nope. And you got a smaller sized of the normal pic ;O

bro, don't even get me started here.



i suck at poetry

This post was edited by Exx on Jan 25 2013 09:30pm

I'm up for discussion

Your love is enough. You talking to me is enough.

Alright here we go

Using a condom and massacring those with the disease is the best cure.

gg genocide

Sometimes I wish everyone was more like you. Then the world will be a much better and efficient place.

tried to make it threw condor hero a second time but that shitty ass chineese after the first season is 2 hard to handle

They got married and made a buncha kids.

1) What protein?
HIV 1 - TAT

2) Cool, but all the viruses in the body are producing functional proteins. Injecting a bunch of non functional proteins into the body won't prevent virus replication. Not to mention that the proteins would never pass into the cell without being degraded (unless it just happens to match to a receptor by chance which is highly unlikely.)

They're not injecting "non functional proteins" into the blood stream. They modified the HIV1-TAT protein through mutation, now called "nullbasic" which inhibits/interferes HIV Rev trafficking.

3) I'm 99.9% sure this is done in cell culture, where it was incubated with the lack of functional mutant. But guess what, what goes in comes out. If they were able to prevent infection in the presence of functional viral particles, then it's worthwhile to mention.

Cells that express "nullbasic" gene showed prominent result against functional HIV-1 dose infection

4) Right I wanna see you injecting proteins into all the permissive cells in your body

Gene therapy

At first, I misinterpreted your statement and Cyche's article since I thought it was just another sort of HIV protease inhibitor drug and that's what I meant by "you try to kill all at once". But after further reading this article, I can see why its promising (even though there are so many drugs out there that deters HIV)


"The potential therapeutic value of Nullbasic is illustrated by experiments showing that Nullbasic expression protected cells from high-dose HIV-1 infection (500 ng CA-equivalent virions per 106 cells) by greater than two orders of magnitude compared to control cells (Fig. 8D). Furthermore, Nullbasic-expressing cells were protected against HIV-1-induced syncytia formation and cell death, indicating that Nullbasic expression protected cells against a spreading infection. All three of the previously described antiviral activities of Nullbasic (inhibition of transactivation, Rev function and reverse transcription) likely combined to suppress this spreading infection.
In conclusion, we demonstrate the potent antiviral activity of a transdominant Tat mutant and show that multiple steps in the HIV-1 replication cycle are targeted. In addition to negative effects on viral gene expression, we report for the first time that Nullbasic also inhibits Rev-dependent viral mRNA transport and intravirion reverse transcription. Moreover, these inhibitory effects combined potently to reduce HIV infection, illustrating Nullbasic and its activities as potential avenues for the development of new therapeutic interventions. Identification of the cellular or viral factors that interact with Nullbasic to induce Rev and reverse transcription inhibition may also reveal novel aspects of HIV-1 replication."