Phage , the virus that cures

[William Gaatjes]

To support modestgamer with his claim that vaccinations can be a serious risk :

It seems some people acquired an autoimmune disease similar to multiple sclerosis after an HPV vaccination in Australia. The Gardasil vaccin is used to prevent a possible cancer of the cervix or other parts of the female reproductive system.
http://www.tga.gov.au/alerts/medicines/gardasil.htm

The TGA is also aware of a small number of cases in which neurological symptoms, similar to those experienced in patients with a demyelinating disorder such as multiple sclerosis, have been reported shortly after HPV vaccination. In some of these cases symptoms were present prior to the vaccination. These reports have been actively investigated by an independent panel of clinical and scientific experts in immunology, neurology, epidemiology and paediatrics. Based on the available reported cases, the incidence of demyelinating disorders amongst recipients of Gardasil is not demonstrably higher than would be expected to occur by chance.

I do not feel comfortable with the results.


How are vaccines made today ?
Are there still animals used or are there cultured cells used as in for example petri dishes ?

 

[Gibsons]

Another possibility may be that in the process of a virus infection a protein is created that looks like a protein used in the human body in an entirely different part of the human body. As such, one could acquire an auto immune disease. I do not think that auto immune diseases are all a defect in genetic code. That would be to perfect and clean. Nature does not work with closely guarded boundaries.

What you're referring to is called mimicry. Seems to happen with Strep, or at least that's the theory (google rheumatic fever). Probably some other cases out there but not so well understood. I'd guess they're very rare though.

As I said before, there are definitely genetic/inherited components to some autoimmune diseases as well as some environmental contributions. For some really odd stuff, look at the geographic associations (37th parallel) with Multiple Sclerosis.

 

[William Gaatjes]

What you're referring to is called mimicry. Seems to happen with Strep, or at least that's the theory (google rheumatic fever). Probably some other cases out there but not so well understood. I'd guess they're very rare though.

Interesting : mimicry, also known as cross reactivity. I have not fully read or understood the mechanism. But that does seem to worry me. I think research to find out how the immune system can be strengthened and partially reset on a certain group of antibodies or antigens if necessary will be a very good advancement.

As I said before, there are definitely genetic/inherited components to some autoimmune diseases as well as some environmental contributions. For some really odd stuff, look at the geographic associations (37th parallel) with Multiple Sclerosis.

I did, but what i read, is that everything can be blamed.
Metals in the soil to low radioactivity to low hygiene in houses.

This could however be once again a combination problem. Heavy metals or chemicals or radiation would weaken the immune system. Then the virus would be able to do it's damage more easy and in the end multiple sclerosis as a result. Maybe even more variables have to be met though. Multiple infections with different viruses perhaps or bacteria... Past events from infections.

EDIT:
However, if the soil has a certain chemical or elemental composition, then it must also have a certain bacterial composition and a certain virus composition.

 

[Gibsons]

To support modestgamer with his claim that vaccinations can be a serious risk :

You're better off ignoring modestgamer if you want to understand anything. He's either a drooling moron or a very persistent troll.

I suspect the article you're linking is referring to Guillain Barre syndrome. Chances of it occurring are about one in a million. Vaccination might raise that chance slightly, and a viral infection might raise it as well.

The rest of what you're talking about is just too speculative to specifically discuss. Yes, it could be this or that, and we also could be in the matrix.

 

[Mr. Pedantic]

I do not feel comfortable with the results.

Did you read your own exerpt? "Based on the available reported cases, the incidence of demyelinating disorders amongst recipients of Gardasil is not demonstrably higher than would be expected to occur by chance."

How are vaccines made today ?
Are there still animals used or are there cultured cells used as in for example petri dishes ?

The nucleic acid coding for surface proteins (or any other antigen that can be used by the immune system to identify the virus) is extracted from the virus and reinserted into another, attenuated virus - one with all virulence factors removed, or one cultured to infect at above or below body temperature, etc.

 

[tcsenter]

I suspect the article you're linking is referring to Guillain Barre syndrome. Chances of it occurring are about one in a million. Vaccination might raise that chance slightly, and a viral infection might raise it as well.

Its about one in 1000 for persons who have a bout of Campylobacteriosis. Campylobacter is one of the most common (often cited as THE most common) types of food poisoning or causes of invasive diarrhea (in the developed world).

 

[William Gaatjes]

You're better off ignoring modestgamer if you want to understand anything. He's either a drooling moron or a very persistent troll.

