will pharmaceutical companies develop drugs to destroy mutations their new drugs created?

I guess many of us wonder what will happen if you mutate with the new PIs From what I have read, it seems that most mutations die off, but occasionally the mutations become dominant.

Anyone know what happened with the HIV drugs? Were the people on the first PIs out of luck if they mutated? I thought that they developed and they continually change the drugs for people with HIV when they mutate. I realize that HCV mutates more rapidly, but still HIV research has led the way to this class of drugs.

[Bill1954]

Others more knowledgeable than I will hopefully chime in with more info, but I believe that to date, protease inhibitors have been offered with interferon for just this reason; the IFN helps mop up most of the escape variants as they develop. I say most; I’m unsure if/how many leak past this defense.

I agree wholeheartedly though; if used as monotherapy, I believe the NS3, NS4A inhibitors targeted by first generation PI drugs would leak monsters.

--Bill

[Willy50]

I'm not more knowledgeable, but I'll chime in with my opinion.

HCV is considered by some to be a self limiting disease.  Most of us will not re-transmit the virus to others.  We will either become cured or may die with the virus without much concern of spreading it.

Bill used the term "leak".  My simplistic way of thinking of some of these types of TX is that these various types of treatments are like nets that let some by and catch others.  Basically, one net by itself lets a lot by but when they are all combined they may catch about everything.  That is what is happening now.  We geno 1's are going from a 45% SVR rate to a 75-80% cure rate when they add TVR or Boceprevir.  

OK, say that means that 20% may sneak by...... but there will be even more potent compounds that will be combined and we will only continue to see increasing success rates.

The new dual acting antivirals may produce viral declines in the order of 7, 8, 9 log drop in a matter of weeks.  When you squash the viral load so quickly there is far less chance of resistance issues.  Besides, not all compounds will have the same resistance issue that protease inhibitors do.  Before too long, our population is really going to dwindle.

Even in a situation where PI's or twin PI's may fail, one may be able to add another form of TX; maybe plain old IFN and RBV and finish off the virus that the new kids on the block couldn't.

I think that it's going to be vastly improved, maybe not perfect but so much better than what we've had for decades.  I see it more as a great solution than as a potential problem.

willy