Treatment with Flavocoxid or ETV or with drugs combination started 3 hours after transfection and was renewed every other day for 5 days. Total HBV replicative intermediates, viral transcripts and cccDNA levels were evaluated in untreated and treated HepG2 cells by quantitative real-time PCR, Southern and Northern blots experiments. To analyse the epigenetic modulation of HBV cccDNA the cccDNA-ChIP assay was applied to untreated and treated cells.
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..
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.
What are my chances of getting infected. Another question was administered a PEP drug emtricitabine and tenofovir, can it prevent me from contracting HiV.
FTC is Emtricitabine.
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.
s ability to readily detoxify the reactive intermediates or easily repair the resulting damage. Disturbance in this normal redox state can cause toxic effects through the production of peroxides and free radicals that damage all components of cells, including protiens, lipids and DNA. Uric Acid is increased by diet of high fructose intake (corn syrup) and purines found in high amounts or animal food products. Check your diets, my husband drank alot of Mountain Dew and likes to hunt.
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.
Good afternoon. There is a double-acting drugs - lamivudine, emtricitabine, tenofovir. This is known. Are there any similar action in the protease inhibitor, such as Kaletra (lopinavir) for example?
Have you ever thought about that?
I read - sometimes laugh. Simvastatin, vitamin D, which the Chinese poeben, mythical new drugs, masturbation with measurements of the level of HBsAg, and other nonsense....
m thinking about taking Tenofovir only because I will move to a place where Emtricitabine is not available. I know it is better to combo. But can you tell me how risky it is if I take tenofovir only (LAM resistance)? stef2011?
Thanks JB.
to mike1105: thanks.
You say it's a bit tricky to get the "intermediates" right. Since posting I located an old friend out of town(who is a D.D. but no longer practicing) and he told me over the phone several things: 1) he never heard of "intermediates" for the type of denture replacement I described. I had a functioning set of dentures which were there to be used for control prior to the surgery - they were not.
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.
the second component is unchanged, 200mg of emtricitabine, also called FTC, a fluor substituted form of Lamivudine, that provides protection from the development of mutants that will lower the responsiveness to tenofovir.
it's side effects are generally considered very mild, equivalent to lamivudine.
This is theoretically good news for hbv patients waiting eagerly for TAF to be available for HBV.
The problem is the high price: 1500$ for one month supply of 30 pills.
It is probable that these cells could support viral replication because hepatitis B virus DNA replicative intermediates, viral transcripts and HBsAg and HBcAg proteins were detected in most. These findings may be relevant to the initiation of extrahepatic syndromes associated with chronic hepatitis B virus infection such as vasculitis, glomerulonephropathy, neuropathy and dermatitis.
Similarly, extensive analyses of intrahepatic woodchuck hepatitis virus (WHV) and duck hepatitis B virus (DHBV) DNA intermediates under nucleoside analog therapy clearly demonstrated that cccDNA become the predominant form of viral DNA replication intermediates upon long-term suppression of viral DNA replication40 and 41. These findings strongly suggest that cccDNA is the most stable HBV replication intermediate and elimination of cccDNA is the key to cure HBV infection.
Alan McLachlan at the University of Illinois-Chicago, dramatic reductions in viral transcripts, viral replicative DNA intermediates, and intracellular HBV core antigen were observed in the liver after two weekly doses.
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.
Nicotinamide suppressed both HBV DNA replicative intermediates and 3.5-kb mRNA expression. Moreover, nicotinamide treatment also suppressed core protein expression and the secretion of the hepatitis B surface antigen (HBsAg) and the hepatitis B e antigen (HBeAg) in HBV-expressing cell models. Importantly, nicotinamide treatment suppressed serum HBV DNA, HBsAg and HBeAg levels and liver HBV DNA in HBV-transgenic mice.
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