I suspect the article you're linking is referring to Guillain Barre syndrome. Chances of it occurring are about one in a million. Vaccination might raise that chance slightly, and a viral infection might raise it as well.

The rest of what you're talking about is just too speculative to specifically discuss. Yes, it could be this or that, and we also could be in the matrix.

I wil look it up, thank you.

Babylonical translation errors are the burden of human society.
I do not agree with that cancer is an virus.
But i understand what he is trying to write about vaccination.
However, i personally think contamination of vaccination serums is the real problem.


EDIT:

The rest of what you're talking about is just too speculative to specifically discuss. Yes, it could be this or that, and we also could be in the matrix.

Well, then you have a future for you. ^_^
Don't be silly. The matrix... That is the most worst idea to generate electricity i have ever seen.

 

[William Gaatjes]

Did you read your own exerpt? "Based on the available reported cases, the incidence of demyelinating disorders amongst recipients of Gardasil is not demonstrably higher than would be expected to occur by chance."

Afcourse i read it.
I did. But i do not always like the results of data massage. When smoothing the unknown, there might be something hidden as well.
When somebody tells me that it is statistical insignificant, what he or she is actually meaning that he/she does not know. I am difficult sometimes i know.

The nucleic acid coding for surface proteins (or any other antigen that can be used by the immune system to identify the virus) is extracted from the virus and reinserted into another, attenuated virus - one with all virulence factors removed, or one cultured to infect at above or below body temperature, etc.

That is interesting. But in what are the weakened viruses with desired antigen injected to, to make more copies ? Bacteria ? Animals ? Special cultured human cells ?

 

[Mr. Pedantic]

Afcourse i read it.
I did. But i do not always like the results of data massage. When smoothing the unknown, there might be something hidden as well.
When somebody tells me that it is statistical insignificant, what he or she is actually meaning that he/she does not know. I am difficult sometimes i know.

It does not mean he/she does not know. It means that the results are sufficiently similar that given the experimental error involved it is likely that any differences are due to chance. There is a difference. An important difference.

That is interesting. But in what are the weakened viruses with desired antigen injected to, to make more copies ? Bacteria ? Animals ? Special cultured human cells ?

Chicken embryos, as far as I'm aware. This is expensive, since 1 embryo provides roughly 3 doses of vaccine, so something else is probably used now.

 

[Gibsons]

That is interesting. But in what are the weakened viruses with desired antigen injected to, to make more copies ? Bacteria ? Animals ? Special cultured human cells ?

Okay, I guess I'll try to clear this up.

Vaccines can be divided into two categories, passive and active. We're talking about active vaccines in this case.

Active vaccines can be divided further into two categories, generally called attenuated and inactivated.

An inactivated vaccine is denatured (sometimes called "killed" although a virus isn't technically alive by some standards). The common flu vaccine is this kind. Virus is grown up in chick embryos, then denatured. The viral proteins are then injected into the vaccinee. The immune response to this is usually solely antibody based, specifically serum IgG. This isn't the strongest immune response around, but for some diseases it's enough. The failure rates from this approach can be pretty high, but they're generally safe.

An attenuated vaccine is one where the vaccine agent is 'alive' or capable of infecting, maybe even reproducing. The classic example of this is the cowpox-chickenpox story. The cowpox and smallpox viruses are closely related, so an immune reaction against one is effective against the other. When cowpox infects a human, it's a very mild disease, zero percent mortality assuming a normal immune system. But the immune response against it is extremely effective against smallpox. Smallpox has a ~30% mortality rate. Attenuated vaccines tend to be more effective than inactivated, they raise different 'arms' of the immune response as well as the serum IgG response, usually a much better memory response.

Nature isn't always kind enough to provide us with a closely related animal version of a particular virus however, so we have to attenuate it ourselves. This usually means growing it at a lower temperature, and maybe in other animal cells for several generations. Basically, you let evolution take its course and the virus adapts to the new cells and temperature, such that when it is later introduced into humans at a higher temperature, it's no longer pathogenic. Can't use it in the immunocompromised, and there's some chance that it can revert to pathogenic. So, it's more effective, but less safe.

We are getting much more sophisticated now though. Different variations on this approach with hybrid viruses, single cycle viruses etc are being tested and show some promise against some previously intractable diseases. DNA vaccines are another matter. DC vaccinations might be the best approach of all but they're too expensive for widespread use.

Regarding my matrix comment - yes, humans as living batteries is a very dumb idea. But are we all a computer simulation? It's an interesting question. link As with your more speculative ideas - yes it's possible, but so are lots of things that aren't worth worrying about.

