Ebola... Is Reston a last ditch possibility?

I'm putting this in the Gray area for a reason.

This is pure conjecture.

There is a strain of ebola called Reston. It was discovered in a group of primates that were being studied in a lab in Reston Virginia run by Hazleton research.

The involved primates were macaques from the Philippines.

They were tested and found positive on tests for Ebola Zaire. The infection moved into other primates in the facility without actual physical interaction. Ultimately, the entire population of the primate facility was euthanized.

During the 3 month process the lab technicians in the facility did not use protective clothing until ebola was actually found. None of the humans got sick. The strain was Named Ebola Reston. It is the only known strain of ebola that is not fatal to humans.

After the Reston outbreak, Hazelton Research Products was purchased by a company called Covance Inc.

I haven't found a specific reference to who actually owns the Reston virus patent but I expect it is owned by the Government via a contractor.

The issue I am thinking about is that this particular strain tested positive for Ebola Zaire so it is very close to it. Reston was not harmful to the humans that came into contact with it. Only the monkeys were affected.

Is it reasonable to expect that a human who was infected with Reston and survived would have antibodies that would protect the individual from other ebola strains?

If this were true, wouldn't it make sense to test as a possible vaccine?

I wouldn't be surprised if this remedy were top be used as a last ditch effort in case of extreme pandemic.
I'd be even less surprised if it was suddenly on the market and making some company a hell of a lot of cash.

Just wondering if this is a real possibility.

The lack of information on studies of Reston since it was discovered makes me wonder if it's a real solution that's been kept under wraps.

So,
I've thrown it out there. Any thoughts? Anyone have more info on Reston research?

That does sound possible. In the past, it was discovered that giving cowpox to humans was known to be a way of immunizing people against smallpox.

It would be interesting to know what the differences between the (Reston and regular Ebola viruses are. Is is the receptors that attach themselves to the cell membranes, the viral capsule or just the genes?

a reply to: badgerprints

Google scholar may assist you with what you're seeking.

Quite a few papers on it, and perhaps some on the antibodys created from it.

I have read about the use of cowpox to inoculate against smallpox.
I wish I knew more about this subject so I could discuss it more coherently.
I just don't have the background to discuss receptors, viral capsules and genes.

The record shows that the testing on the virus during the outbreak was strongly positive for Zaire but less so for others.
This must mean that there are significant genetic differences between the strains.

Still, the general similarities may be enough to create effective antibodies.

originally posted by: AlphaHawk
a reply to: badgerprints

Google scholar may assist you with what you're seeking.

Quite a few papers on it, and perhaps some on the antibodys created from it.

Never used google scholar.
I assume i've passed up a decent resource then.
I'll check it out.

a reply to: badgerprints

From what I heard having one strain does not protect you from the others.

It was mentioned on CNN health 2 minutes to understanding ebola also. Appearently immunity is 10 years for the specific strain you catch not others.
I am not a scientist though that specializes in this sort of thing and I also have been taking info at face value for the moment.

a reply to: AnteBellum

Ten years sure sounds like an arbitrary number. It takes 3,650 days? Sounds like it takes a certain amount of deviation from it's current form, which could take maybe a year, or 30. I would think the amount of cases over a given period of time (hosts for viral load to increase and mutations to occur) would be the main factor, not necessarily time itself.

originally posted by: AnteBellum
a reply to: badgerprints

From what I heard having one strain does not protect you from the others.

That's too bad.
It would mean that any mutation would likely render antibodies useless.
Someone who survived it once might succumb to a mutation at a later date.

a reply to: badgerprints

glad you brought this up...ive mentioned a few times I just read "the hot zone" which specifically tells of this story. From what I am understanding it is still only theory that their blood would help but it was a fact that something like 4-5 employees there were infected with it.

Would be a good start but I don't know enough about how different a virus is after a mutation.

a reply to: rockpaperhammock
I read Hot Zone years ago by accident.
I thought it was a book by a different Preston.
Ended up finishing the entire thing and it was fascinating.
Just bought it last night on Kindle so I'll be reading it again.

I am really curious about what kind of research has been done on Reston behind closed doors.

a reply to: badgerprints

Let me sum this up to make sure I have it right.

The Reston type of Ebola is non lethal to humans, infect humans and hope that it protects us from the other strains of Ebola.

If that is correct, the only problem I see (if it works) is infecting everyone before they catch another strain of the virus. To say that is a tremendous undertaking is stating things lightly.

a reply to: QuietSpeech

Yes,
Like I said, "Last ditch effort" and "Conjecture".
I'm only throwing it out for discussion.

The one point would be that reston could be a likely subject for manipulation as an inoculant because it didn't make humans sick.

The second would be a last ditch such as airborne spraying over populated areas in event of a massive pandemic in hopes that some of the population would produce working antibodies.

