I love to understand how things actually work.
I have found minimal research on deeper understandings on how these drugs work and what the body is actually experiencing
in the process.
I understand that they are DAA inhibitors; inhibiting virus replication and also inhibiting the protein which splices the virus.
So my speculation is that the waves of side effects could be due to the liver then having to also process high volumes of dying virus from the blood, not to mention dealing with the medications themselves?
Does anyone have any resources or links that explain this in more detail?
Hi Nzlisa, I had very few minor side effects from generic harvoni,
May we know if you have already treated or are considering doing so? Most people here put their basic Hep history on their signature so anyone knows the basics at a glance. You see, without knowing your history, no-one knows if you are being curious or anxious. So have you been treated before or have cirrhosis?
M, 57, Live in Wellington,NZ.
Genotype 1a diagnosed in 2013.
Treating for the first time since October 31 with Buyers Club Sof/Led. Thanks so much guys. Minimal side effects apart from sore throat at the start..
Viral load 5.4m when treatment started, Undetected at 4 weeks, 8 weeks, End of Treatment and 12-weeks post EOT. Yay!
Here is a link to a fairly simple explanation of the process for DAAs. The same basics apply to the various different DAAs being used for HCV treatment although the exact mechanism varies a little depending on which one.
You can also think of it as a bit like a lock and key. Lots of keys will fit the lock but only one will open it and allow the virus to replicate. Normally the virus finds the correct keys in our bodies but if we flood our bodies with lots of faulty keys (Sofosbuvir) that the virus thinks look the same as the one it needs it will use them and block the lock mechanisms stopping the replication from occurring.
So while we often think of the medication killing the virus sort of like a poison or something, it isn't really. It is just slowing its replication down enough for our immune systems to get back in control and do their job properly.
The side effects (which for most people are fairly mild) are probably a combination of our immune system working hard and as you say the rapid viral die off plus the fact that anything new we add to our metabolism will have some sort of effect until we are used to it.
(Apologies to molecular chemists and biologists everywhere )
G3a since '78 - Dx '12 - F4 (2xHCC)
24wk Tx - PEG/Riba/Dac 2013 relapsed
24wk Tx - Generic Sof/Dac/Riba 2015/16 relapsed
16wk Tx - 12/01/17 -> 03/05/17 NS3/NS5a + Generic Sof
SVR7 - 22/06/17 UND
SRV12 - 27/07/17 UND
SVR24 - 26/10/17 UND
Laughing Gaj at your apology to chemists and biologists.... however perfect explanation for my limited knowledge of chemistry and biology.
Thank you also to Chapel & Greedfighter who took the time to respond. I'm sorry if my communication was unclear, I wasn't so worried about
side effects but rather wanting to satiate my inquisitiveness into how the drug actually works.
I appreciate you all in this supportive and helpful community.
PS; and now can report that the effects of insomnia are kicking in... reporting live at 1.37am Colorado time.
Have you seen this video? At the time it helped me to understand virus replication and the complexities
gt 1a VL 6m
F2/3 FibroScan - 9KPa in 2011 and 7KPa in 2015
sof/dac 10 December for 12 weeks
pre tx alt 85 ast 51
4 wk alt 34 ast 31 UND <35
8 wk alt 29 ast 32 UND <15
12wk alt 25 ast 25 EOT 3.3.16
SVR24 UND KPa5.3 F0 in normal range
I am well
.forever grateful to fixhepc
nzlisa, these drugs block the ability of the virus to replicate (if successful) So the virus only lives so long, and if it can't replicate itself then the VL goes down, eventually to 0. I hope that helps. The side effects are small for most people, usually just a few headaches at the start of treatment.