 

[William Gaatjes]

Okay, I guess I'll try to clear this up.

Vaccines can be divided into two categories, passive and active. We're talking about active vaccines in this case.

Active vaccines can be divided further into two categories, generally called attenuated and inactivated.

An inactivated vaccine is denatured (sometimes called "killed" although a virus isn't technically alive by some standards). The common flu vaccine is this kind. Virus is grown up in chick embryos, then denatured. The viral proteins are then injected into the vaccinee. The immune response to this is usually solely antibody based, specifically serum IgG. This isn't the strongest immune response around, but for some diseases it's enough. The failure rates from this approach can be pretty high, but they're generally safe.

An attenuated vaccine is one where the vaccine agent is 'alive' or capable of infecting, maybe even reproducing. The classic example of this is the cowpox-chickenpox story. The cowpox and smallpox viruses are closely related, so an immune reaction against one is effective against the other. When cowpox infects a human, it's a very mild disease, zero percent mortality assuming a normal immune system. But the immune response against it is extremely effective against smallpox. Smallpox has a ~30% mortality rate. Attenuated vaccines tend to be more effective than inactivated, they raise different 'arms' of the immune response as well as the serum IgG response, usually a much better memory response.

Nature isn't always kind enough to provide us with a closely related animal version of a particular virus however, so we have to attenuate it ourselves. This usually means growing it at a lower temperature, and maybe in other animal cells for several generations. Basically, you let evolution take its course and the virus adapts to the new cells and temperature, such that when it is later introduced into humans at a higher temperature, it's no longer pathogenic. Can't use it in the immunocompromised, and there's some chance that it can revert to pathogenic. So, it's more effective, but less safe.

We are getting much more sophisticated now though. Different variations on this approach with hybrid viruses, single cycle viruses etc are being tested and show some promise against some previously intractable diseases. DNA vaccines are another matter. DC vaccinations might be the best approach of all but they're too expensive for widespread use.

Regarding my matrix comment - yes, humans as living batteries is a very dumb idea. But are we all a computer simulation? It's an interesting question. link As with your more speculative ideas - yes it's possible, but so are lots of things that aren't worth worrying about.

Well, i for large part know about this in a rudimentary, but i a have some questions anyway.
I was interested in the chicken embryos, are these grown/born in a sterile environment or is the vaccine a combination of the inactivated virus and other viruses naturally present in the chicken ?
Denatured, does that mean process the alive viruses with formaldehyde ?


An attenuated virus, that sound like let it adapt to another host or another species. Then use that same virus to infect humans. I am interested in the hosts for the same reason that no animal is possibly free of viruses. Because this reminds of the poliovirus accident from the 1960s.
We both would agree sterile hosts are needed, yes ?

You mention temperature. Why is temperature so important to viruses ? I know that an increase in temperature speeds up chemical reactions. Must i see it in that direction ?

 

[Gibsons]

Well, i for large part know about this in a rudimentary, but i a have some questions anyway.
I was interested in the chicken embryos, are these grown/born in a sterile environment or is the vaccine a combination of the inactivated virus and other viruses naturally present in the chicken ?
Denatured, does that mean process the alive viruses with formaldehyde ?


An attenuated virus, that sound like let it adapt to another host or another species. Then use that same virus to infect humans. I am interested in the hosts for the same reason that no animal is possibly free of viruses. Because this reminds of the poliovirus accident from the 1960s.
We both would agree sterile hosts are needed, yes ?

You mention temperature. Why is temperature so important to viruses ? I know that an increase in temperature speeds up chemical reactions. Must i see it in that direction ?

Chicken embryos = eggs, more or less. They grow the virus, purify it, then heat+formaldehyde denature it. Other viruses aren't a big concern with chicken eggs (not saying it should be ignored however). But, the heat and formaldehyde, if properly done, will denature any virus, so there's not much issue with another virus anyway. No real concerns with 'bits of RNA and DNA' here either since formaldehyde was used.

dunno exactly what you mean by a "sterile" host. That's hard to quantify when you get concerns with endogenous viruses. The attenuated polio vaccine is/has been grown in monkey cells. Some other virus running around there is a possibility. Need to be very careful in choosing host cells, for sure. And, you can learn a bit from testing the vaccine in the right animal host. Finally, if there is some other virus in there, it should be specific for the other animal, but of course you can't be certain of that.