Total conjecture on that point.
Just thinking about the kind of thing that might happen if ebola mutated and started wiping out large portions of the population.

originally posted by: pl3bscheese
a reply to: AnteBellum

Ten years sure sounds like an arbitrary number. It takes 3,650 days? Sounds like it takes a certain amount of deviation from it's current form, which could take maybe a year, or 30. I would think the amount of cases over a given period of time (hosts for viral load to increase and mutations to occur) would be the main factor, not necessarily time itself.

I think that's actually how long your body will keep effective antibodies just to that un-mutated strain. It's an average number obviously. It has nothing to do with predicting speed of mutations. So it's a number about human antibodies not viruses.

I am speaking out of school on this subject though.



And as far as the OP goes, How do the antigens of the two strains coincide? If they are the same antigens then the same antibodies will work. I'm working to that answer, but I appear to be in over my head haha.

One thing that's promising is that I am pretty sure when you test for a virus you are testing for the antigen. So if you are getting a false positive for the Zaire strain then it should be a close relationship to reston strain.


This Paper seems to say that there is cross antibody effectiveness with reston and Zaire strains. But Its really hard for me to understand I might be reading wrong. I might be reading about another way of finding the antigens of ebola that works for both zaire and reston.. It's hard to know for me haha.

Link



OK so yea it's just for testing for Ebola, and the fact that they cross test positive.. NVM

a reply to: badgerprints

My brain is starting to hurt. What I am seemingly noticing is that zaire and reston are the two closer linked strains in antibody/antigen detection. Should be closer linked with vaccines but that's just me making a guess more or less.

Anti-HIV Protein from Blue-Green Algae Also Inhibits Ebola Infection

Researchers have discovered that a bacterial protein known to reduce the ability of the human immunodeficiency virus (HIV) to infect cells also inhibits infection by the Ebola virus. The antiviral protein, known as cyanovirin-N (CV-N), can extend the survival time of Ebola-infected mice,

So there's that.

What's important, is apparently if you can build up some amount of antibodies in the early stages of infection you have a much higher chance of survival. So getting that CV-N at the onset could give you some extra time to get up antibodies before too much spread and damage occurs.

I started a thread here on how there is a possiblity that the virus was created via low moisture mulch farming being taught in not just Western Africa but in all of Africa.
www.abovetopsecret.com...

originally posted by: KnightLight

And as far as the OP goes, How do the antigens of the two strains coincide? If they are the same antigens then the same antibodies will work. I'm working to that answer, but I appear to be in over my head haha.

One thing that's promising is that I am pretty sure when you test for a virus you are testing for the antigen. So if you are getting a false positive for the Zaire strain then it should be a close relationship to reston strain.

Yeah,

It seems that the test would indicate genetic similarity.
I'm over my head too.


I find it funny that there seems to be a definite idea that reston antibodies won't work at all with no explanations in literature as to why. Haven't found any testing literature yet.

Maybe it does work but that's something that the patent holder doesn't want us to know.
There's a conspiracy theory to think about.

Big drug keeps simple cure in reserve while ebola spreads.

Just being a conspiracist here. Not actually suggesting it's true.

a reply to: badgerprints

Yikes, you're making me remember some stuff that's all too close to where I live (Reston.)

I don't know if what defeats one marburg type virus would defeat another. It would depend alot upon the particular strain of the virus I think.

originally posted by: pl3bscheese
a reply to: AnteBellum



Ten years sure sounds like an arbitrary number. It takes 3,650 days? Sounds like it takes a certain amount of deviation from it's current form, which could take maybe a year, or 30. I would think the amount of cases over a given period of time (hosts for viral load to increase and mutations to occur) would be the main factor, not necessarily time itself.

The 10 year figure is referencing the 'acquired immunity' from that particular exposure and immunity; that is approximately how long the T-cells buried in your tissues will remain alive and ready to activate at the next exposure to that agent. If you are exposed within that time, they will activate, multiply, and attack by generating more antibodies, and some will return to the tissues and reservoirs to remain waiting for the next exposure.

No exposures in that period of time, will mean you will likely no longer have enough 'acquired immunity' to attack it if exposed again after the remaining T-cells recognizing that pathogen have died off.

If the virus mutates enough that it is not recognized as the agent that your 'acqired immunity' has adapted to, then there will be no attack, and therefore there will be a new infection by a new agent with no acquired immunity to stop it.

a reply to: lakesidepark
a reply to: KnightLight

Thanks to the both of you for helping me understand where this 10 year number came from. I'm guessing this is the duration of the T-cells lifespan before they will be replaced. Some die out, some remain, but the last will die out in ~10 years.

a reply to: pl3bscheese

That makes much more sense to me also and that's the problem I'm having believing anything the cdc or anyone right now is saying. There is no direct evidence.

I will say I heard that having specifics on certain diseases is impossible to determine, even with clinical studies over long times and numerous people. Why can't they just say it's all unconfirmed at the present time? Are they in denial also?