Anyone Got A "Typical" Viral Load Drop Graph?

[RobertBeWell]

I sat down with the research doctor today at my study visit, because I wanted to discuss with him his feelings on whether or not I should continue on. Though he couldn't come right out and say it, he absolutely didn't disagree when I told him that based on my results, I was not getting the study drug.

Anyhow... he told me that as time goes on, and the viral load drops, the remaining virus are "harder" to kill, because they are "tougher". In other words, in patients that respond to treatment, they usually expect to see large viral drops initially, followed by progressively smaller and smaller drops until UND.

I was a bit skeptical, but I didn't let on because I didn't want to insult the man, as he's pretty respected in his field as a researcher.

How can one virion be any harder to kill than another.

Anyone got a link to a graph of a "typical" viral load drop in a "good response" scenario?

Thanks

RBW

[willing]

thanks for asking  - I posted a journal article with a vl pic and summary since it may be of use to others planning their next PI-based attack. Insomnia is a problem with me in any case and none of this has helped but I couldn't tell you whether the SAMe is a factor. I've just gotten in the habit of  being up for a couple of hours somewhere between 3 and 5 and have re-arranged my life to sleep later in the mornings. Also, I  make a protein-powder shake every night which helps with  the middle-of-the night stomach growling.

I'm actually fairly clueless about diet-related issues (topologically, human anatomy is isomorphic to a doughnut and I've  assumed whatever goes through the middle of the doughnut has little more impact on the doughnut than what's outside). Though normally I keep to a pretty good diet (low sugar/fat, high fiber, yadda, yadda)  for now I could care less. My stomach has given me so much grief this tx that as long as it keeps quiet it can eat whatever it wants (weird stuff : lots of bok choy and plates of plain noodles with butter...) Fine by me - if it stays happy I'm happy.

Good luck with your tx planning!

[merryBe]

the CTLs?  well isn't that regulated by how well the antigens are recognized..?

I mean the nose knows right??

That's why I opted to up the LDL profile, the softer fats create a less hydrophobic cell...meaning more permeation by the drugs to the surface, but also, if macrophages are sensory, we don't know by what process they detect...chemical detection...the little buggers may have plenty of adenoidal tissue who nose (jk).

But however they do it, they may be able to detect better through a more permeable shell.

That the viron always puts on a raincoat, a fat layer, before jumping out into the bloodstream for a day at Disneyland (rollercoasters) seems to me the greatest argument for calorie restriction because they are pulling their coats from the livers stores, yes??

While I agree that recognition is a big part of the equation, I think that Riba penetration is even greater, especially when viewing the Lindahl studies where SVR and Riba plasma levels were so integrally linked. What do you think??

Could the type of fat we consume be more crucial than once thought?
I'm kind of likening the idea to maybe wearing a wool coat vs. a vinyl coat. The vinyl is impervious to the water coming by, none gets in, inside its all dry and the rain has no effect....whereas the woolen coat offers so protections, but not completely. Even if it's a thicker coat it's still got a permeability factor that the vinyl just doesn't have, so eventually, given enough rain, the person will eventually get wet...the coat will fail to some extent.
Now imagine that HDL is the vinyl coat, and LDL being sofeter and more permeable, is the fatty layer that eventually the riba can penetrate. So then which should I eat the tough coat or the tender one?

Am I making any sense here?

I wish they would test Riba plasma levels...it would make life so much easier...we could all get more quickly to steady state and have a much better chance at SVR without going over. Do you think that will EVER happen?? I think just watching blood labs is inept, since age and marrow health can effect blood results regardless of whether riba is optimum.

mb

[merryBe]

First, how are you holding up?? How's your bloodwork holding??
Is the Sam-E making it hard to sleep?  I'm very curious as to how others are fairing with this adjunct while on tx.

I was with you on nixing the IL28 until I realized for a relasper having the proof of genetic incompetance would make the case for ntz more valid.
Assuming we use a four pronged approach (4 pharmaceuticals) as well as our adjuncts would provide a lesser chance of resistant mutations so why not get the test??  The liklihood is high that relapsers would have CT or TT, and this give my doc rational for ordering anything off label he wants to.
I've even given thought to buying a pound of clemizole..same reasons, more prongs.

BTW, can you PM me the studies you have on the 4 pronged stuff..I can't find them.

Also, how are you doing???

Did you see the thread on isonine genetics??
It came on the heels of a thread of mine on purines and isonine from last week.
It would be great if you could take a look there, I'd value your opinion.
It might also help you to be aware of what purines and isonine do to riba absorption if you don't already know that.
take care.

mb

[justfinethanks]

i dont think that critter exists   typical results is kind of an oxymoron when it comes to hcv and treatment  also imo the hcv virus is capable of producing trillions of copies daily the more in the body the easier for the meds to target them  as far as mutation with peg and riba theres not much of that on treatment unless they are inf resistant  is this a mutation  im not sure  as we get more advanced genetically with our dna and the viral rna  things will change  there are so many positive and negative predictive factors involved - all we can tell from a graph is if we are undetectable before 12 weeks - treatment will most likely work  and if we arent undetectable by 6 months treatment will most likely fail

[willing]

yes, there's this eternal dance between  host, virus and  meds and the games they all play. The host can fail to respond to ifn for various reasons which regularly come up here. It's amazing how often this can be reversed : stories like CS's or jt57's are very dramatic but even I saw a better vl curve this time around by adding ntz, high dose rbv and SAMe.

Regardless of the host response, Trin's paper suggests that just as PIs  have a clearly defined set of sequences which will not be affected by the drug, there are "tougher buggers", mostly already present, but some of which can come into existence during tx, that thrive notwithstanding the ifn. Ifn's mechanism of action is way more complicated that that of PIs - after binding to its cell receptor it fires off on the order of a hundred genes with wide ranging effects  so what it takes for the "tough buggers" to withstand that firestorm remains a  mystery.

As I wrote above, my hunch is that at least part of the problem is a failure of the class-I MHC/CTL mechanism. This is the major component of the immune system that enables the immune police to detect infected cells by scanning the cell surface for bits of "foreign" antigen. Virus that presents no MHC-binding antigen, just like the stealth fighter jet China tested last week, is invisible to radar and the infected cells presumably remain in business until some mutation in viral sequence finally gives them away.

[Trish77]

From the study:  "The persistence of variants present before treatment in patients who fail to respond or who experience a breakthrough during therapy strongly suggests the preexistence of viral strains with inherent resistance to IFN. Thus, the study of the evolution of the HCV quasispecies provides prognostic information as early as the first 2 weeks after starting therapy and opens perspectives for elucidating the mechanisms of treatment failure in chronic hepatitis C. "

willing:  "On one hand it's well accepted that there is no such as soc resistance and if one fails it's perfectly reasonable to try again. On the other that study suggests that if one's tx is reasonably successful there is a great narrowing of sequence diversity towards the end of tx. "

Hm - well, the way I read that excerpt I quoted from Trinity's post is that there already existed a tougher bugger amongst the virons and it's identifiable as early as 2 weeks in.  The others may die off but this one doesn't and is likely the one responsible if there is a relapse or failure to respond.  To me, this is less of an explanation as to why you don't jump back in right away but moreso why it's generally accepted that, if you do this again, you do something differently next time around.  Either you double-dose with interferon for awhile, increase the ribavirin, add Alinia or a PI - but not the same thing.  Why?  Because you've already learned that the virons you have need something more.  

Whatcha think, willing?  Interested in your take on this.

Trish