Temperature is important because you can grow the virus at a low temperature for many generations. This will allow the whole viral population to accumulate temperature-sensitive mutations. i.e. the mutated gene now encodes a protein that works fine at 30C, but at an elevated temperature (37C) it tends to misfold and function poorly or not at all. Thus the virus has a very difficult time reproducing in a human host. With the attenuated version of the influenza vaccine, it can mean that it reproduces in the nasal passages, but not deeper in the respiratory tract.

 

[William Gaatjes]

Chicken embryos = eggs, more or less. They grow the virus, purify it, then heat+formaldehyde denature it. Other viruses aren't a big concern with chicken eggs (not saying it should be ignored however). But, the heat and formaldehyde, if properly done, will denature any virus, so there's not much issue with another virus anyway. No real concerns with 'bits of RNA and DNA' here either since formaldehyde was used.

dunno exactly what you mean by a "sterile" host. That's hard to quantify when you get concerns with endogenous viruses. The attenuated polio vaccine is/has been grown in monkey cells. Some other virus running around there is a possibility. Need to be very careful in choosing host cells, for sure. And, you can learn a bit from testing the vaccine in the right animal host. Finally, if there is some other virus in there, it should be specific for the other animal, but of course you can't be certain of that.

Temperature is important because you can grow the virus at a low temperature for many generations. This will allow the whole viral population to accumulate temperature-sensitive mutations. i.e. the mutated gene now encodes a protein that works fine at 30C, but at an elevated temperature (37C) it tends to misfold and function poorly or not at all. Thus the virus has a very difficult time reproducing in a human host. With the attenuated version of the influenza vaccine, it can mean that it reproduces in the nasal passages, but not deeper in the respiratory tract.

Ah thank you.
The bold part i find very amazing. It is so obvious that i would not think about it. The temperature has effect on the folding. I learn every day something new.


I do worry about contamination though. I find it very likely that the human immune system has no problem with weakened viruses. But alive and kicking viruses from another species ? This would be creating a situation where a virus can jump between species. And that is not an impossible scenario, taking into account food habits, diseases, inoculation from contaminated vaccines, the environment, genetic make up. When taking epi-genetics into account, most of the above mentioned variables have an epi-genetic influence it seems, maybe even all of them. And i am sure that certain rules can be laid out that one can predict that a certain stimulus would cause a genetic mutation or epi - genetic change in a certain direction...:hmm:



I did some reading, and some people are worried about the use of formaldehyde. They claim this can have an effect when received in the blood through inoculation. But i find it hard to believe that a small amount could have such an effect on the immune system. I would think the heart especially would not be so happy about it. But then again, i am not a chemist or biologist. I do not know how much is needed for a serious effect. And there is a linkage between formaldehyde and food. If the people who got an inoculation also ate prepared food where high concentration of formaldehyde would be present, then this would seem that it is the inoculation responsible for the elevated levels of formaldehyde found in the body. It is once again all very complex.

 

[Mr. Pedantic]

I do worry about contamination though. I find it very likely that the human immune system has no problem with weakened viruses. But alive and kicking viruses from another species ? This would be creating a situation where a virus can jump between species. And that is not an impossible scenario, taking into account food habits, diseases, inoculation from contaminated vaccines, the environment, genetic make up. When taking epi-genetics into account, most of the above mentioned variables have an epi-genetic influence it seems, maybe even all of them. And i am sure that certain rules can be laid out that one can predict that a certain stimulus would cause a genetic mutation or epi - genetic change in a certain direction...

It's what happens every time we get a flu 'outbreak'. Influenza A is mainly an avian virus, except we get outbreaks every couple of years when the NA and HG receptors mutate so that the virus can infect human cells. Of course, this is far more likely to happen if you are actively feeding the virus new material by packaging it in with a vaccine.

 

[William Gaatjes]

It's what happens every time we get a flu 'outbreak'. Influenza A is mainly an avian virus, except we get outbreaks every couple of years when the NA and HG receptors mutate so that the virus can infect human cells. Of course, this is far more likely to happen if you are actively feeding the virus new material by packaging it in with a vaccine.

I know. But if the biological researchers are going to create a virus, i prefer they create one that is easily recognized and defeated by the human immune system. Maybe one day it will be possible to steer mutations towards a direction where it is easily to control the mutation of the virus. Viruses will mutate and recombine and some diseases will be the result. If it would be possible to create a means to steer the lethality from the virus into a direction where it is not as dangerous anymore. I have read in the past about that some advanced and expensive chemical cocktails do just that with HIV. HIV starts to mutate into a certain direction when the body is flood with certain chemicals.

I found what Gibson mentioned about viruses and temperature very interesting.

