HIV-1 Viral Protein R Displays Anti-Cancer Effects.
43 replies, posted
In a first time effort on my part, I bring you my own reporting on primary sources of scientific research and interest. Exclusive to the [i]In The News[/i] section. Let hope this goes as well as I hope.
[b]Introduction and [i] in vivo[/i] Results:[/b]
Published in the open access journal PLoS ONE, a team based out of the University of Maryland recently reported on a novel application of a protein that is generated by the HIV-1 strain of the AIDS causing virus. This research shows a significant reduction of cell growth [i]in vitro[/i] and a sizable decline of around 50%-75% in tumor size of chemotherapeutic resistant types of neuroblastoma (A malignant tumor formed on nervous tissue). These effects are thought to be largely due to the impact HIV-1 Viral Protein R (VPR) has on the cell life-cycle.
These effects are caused via multiple pathways, firstly, it seizes the cell life-cycle of quickly dividing cells in the G2-interphase period (Longest phase of cell division where the cells gather resources to divide), leading to the cessation of meiotic activity (cell division) within the fast growing cells, resulting in their eventual deaths. The net effect of this is shown in figure 1 below:
[tab]VPR induced G2 arrest (stoppage of cell division) shown on the right in multiple cell lines (cells grown in culture) of varying types of cancers Cervical Cancer(HeLa) osteosarcoma (SaOS2), and breast adenocarcinoma (MCF-7)[/tab] [img]http://www.plosone.org/article/fetchObject.action?uri=info%3Adoi%2F10.1371%2Fjournal.pone.0011466.g001&representation=PNG_M[/img]
Secondly, it induces apoptosis (cell death) via normal p53 tumor suppressor related signaling pathways. This induces cell death at any stage of the mitotic (cell division) process. This, along with the G2 arrest is seen in cell lines that are resistant to traditional chemotherapeutic agents.
Figure 2:
[tab]On the left is a normal variant of the cancer, and on the right is a drug resistant strain. The two graphs are similar due to the novel treatment's ability to bypass normal resistance[/tab][img]http://img535.imageshack.us/img535/526/journalpone0011466g003.png[/img]
This figure shows the death of cells on the verical axis using Trypan blue flow cytometry (establishes viability of the cells in culture as well as counts them) for both Wide Type (normal variety, not drug resistant), and DOX (Chemotherapeutic agent) resistant neuroblastoma in the first row of graphs. The second row is cell viability based on the MTT assay (another form of viability determination). The horizontal bar is the multiplicity of infection (or effectiveness) of the viral vector they used to have the cells generate the Viral Protein R. Fig 1 b. is a quantitative western blot (protein detection test) analysis of the amount of Vpr generated for each MOI level.
[b][i]In Vivo[/i] Results:[/b]
In addition to the [i]in vitro[/i] tests, they also performed [i]in vivo[/i] testing of the efficacy of the same treatment of human neuroblastoma in a mouse host. Table 1 is a summary of the effects seen in reducing the size of both wide type and DOX resistant neuroblastoma:
[img]http://www.plosone.org/article/fetchObject.action?uri=info%3Adoi%2F10.1371%2Fjournal.pone.0011466.t002&representation=PNG_M[/img]
As seen in this table, the viral protein has a promisingly positive effect in the reduction of tumor sizes [i]in vivo[/i]. With tumors being reduced by up to 75% over the control groups. This is an incredible reduction in size over the standard treatment course.
[b]Summary and Discussion of Implications:[/b]
Based on this research, this novel application of HIV-1 Viral Protein R seems to be quite promising at least in the early stages. However, some difficulties lie ahead in the adoption of these treatments. One of these could be that the same cancer-fighting effects are not seen in humans, as most treatments die in Phase I human testing.
More worryingly is the delivery system. In this paper, they used an adenovirus vector to transcribe the host's DNA with the strain of DNA required to assemble the protein, this has the side effect of being very long lasting. A better way might be to simply inject the viral protein into the patient directly, this would also allow for a better control over the dosage and duration of treatment.
Patients may not savor the thought of having something that a virus with the reputation of HIV produces injected into their bloodstream, and this may serve as the greatest barrier to the adoption of this new treatment, if indeed it does pan out in the later phases of testing. But this protein is not infectious on its own, and will not cause you to generate serum antibodies against HIV.
Primary Article/Source:
Zhao RY, Liang D, Li G, Larrimore CW, Mirkin BL (2010) Anti-Cancer Effect of HIV-1 Viral Protein R on Doxorubicin Resistant Neuroblastoma. PLoS ONE 5(7): e11466. doi:10.1371/journal.pone.0011466
Wow.
good job.
HIV kills cancer? Well i never....
impressive
At first I thought it just said "Most die in human testing" instead of "Most treatments dies in human testing".
I understood everything in the op
Usually in the joke, the cancer kills the aids.
An epic discovery of cellular proportions, indeed.
The advancement in Cancer curing lately is fantastic, but a thought it the back of my head is screaming "I am legend" I wonder if something like could ever come from treatments like this.
Cool, we can cure cancer by giving people aids?
HIV may lead to AIDS, but it is not AIDS. This is just a protein from HIV, and seeing as it is for medical use, it would not actually give the person HIV.
This pretty much explains it: "This protein is not infectious on its own, and will not cause you to generate serum antibodies against HIV."
