Hepc, so what is being done to eradicate

[geterdone]

So what is being done to eradicate

the host virus cell and are we and research just being reactive when fighting this virus. Is there anything being done to eradicate the virus cells itself before having sex with the liver?

jasper

[jack1642]

I am glad you got what you wanted from the ling i gave you. I have been reading some promising development by some scientific herbalist in the West African State - Ghana.
This not particularly to do with HCV but HBV and HIV. It is my opinion that if as they claimed to cure people with HIV and HBV it is possible the said concortion could help fight against HCV.
At this stage no stone sholud be left unturned in the fight agaisnt the horrors we facing.
I will get back to you should any information on their work is further reveal.

[geterdone]

It is not so much as the liver protecting it self as it is with the “virus cell” floating around and hitching a ride on the plaque in the veins and in some instances being coated additionally by the tumbling lipids and sticking to the plaque and eventually being encapsulated in it over time which brings me back to the virus cell and the thickness of the cell envelopes which is not soluble and floats at various degrees with in the blood stream in which the cells act as balloons because of the chemical make up of the inner membrane and outer coating and the varying buoyancy of each cell given that make up and coating.

Hope HR is lurking because I doubt if I’ll remember this scenario, in which all probability is totally wrong but here goes.

Using hr’s example of the ten vials of 1ml of infected blood serum all from the same draw and using ten centrifugal mixers (lack of better word) and set at different speeds among the ten vials what would be the viral content at the various speeds and the viral buoyancy of the virus cell at each speed. Now if going by the different centrifugal speeds and all ten vials show different concentration of virus cells and virion at those different levels what would cause those virus cells and virions to stay buoyant at that given speed, and of that, what would be the thickness of the envelopes in each virus group? In looking at it this way the newly created virus cells and virions would be lighter and would sink to the bottom at the slower speed because they have not had the time to mature and flow through the blood stream and pick up additional protein coatings of its outer cell envelope and in contrast; the maximum centrifugal speed would yield the most hardy of the virus cells and virions because of the length of time floating in the blood system (years) and picking up the additional proteins of insoluble coatings of the outer envelope along the way in which it makes them more buoyant in our water based blood system and would it not make more sense that the newer virus cells and virions get eradicated faster in the beginning of treatment because of this lack of additional protection of each? Sounds far out but to the layman sounds logical for a hepc 101 class minus all the sifi wording.

So, say out of the ten vials centrifuged, vial one has 500k virus cells and virions at the lowest rpm and viral 10 has 5000 of the virus cells and virions at the maximum rpm would it be safe to say that what in the virus cell has made it so resistant to the downward pressure of the spinning centrifuge.

It might be interesting to also consider why alcohol, which is a solvent and has a cascading effect on lipids and cell membranes, also escalates the virions invasive abilities ten fold.

Haven’t got to that chapter yet, why would this effect viral replication?

BTW good luck with the surgery.

jasper

[merryBe]

loved your spikey analogy!!
sounds to me like they all had an exciting time, and then the cherry got popped and things went limp weak and vunerable in due course!!
Battle of the sexes is more like it : ))))))))))))))))))))))

I think you are asking why the liver cells don't protect themselves from the big spiked, hard, and tatooed dudes...
good question...
maybe it's similar to why plaques form in the veins, based also on the stickyiness of lipids....it's a connundrum that may be partially explainable by looking at what HepatitisResearcher has been saying about all the conservation chemicals which do influence lipids and penetrability of cell membranes.
It might be interesting to also consider why alcohol, which is a solvent and has a cascading effect on lipids and cell membranes also escalates the virions invasive abilities ten fold. Maybe if we could reverse engineer the alcohol effect and push that process to it's logical conclusions in the opposite chemical directions we might get somewhere. I'm sure this may have already be thought of.
maryB

[geterdone]

Thank You! very much for the medworm link. I found what I was looking for right off the bat about the centrifuging of blood serum and virion levels.

jasper

[geterdone]

Thanks! for the link.

charm hope all is well with you.

jasper

[geterdone]

Ok, so some may be wondering, (well maybe) what the heck is getter talking about now. Well, looking at it with a warped sense of humor it’s kind of goes like this, these virus cells are floating around in the blood stream in their protein and lipid envelopes which contain the positive RNA strand and with its spiked hair doo and are looking for a recipient or vulnerable coated host cell. As all things in the body, they have to pass through the liver for proper processing and as these virions float by and bounce around on the liver surface there are times where there is a chemical charge reaction and enough that in the caveloa (shallow dent) will cause an attraction in the virion cell as well as the surface in which the caveloa and the hair doo spike on the virion has become embedded and because of the lipid coating in the caveloa and the differing degree of lipid formation on the envelope of the virus cell and the chemical mixing and receptiveness of each, it has caused the jelling of the host cell surface membrane in which penetration is imminent. After the stimulation process and once inside, the virion cell sub comes to its own demise after embellishing inside its own now concurred domain but only briefly because of the stimuli and the battle to reach its objective the virion has now become weak and vulnerable itself by the stimulation process to where its once harden protein shells melt away and give way to the positive RNA offspring that lay inside and so goes the rest of the story of the ongoing Battle Of New Orleans.

So is there any research in how to stop the process before it happens at the virus cell level.

jasper

[jack1642]

Guess this web site will be helpfull to you. www.medworm.com
You can find the latest research journals relating to hepatitis.
take care.
jack

[charm27]

This question was helpful to me. lol
Charm


Ive lost it. aha