There is temperature (body temperature) that limits the amount of possible reactions.
There is a certain chemical make up.
If we know about the exact details how the recombination of DNA occurred, there might be a way to severely limit the amount of possible mutations. One can never fully rule out all options to one single candidate but still. Ruling out viruses or bacteria, forget it. It is not going to happen. But steer them in a way that they are non lethal and possibly even more beneficial then they already are. That is a good thing. Combine that with full control over the immune system with respect to alarming it or resetting it for a certain chemical. Most of the sickness that exist will no longer be present.

Grrr. I hate the low infrasonic sounds of helicopters.

 

[Gibsons]

I know. But if the biological researchers are going to create a virus, i prefer they create one that is easily recognized and defeated by the human immune system. Maybe one day it will be possible to steer mutations towards a direction where it is easily to control the mutation of the virus. Viruses will mutate and recombine and some diseases will be the result. If it would be possible to create a means to steer the lethality from the virus into a direction where it is not as dangerous anymore. I have read in the past about that some advanced and expensive chemical cocktails do just that with HIV. HIV starts to mutate into a certain direction when the body is flood with certain chemicals.

I found what Gibson mentioned about viruses and temperature very interesting.

There is temperature (body temperature) that limits the amount of possible reactions.
There is a certain chemical make up.
If we know about the exact details how the recombination of DNA occurred, there might be a way to severely limit the amount of possible mutations. One can never fully rule out all options to one single candidate but still. Ruling out viruses or bacteria, forget it. It is not going to happen. But steer them in a way that they are non lethal and possibly even more beneficial then they already are. That is a good thing. Combine that with full control over the immune system with respect to alarming it or resetting it for a certain chemical. Most of the sickness that exist will no longer be present.

Grrr. I hate the low infrasonic sounds of helicopters.

There's no "steering" of mutations, not in the sense you're describing anyway. It's right next to impossible, even in theory, as long as you're talking about nucleic acid based reproduction.

There are some sophisticated approaches being developed right now. One idea is to take a harmless virus and engineer it to express a protein or three from your target virus. The immune reaction to this will target everything, and can be effective against the real thing. Look up RV 144. The idea I've always liked is DNA vaccines, they just haven't worked too well in the real world, at least not yet.

 

[William Gaatjes]

There's no "steering" of mutations, not in the sense you're describing anyway. It's right next to impossible, even in theory, as long as you're talking about nucleic acid based reproduction.

There are some sophisticated approaches being developed right now. One idea is to take a harmless virus and engineer it to express a protein or three from your target virus. The immune reaction to this will target everything, and can be effective against the real thing. Look up RV 144. The idea I've always liked is DNA vaccines, they just haven't worked too well in the real world, at least not yet.

Ok, what are your thoughts then about what i mentioned about HIV and the cocktails ? According to research at the time the virus seemed to mutate to a certain direction depending on the composition of the chemical cocktail. This was not a petri dish experiment. But the results of an experiment with real life infected humans.

 

[Gibsons]

Ok, what are your thoughts then about what i mentioned about HIV and the cocktails ? According to research at the time the virus seemed to mutate to a certain direction depending on the composition of the chemical cocktail. This was not a petri dish experiment. But the results of an experiment with real life infected humans.

HIV has a high mutation rate, and the mutations are mostly random. What happens with the drug treatments is you then get selection of those mutants that are resistant. Basic evolution.

 

[William Gaatjes]

HIV has a high mutation rate, and the mutations are mostly random. What happens with the drug treatments is you then get selection of those mutants that are resistant. Basic evolution.

Exactly. And what they found out is that you can push evolution to make the virus mutate in such a way it becomes more sensitive to other chemicals in the next cocktail. The resistance for chemical A made the virus more sensitive for chemical B. where chemical B would kill or at least disable the virus.

Now here is my theory :
Afcourse when using chemical B, mutation starts the other way around. Now this was not clear about what i read then, but i would think myself that the virus would have become resistant to chemical B but once again became more sensitive for chemical A. Now if that is the case, which i am willing to bet it is (And i do not like to bet) There is a pattern to be found. And that pattern is hidden in what you mentioned with temperature and the chemical composition. The chemical composition itself is depend on what atoms are used and on the sequence of RNA/DNA and enzymes used. Now i do not know all the details but i think this can be the case. Now afcourse this would still mean there are a lot more variables to account for like simultaneous infections of other viruses. But i truly think something can be found here. If one could reduce the number of possible mutations from for example 1000.0000.0000 to 1000.000 (just a random number as an example). That means a lot in favour of the immune system.