[QUOTE=|FlapJack|;23249744]Cool, we can cure cancer by giving people aids?[/QUOTE]
Not quite, this uses just one of the proteins that HIV-1 uses in its replication cycle. this protein is only immunogenic (active in the immune system) on a very low-level, it is not infectious and does not cause any form of systemic response, or lead to AIDS.
I sat there the entire time stroking the small amount of hair I have on my chin at the moment, nodding, and occasionally saying, "uhhu, uhhu..." out loud.
I understood next to NOTHING in the OP :saddowns:
[QUOTE=sltungle;23250476]I sat there the entire time stroking the small amount of hair I have on my chin at the moment, nodding, and occasionally saying, "uhhu, uhhu..." out loud.
I understood next to NOTHING in the OP :saddowns:[/QUOTE]
I'm working on trying to define more of the terms clearly without interrupting the flow of the text, it's not very easy. It's already a great deal more simple than the original paper. Not sure how much easier I can make it. Suggestions and comments are appreciated.
So one of mankind's most reviled diseases has a component that can destroy another of mankind's great enemies; cancer.
Well i'll be darned.
[QUOTE=sltungle;23250476]I sat there the entire time stroking the small amount of hair I have on my chin at the moment, nodding, and occasionally saying, "uhhu, uhhu..." out loud.
I understood next to NOTHING in the OP :saddowns:[/QUOTE]
Not that hard to understand if you actually [i]read it[/i]
Just wondering, are you guys interested in having me do more of these? I'll try and look through the scientific literature for some important and interesting, but unnoticed by the general media/popular science media and do writeups one them. I would be focusing on biotechnology related areas, as that's where my expertise lies.
I found this really interesting, so yeah if you can find some more in this field.
[QUOTE=Kai-ryuu;23250536]Not that hard to understand if you actually [i]read it[/i][/QUOTE]
I DID read it. There's a lot of words in there I'm not familiar with.
Then again, I never continued with biology past year 10. I took chem and physics instead.
[QUOTE=sltungle;23250670]I DID read it. There's a lot of words in there I'm not familiar with.
Then again, I never continued with biology past year 10. I took chem and physics instead.[/QUOTE]
What sections were particularly bad for you?
[QUOTE=Kagrenak;23250689]What sections were particularly bad for you?[/QUOTE]
Well it'd be nice if you put an explanation next to things like G2-interphase period. You know, in brackets or something. Much easier than everyone having to have 20 wikipedia tabs open just to understand what they're reading.
You can still understand most of it, even if you don't understand a few technicalities.
The brackets idea might be good though.
[QUOTE=sltungle;23250738]Well it'd be nice if you put an explanation next to things like G2-interphase period. You know, in brackets or something. Much easier than everyone having to have 20 wikipedia tabs open just to understand what they're reading.[/QUOTE]
I tried to provide some context for these things, but I'll try and go through and give explicit definitions of the more obscure ones. It's just that I have difficulty separating what my colleagues and I know with what someone with a general background knows. Help determining difficult passages would be nice, along with general comments on the writing of the article.
[QUOTE=Kagrenak;23250785]I tried to provide some context for these things, but I'll try and go through and give explicit definitions of the more obscure ones. It's just that I have difficulty separating what my colleagues and I know with what someone with a general background knows. Help determining difficult passages would be nice, along with general comments on the writing of the article.[/QUOTE]
[b]Anything[/b] that you've been taught in higher education regarding biology is probably gonna need an explanation tagged on with it for optimal understanding.
Also what's up with the 4 graphs? Each of the two graphs with the corresponding other two graphs look nearly identical. It just looks like the y-axis has been compressed on the right hand graphs. They should have used bigger graphs so it's easier to notice the differences.
[QUOTE=sltungle;23250832][b]Anything[/b] that you've been taught in higher education regarding biology is probably gonna need an explanation tagged on with it for optimal understanding.
Also what's up with the 4 graphs? Each of the two graphs with the corresponding other two graphs look nearly identical. It just looks like the y-axis has been compressed on the right hand graphs. They should have used bigger graphs so it's easier to notice the differences.[/QUOTE]
Went through and added more definitions.
The left hand column is a normal variety of the cancer, and the one on the right is the drug resistant one. They are largely the same as the treatment bypasses the drug resistance of the special variety. This is one of the reasons why the research is significant. Added this in a tab next to [i]Fig. 2.[/i]
That's a lot better :) That should help people understand it a bit better. Not me, though. I'd already wiki'd it all and made sense of it :v:
Thanks anyway, though.
TL:DR for those who does not get it/does not want to read:
AIDS kills Cancer.
[editline]04:27PM[/editline]
And i know this used a non-infectious part, but its a TL:DR.
Well, this is an interesting turn of events.
[QUOTE=Aerkhan;23251320]TL:DR for those who does not get it/does not want to read:
AIDS kills Cancer.
[/QUOTE]
No it doesn't. I mean it doesn't have anything to do with this specific topic. AIDS is a disease. HIV is the virus. A protein (VPR) of HIV stops cancer cells from going further than the G2 stage of cell division (so the tumour stops growing) and causes
that, already present, p53 suppressor protein to cause cell death.
Also I think there is a mistake in the 3rd paragraph... it should be mitotic not meiotic, right?
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