the explanation of why tenofovir is so potent on hbv and makes no resistance was explained by the intracellular levels reached by this drug, it is so bad no study ever showed how all other nucs are extremely poor at this and when i found this comparison i was very very surprised
all ohter drugs are so weak as intracellular levels, just look at lam vs tdf.we dont have etv here but it is probably very poor too.
Tenofovir has a excellent resistance profile especially in UND situations. Even if you are resistance to LAM, can you access Entecavir as a possible combo with Tenofovir?
An international study found the antiviral combination of tenofovir and emtricitabine (Truvada) was most effective in treating younger adult hepatitis B patients with high viral load and normal ALT levels.
Doctors historically have not treated this group because there appeared to be no sign of liver damage. However, doctors now know that high viral loads may increase patients’ risk of liver damage and cancer as they age, despite their normal ALT levels.
Does not mean it will happen with everybody but it sure did happen to me taking Entecavir (Baraclude) which was also originally developed for HIV but it failed miserably as they virus developed resistance really fast to it..
You are correct that Truvada is a combination of tenofovir and emtricitabine, and is generally prescribed for patients with HIV. Being a HBV forum, most of us know very little about Truvada except that it is prescribed off-label for HBV by some doctors, and that it is recommended for HBV patients who develop resistance to Tenofovir.
This is a potential concern because the drugs in Truvada – tenofovir and emtricitabine – are active against HBV as well as HIV.
HIV and HBV are spread through some common transmission routes, including sexual transmission, vertical transmission (mother to child) and via multi-person use of injection equipment.
However, I probably can not blame my doctor too much if it dates back ten years ago. But, this failed treatment may induce LAM-resistance in my body. So, I have to take
either tenofovir or Truvada (Tenofovir 300mg/Emtricitabine 200mg). I prefer to take Truvada at the first begining, then switch to Tenofovir after HBV-DNA is undetectable.
Also, I have big concern about my AFP. I am wondering if it is because of liver cell renaissance after damage. Or it is related to HCC?
truvada is just tenofovir+ftc, it is sueless on hbv unless non response to tenofovir, which is extremely rare
it adds toxicity and higher price because truvada patent is not expiring in 2014, no difference on hbsag.
instead of truvada it is best only for those non responding to combo tenofovir+lamivudine.
"Try Truvada. There are reports that it clears surface antigen at 11% per year. The benefit of interferon still will be there as it had a long lasting effect." - do you have this reports ?
"Five years ago they were right on the spot with Baraclude saying it is weak drug and resistance issue will be a problem with HBV..
To evaluate amino acid changes within HBV pol/RT after up to 240 weeks of tenofovir disoproxil fumarate (TDF) treatment and determine their potential association with resistance to TDF. No TDF resistance has been detected through 192 weeks of TDF treatment. Methods: Patients in Studies GS-US-174-0102 (HBeAg-) and GS-US-174-0103 (HBeAg+) were randomized 2:1 to receive TDF or adefovir dipivoxil (ADV) for 48 weeks followed by open-label TDF.
I was also a reciever. After 40 hours I went to the first clinic and they gave me PEP (TenofovirDF, emtricitabine + lamivudine). The clinic looks very unprofessional, but it was my only chance. I didn't do any hiv or std test, a month before the exposure i had HIV test which was negative. After few days I had a mild sore throat, i still have it, i don't have fever, running nose, rash or anything else. My questions are..
What are my chances of getting infected. Another question was administered a PEP drug emtricitabine and tenofovir, can it prevent me from contracting HiV.
Due to the extremely low susceptibility to resistance and very low toxicity this drug became the cornerstone of antiviral treatment for HIV and HBV. It made Gilead Billions, of which Holy has seen a million a year grant for his Institute in Prague.
At the day he died, the FDA had approved Truvada, a combo of tenofovir and emtricitabine (FTC) (300/200mg) for use as a preventative in healthy individuals exposed to risk of infection.
Tenofovir alafenamide (TAF), a new formulation that reaches higher levels in cells but allows for lower dosing, was as effective as the current tenofovir disoproxil fumarate (TDF) formulation but had less impact on markers of kidney function and bone turnover, researchers reported at the 53rd Interscience Conference on Antimicrobial Agents and Chemotherapy (ICAAC 2013) this week in Denver.
yes it is and resistance is very difficult to develop (your doc made the best choice combo for you) but in theory there is no data on lamR respose durability so better always double check although 99% gym/diet can be the cause
in any case consider ntz because truvada only lowers replication but doesn t have any effect for virus eradication and achieving hbe neg is very important because hbe has a very strong effect lowering immune response and inducing immune tollerance
I asked her of her status and she stated clean. I started PEP within 24 hours. (Teneogovir, emtricitabine, lamivudine ) What are the odds of being infected ? is this low risk ?
I started a course of PEP that included Tenvor-EM (Indian version Emtricitabine/Tenofovir DF) and Kaluvia (generic of lopinavir/retonavir) for 25 days and interrupted it for two reasons:
1-My partner tested Negative(Antigen/ Antibody) on 22 days post exposure
2-Thinking that i might be developing facial Lipodystrophy (slight facial fat loss under cheek bones). I cant tell if my face was like this before the treatment or it is just an illusion.
You can develop resistance to a STAT-C drug however. So when someone is choosing a trial with a STAT-C drug involved, you want to choose with care - the same will apply when undergoing treatment with a STAT-C drug when they finally get to market. You want a doctor/treatment team who understands the issues and you'll want to understand them yourself so that your first attempt with a STAT-C drug is as hopefully your last.
Monotherapy using lamivudine has the longest history of use and shows highest rate of resistance. A 2003 study of 998 patients showed 65% lamivudine-resistance mutations in 5 years. Lamivudine should no longer be used as monotherapy.
2. Monotherapy using adefovir has 29% mutation probability in 240 weeks, according to a 2006 study of 125 patients.
3. Entecavir is 100-fold more potent than lamivudine or adefovir.
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