 

[Gibsons]

Exactly. And what they found out is that you can push evolution to make the virus mutate in such a way it becomes more sensitive to other chemicals in the next cocktail. The resistance for chemical A made the virus more sensitive for chemical B. where chemical B would kill or at least disable the virus.

link? something peer reviewed preferably? I think I know what's going on here, but it's still random, not directed, mutations.

 

[William Gaatjes]

link? something peer reviewed preferably? I think I know what's going on here, but it's still random, not directed, mutations.

It was some news item in a science magazine a year or 3 ago.
I do not know if it was peer reviewed. I was hoping you would have something.
But that should not be a major concern since most ground breaking science is ridiculed at first every time.
Although it is possible that it was just chance.

I will see if i can google something about it from the web.

If i remember correctly it was something about that first drug that inhibited something with the RNA to DNA transcription ?
Later on the virus adapted. After that they found another chemical that worked but the virus adapted to that too. But it became sensitive again to the first drug.

I remember a bit more :
reverse transcriptase, protease AZT.
Integrase


Yahooo :
I found something similar i think :

http://www.ncbi.nlm.nih.gov/pubmed/7679778

Wild-type reverse transcriptase has evolved for the survival of human immunodeficiency virus type 1 (HIV-1) by natural selection. In contrast, therapy relying on inhibitors of reverse transcriptase by nucleosides like zidovudine (AZT) or dideoxyinosine (ddI), and by non-nucleosides like pyridinones or nevirapine, may exert different selection pressures on this enzyme. Therefore the acquisition of resistance to reverse transcriptase inhibitors by selection of mutations in the pol gene may require compromises in enzyme function that affect viral replication. As single mutations are unlikely to confer broad resistance when combinations of reverse transcriptase inhibitors are used, multiple mutations may occur that result in further compromises. Certain drug combinations may prevent the co-existence of adequate reverse transcription function and multi-drug resistance (MDR). Unlike bacterial or eukaryotic drug resistance, retroviral drug resistance is conferred only by mutations in its own genome and is limited by genome size. Combining drugs directed against the same essential viral protein may thus prevent HIV-1 MDR, whereas the conventional approach of targeting different HIV-1 proteins for combination therapy may not, because genomes with resistance mutations in different HIV-1 genes might recombine to develop MDR. Here we show that several mutations in the HIV-1 reverse transcriptase gene that confer resistance to inhibitors of this enzyme can attenuate viral replication. We tested whether combinations of mutations giving rise to single-agent resistance might further compromise or even abolish viral replication, and if multidrug-resistant viruses could be constructed. Certain combinations of mutations conferring resistance to AZT, ddI and pyridinone are incompatible with viral replication. These results indicate that evolutionary limitations exist to restrict development of MDR. Furthermore, a therapeutic strategy exploiting these limitations by using selected multidrug regimens directed against the same target may prevent development of MDR. This approach, which we call convergent combination therapy, eliminated HIV-1 replication and virus breakthrough in vitro, and may be applicable to other viral targets. Moreover, elimination of reverse transcription by convergent combination therapy may also limit MDR.

I found some more information but while reading this website i had to acknowledge this is where it ends for me. Perhaps you can make sense of it. It is to detailed and to warm outside for me to decode what they mean.


http://jvi.asm.org/cgi/content/full/79/18/11981

 

[William Gaatjes]

Another example of how beneficial symbiosis with the right bacteria can be :

Now, in a paper to be published in the journal Science, University of Rochester biologist John Jaenike and colleagues document a clear example of a new mechanism for evolution. In previous well documented cases of evolution, traits that increase an animal's ability to survive and reproduce are conferred by favorable genes, which the animal passes on to its offspring. Jaenike's team has chronicled a striking example of a bacteria infecting an animal, giving the animal a reproductive advantage, and being passed from mother to children. This symbiotic relationship between host animal and bacteria gives the host animal a readymade defense against a hazard in its environment and thus has spread through the population by natural selection, the way a favorable gene would.

Jaenike provides the first substantial report of this effect in the wild in his paper "Adaptation via Symbiosis: Recent Spread of a Drosophila Defensive Symbiont," but he says it may be a common phenomenon that has been happening undetected in many different organisms for ages.

Aside from shedding light on an important evolutionary mechanism, his findings could aid in developing methods that use defensive bacteria to stave off diseases in humans.

