistry does the rest.
This may explain better.
Abstract
The cell imposes multiple barriers to virus entry. However, viruses exploit fundamental cellular processes to gain entry to cells and deliver their genetic cargo. Virus entry pathways are largely defined by the interactions between virus particles and their receptors at the cell surface. These interactions determine the mechanisms of virus attachment, uptake, intracellular trafficking, and, ultimately, penetration to the cytosol. Elucidating the complex interplay between viruses and their receptors is necessary for a full understanding of how these remarkable agents invade their cellular hosts....more
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3246895/
Anyway, for Virus to be active, fusion is first need and it can be pH and receptor dependent. Moreover priming if S protein will also be required for attachment to cell and for internalization of genetic material. If so, how these routes are targeted either by anti virals or by vaccine or by changing pH related physiology?
I really am not that well versed in bacteriology. But the one property of quorum sensing seems to be that by not killing the virus or bacteria it leaves the population basically intact and prevents natural selection of the most resistant and virulent survivors.

IMO, it's worthy of note that viruses are only effective on specific cells and rarely attack more than one or two cell types, which would suggest that viruses are a result of a very specific form of natural selection. If so, we should be able to discover the exact mutations and introduce our own "human selection" into the viral matrix.
 
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From what I can tell, it is as if many viruses grow a sort of velcro type grappling hooks. Don't forget the size of viruses. They are so small that allows them entry or attachment in spaces so small, we cannot see with a regular microscope. Once they succeed in attachment, the programmed chemistry does the rest.
This may explain better. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3246895/
Interplay between virus and cellular attachment should be a good target at basic leveks. Few drugs already in use are repurposed as investigational durgs for COVID under active studies. As quoted previously. Hope they can be useful.
 
Write4U ,

Whether "quorum sensing " is related in between to Lag and Log phase of Bacteria life cycle?
https://sciencing.com/bacteria-life-cycle-12211284.html

Accordingly, we need to check Virus life cycle.
The life cycle of bacteria is well documented. They all use the same type of quorum sensing, except for the language. Each species of bacteria has it's own unique chemical intra-species language in addition to a second "common" inter-species language.

But quorum sensing does not have anything to do with bacteria growth, except that when there are sufficient te virulent behavior oh the bacteria is triggered in unison so that they can overwhelm the host's defenses.

As Bassler demonstrated, when bacteria are low in numbers they remain virally dormant but keep dividing until a sufficient number is reached which then "triggers" the virulent part of the bacterial genetic code.

This is different from viruses who cannot self-divide and must use the host's mitotic system to divide. I am not clear if viruses use quorum sensing or if they are viral from the moment they enter the cell and just keep dividing until the cell bursts and dies, giving birth to an army of new viruses.

What’s the Difference Between Bacterial and Viral Infections?
Bacteria and viruses can cause many common infections. But what are the differences between these two kinds of infectious organisms?
Bacteria are tiny microorganisms that are made up of a single cell. They’re very diverse and can have a large variety of shapes and structural features.
Bacteria can live in almost every conceivable environment, including in or on the human body.
Only a handful of bacteria cause infections in humans. These bacteria are referred to as pathogenic bacteria.
Viruses are another type of tiny microorganism, although they’re even smaller than bacteria. Like bacteria, they’re very diverse and have a variety of shapes and features.
Viruses are parasitic. That means they require living cells or tissue in which to grow.
Viruses can invade the cells of your body, using the components of your cells to grow and multiply. Some viruses even kill host cells as part of their life cycle.
Read on to learn more about the differences between these two types of infections.
https://www.healthline.com/health/bacterial-vs-viral-infections
 
Now for OP,
In view of these discussions, plasma therapy and anticipated antibody tests by CDC, labsonline etc. but no indication of long term immunological memory, it is still indicative that short term immunity is developed in some patient after getting infection. So, how aggressive avoidance measures esp at initial stages of low exposure of COVID 19 infection impacted this pademic, need to be deeply thought. What past history of any epidemic or pademic can suggest to this effect where such aggressive measures might had not kept?
 
This link of CDC tell about Serology tests for COVID 19 which can be indicative of fevelopment of short term natural immunity on exposure. Moreover many got cured, is also similarily indicative.
They've had this for a while, but it's not very accurate.

From the report: "Currently, CDC’s serologic test is designed and validated for broad-based surveillance and research that will give us information needed to guide the response to the pandemic and protect the public’s health. The test is not currently designed to test individuals who want to know if they have been previously infected with COVID-19." That means that it's accurate enough to give _general_ information on how many people have antibodies, but is not accurate enough to tell if _you_ had the infection or not.
 
They've had this for a while, but it's not very accurate.

From the report: "Currently, CDC’s serologic test is designed and validated for broad-based surveillance and research that will give us information needed to guide the response to the pandemic and protect the public’s health. The test is not currently designed to test individuals who want to know if they have been previously infected with COVID-19." That means that it's accurate enough to give _general_ information on how many people have antibodies, but is not accurate enough to tell if _you_ had the infection or not.
Yes, it is yet to be validated fully for the the individual infection and cure. A BBC link, I posted earlier, gives the right picture about antibody development and how few people are getting cure. They also linked to to T cells and innate immune system.
 
IIND PART:

As we are discussing about COVID-19, we can also have a gross look on possibility of better treatment side. I give below two links content of which which can be refereed here:-

1. "Research and Development on Therapeutic Agents and Vaccines for COVID-19 and Related Human Coronavirus Diseases"
https://pubs.acs.org/doi/10.1021/acscentsci.0c00272

2. "Antiviral drugs"
https://en.wikipedia.org/wiki/Antiviral_drug

It is mentioned in 2nd link

Viral life cycles vary in their precise details depending on the type of virus, but they all share a general pattern:

  1. Attachment to a host cell.
  2. Release of viral genes and possibly enzymes into the host cell.
  3. Replication of viral components using host-cell machinery.
  4. Assembly of viral components into complete viral particles.
  5. Release of viral particles to infect new host cells.
ALSO
Anti-viral targeting[edit]
The general idea behind modern antiviral drug design is to identify viral proteins, or parts of proteins, that can be disabled. These "targets" should generally be as unlike any proteins or parts of proteins in humans as possible, to reduce the likelihood of side effects. The targets should also be common across many strains of a virus, or even among different species of virus in the same family, so a single drug will have broad effectiveness.
Approaches by life cycle stage...
Before cell entry,
Entry inhibitor,

Uncoating inhibitor
During viral synthesis,
Reverse transcription,
Integrase,
Transcription,
Translation/antisense,
Translation/ribozymes,
Protein processing and targeting,
Protease inhibitors,
Long dsRNA helix targeting,
Assembly,
Release phase
--------------

Other approach is
Immune system stimulation

Details can be read here:-
https://en.wikipedia.org/wiki/Antiviral_drug

Hence, under above referance, targetting which approach or which stage of life -cycle of Virus
can be more logical in this case?

Best wishes.

 
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