Researchers at the Stanford University School of Medicine and their collaborators elsewhere have opened up a new front in the war on HIV/AIDS. Using the tools of the geneticist to insert a series of HIV-resistant genes into T cells--the body's immune cells that are actively targeted by HIV and AIDS--researchers have a found a potent means of fending off HIV cells that would otherwise inhabit and destroy the cells.
HIV and AIDS are usually treated through a cocktail of antiretroviral drugs that essentially attack the viruses at various phases of their replication processes. Because the lifecycle of HIV/AIDS is so short (just a few days, if that) it can mutate quickly as it replicates, so this kind of therapy usually involves a complex combination of drugs--many of which carry undesirable side effects.
This new gene therapy attempts to choke off HIV replication at the point the virus tries to infiltrate a healthy T cell, keeping that T cell healthy and denying the virus its chance to replicate--at least via that particular T cell. The virus usually gains access to the T cell by attaching itself to surface proteins known as CCR5 and CXCR4 (different strains of the virus target different surface proteins). Researchers have previously been able to deactivate the receptor protein CCR5 by developing a special protein that attaches to it and smashes its receptor gene, rendering it inactive for HIV's purposes.
The Stanford team's technique does the same thing but also goes a step further. It uses the same protein to target the DNA that lends the CCR5 its receptor status. But rather than simply smashing that DNA, this protein breaks the DNA sequence and inserts a few new genes in there that are known to express resistance to HIV. This technique of placing certain genes within the genome is known as "stacking," and it's the secret sauce in the Stanford team's anti-HIV recipe.
In lab tests in which T cells carrying these modified genes were introduced to HIV, this method blocked HIV infection via CCR5 and CXCR4 with surprising efficacy, providing 1,200-fold protection against HIV carrying the CCR5 receptor and 1,700-fold protection against those carrying the CXCR4 receptor. The control group of T cells all succumbed to HIV in less than one month.
It's important to note that this isn't a cure or a vaccine. But it is a way to insert a group of healthy, resistant T cells into an HIV/AIDS patient to stave off immune system collapse--and do so without a heavy regimen of antiretrovirals. There are certainly potential drawbacks--tinkering with genomes always carries the risk that something could go wrong, leading to cellular aberrations (like cancer). And it's not necessarily easy to ensure that the protein delivers the resistant genes to the right place in the genome.
Nonetheless, the team plans to keep working on its technique, and the hope is to get into clinical trials within five years. We haven't quite arrived at a cure, but we're certainly getting closer.
Please remove "cells" from the phrase "HIV cells". For any readers who would like to know the difference:
Viruses are not cells, they are particles composed of a protein coat stuffed with DNA. Basically, some code in a box designed to move the code.
Cells have a flexible, fatty, lipid membrane surrounding them, creating an inside and an outside volume. Resources are shipped inside, wastes are shipped out, and when the cell grows enough, the flexible, fatty, lipid membrane can be pinched off into two "daughter cells".
Debate exists on whether or not viruses are considered "alive," but my own interpretation and interpretation I have heard by others is that they are not considered to be living.
Well, this certainly looks promising. However, like Clay Dillow said, modifying DNA is a very risky business.
The way I see it any research towards curing or treating any virus is waste of time with the strong developments of the draco drug. I wanna hear more about DRACO when it comes to viruses. Nothing else. As a matter of fact I don't know why that's not bigger news
Generally I can see this leading to a cure if early detection can be developed. Due to the suppressive nature it could inhibit cell infection, mutation and migration long enough for the virus to die out. It has an exceptionally short life span and requires the infection, mutation and migration process to ensure its propegation process. If inhibited long enough (say 7-14 days to allow for aberant mutation/migration of the HIV/Aids infection) it would allow for the virus to "burn out" naturally without mutation/migration being allowed to overcome a healthy system.
Mikemike141111: DRACO like any drug has 1 defined unalterable flaw, some people wont benefit from it. No matter how good a drug is, some people will either be immune/resistant to it or allergic to it. In these cases it would be useless. Now this holds true for any treatment, some people just wont benefit from it. This kept in mind I think the public could benefit from gene therapy and a good drug oriented cure so both should be pursued.
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I pray that medical science frinds a solution SOON!