Jaenike studied a species of fly, Drosophila neotestacea, which is rendered sterile by a parasitic worm called a nematode, one of the most abundant, diverse, and destructive parasites of plants and animals in the world. Nematodes invade female flies when they are young by burrowing through their skin and prevent them from producing eggs once they mature. However, when a female fly is also infected with a bacteria species called Spiroplasma, the nematodes grow poorly and no longer sterilize the flies, Jaenike found. He also discovered that, as a result of the Spiroplasma's beneficial impact, the bacteria have been spreading across North America and rapidly increasing in frequency in flies as they are passed from mother to offspring. Testing preserved flies from the early 1980s, Jaenike found that the helpful bacteria were present in only about 10% of flies in the eastern United States. By 2008, the frequency of Spiroplasma infection had jumped to about 80%.

"These flies were really getting clobbered by nematodes in the 1980s, and it's just remarkable to see how much better they are doing today. The spread of Spiroplasma makes me wonder how much rapid evolutionary action is going on beneath the surface of everything we see out there," Jaenike said.

He reasoned that the substantial increase in Spiroplasma infection was an evolutionary response to the recent colonization of North America by nematodes. As the nematodes invaded the continent, the bacteria proved to be a convenient and potent defense against the nematodes' sterilizing effect. Now, the majority of flies in eastern North America carry the bacteria, and the bacterial infection appears to be spreading west. Without any mutation in their own genes, the flies have rapidly developed a defense against an extremely harmful parasite simply by co-opting another organism and passing it on from generation to generation.

"This is a beautiful case showing that the main reason these Spiroplasma are present in these flies is for their defensive role," said Nancy Moran, the Fleming Professor of Ecology and Evolutionary Biology at Yale University. Moran studies the role of defensive symbionts in aphids. "These heritable symbionts are a way for an animal host to acquire a new defense very quickly. One way to get a truly novel defense is to get a whole organism rather than mutating your own genes that aren't that diverse to begin with."

Jaenike's work could also have implications for disease control. Nematodes carry and transmit severe human diseases, including river blindness and elephantiasis. By uncovering the first evidence of a natural, bacterial defense against nematodes, Jaenike's work could pave the way for novel methods of nematode control. He plans to investigate that prospect further.

Jaenike's coauthors on the paper are Robert Unckless and Lisa Boelio from the University of Rochester, and Steve Perlman and Sarah Cockburn from the University of Victoria in British Columbia. The work was funded by the National Science Foundation.

http://www.sciencedaily.com/releases/2010/07/100708141533.htm

 

[William Gaatjes]

How to become protected against viruses if you are a single cell organism ?

http://www.sciencedaily.com/releases/2008/10/081026094351.htm

These results enable a clearer understanding of the origin of, and reasons for, sexual reproduction in eukaryotes (1).

The researchers studied the impact of marine viruses on Emiliania huxleyi, one of the most abundant unicellular eukaryotes in oceans that significantly influences the carbon cycle and climates. In their diploid form, i.e. when they contain a pair of chromosomes (2N), Emiliania huxleyi produce mineral scales and form gigantic populations that are visible from space. But when attacked by marine viruses, they transform into haploid cells which only contain a single chromosome (N). These new, non-calcifying, highly motile cells are totally invisible to viruses (and undetectable on satellite photos) so that the species can live in peace to await safer times.

These scientists have called this the "Cheshire Cat" strategy, in homage to Lewis Carroll's novel " Alice in Wonderland". In this book, the crafty and philosophical Cheshire Cat escapes being beheaded on the order of the Red Queen by rendering his body transparent. In the same way, by changing their form during the haploid phase, eukaryotes can evade biotic pressure and reinvent themselves within their own species.

Our ancestors, unicellular eukaryotes, appeared in oceans some one billion years ago and "invented" sexuality. These species are characterized by a life cycle where haploid individuals (carrying a single copy of the genome, like gametes(2)) unify to form diploid individuals that will subsequently generate haploid cells once again. During this eukaryote "double life", humans and other multicellular eukaryotes whose haploid gametes remain imprisoned within a diploid body, tend to be the exception. Originally, and in most eukaryotes, haploid cells multiply in their environment to form independent populations. Sexuality has allowed eukaryotes to evade constant attacks by viruses so that they could evolve towards more complex, high-performance organisms, the ecological importance of which is still markedly underestimated.

Notes:

1) Cells where genetic material is preserved within a nucleus

2) Reproductive cells

The bolded part is interesting for climate research. What happens when the water gets colder or warmer ?


EDIT:

These cells have an impact on the carbon cycle with respect to the sea it seems.

I wonder if pollution could force these cells into their haploid cell state.
Or if pollution would make it easier for the viruses to infect these organisms called Emiliania huxleyi.

 

[Gibsons]

I found something similar i think :
http://www.ncbi.nlm.nih.gov/pubmed/7679778

The idea here is about what happens during antibiotic selection. A particular target of an antibiotic (in this case reverse transcriptase, RT) acquires mutations and in many cases a single point mutation renders the target resistant to the antibiotic, but still functional. it might not work quite as well as the the wild type enzyme, but it works well enough to get the job done.

You can then work at least two ways from there. 1. Treat (preferably at the same time) with a second drug that works by binding a different site on the enzyme. The enzyme now needs a second mutation in order to be resistant to both drugs. Also, the enzyme with two mutations might be even less efficient than the one mutation version. HAART therapy works along this strategy. It's usually a cocktail that includes two RT inhibitors and they bind at different sites on the enzyme. It's not so much the idea of 'making the enzyme less efficient,' it's that finding a virus with both mutations is less likely than finding a virus with either one. Thus at least one drug is effective against every virus in an infected person. (for the nit pickers - yes, HAART usually includes a protease inhibitor as well)

2. Treat with a second drug that's designed to be effective against the most common resistance mutation, but works in the same way (i.e. binding to the same site on the enzyme). Problem here is that you need to know the mutation(s), and be relatively certain that there's not a third mutation that's resistant to both. This isn't used too much or at all. Well sort of in bacteria, but not in a combination type approach. We find resistant bacteria, we develop a new drug that works against them, then we find bacteria resistant the that, we develop a new drug, etc. We're on like the 5th or 6th generation of cephalosporins for example.

Now, none of this involves 'guiding' evolution, that's kind of bizarre weird and I can't imagine how it might be done in any thing outside of Star Trek. It's really pretty standard stuff. And a point that can't be stressed enough, b/c sooo many people get it wrong: antibiotic treatments don't cause the mutations. They select for naturally occurring mutations. Given a large enough population, the mutations are already there. The antibiotic treatment just selects for them. Note there are a a few antibiotics out there that are mutagens in some sense, but it doesn't have much relevance here.

 

[William Gaatjes]

The idea here is about what happens during antibiotic selection. A particular target of an antibiotic (in this case reverse transcriptase, RT) acquires mutations and in many cases a single point mutation renders the target resistant to the antibiotic, but still functional. it might not work quite as well as the the wild type enzyme, but it works well enough to get the job done.

You can then work at least two ways from there. 1. Treat (preferably at the same time) with a second drug that works by binding a different site on the enzyme. The enzyme now needs a second mutation in order to be resistant to both drugs. Also, the enzyme with two mutations might be even less efficient than the one mutation version. HAART therapy works along this strategy. It's usually a cocktail that includes two RT inhibitors and they bind at different sites on the enzyme. It's not so much the idea of 'making the enzyme less efficient,' it's that finding a virus with both mutations is less likely than finding a virus with either one. Thus at least one drug is effective against every virus in an infected person. (for the nit pickers - yes, HAART usually includes a protease inhibitor as well)

2. Treat with a second drug that's designed to be effective against the most common resistance mutation, but works in the same way (i.e. binding to the same site on the enzyme). Problem here is that you need to know the mutation(s), and be relatively certain that there's not a third mutation that's resistant to both. This isn't used too much or at all. Well sort of in bacteria, but not in a combination type approach. We find resistant bacteria, we develop a new drug that works against them, then we find bacteria resistant the that, we develop a new drug, etc. We're on like the 5th or 6th generation of cephalosporins for example.

Now, none of this involves 'guiding' evolution, that's kind of bizarre weird and I can't imagine how it might be done in any thing outside of Star Trek. It's really pretty standard stuff. And a point that can't be stressed enough, b/c sooo many people get it wrong: antibiotic treatments don't cause the mutations. They select for naturally occurring mutations. Given a large enough population, the mutations are already there. The antibiotic treatment just selects for them. Note there are a a few antibiotics out there that are mutagens in some sense, but it doesn't have much relevance here.

I see, you are right. ^_^
The mutations where already present. That makes sense, now i think of it, because if the medicines would cause heavy mutations on these enzymes the virus and the host uses or on the DNA /RNA, then the host would very likely experience such serious effects as well.
But the selection method still has a lot of opportunity i would think. Meaning you can still steer the selection in a way. And thus you could say you are indirectly controlling evolution, because you are laying out a path of survival for those pathogens that will survive. And those survivors must have a weakness as well. It might not be an direct way. But for now it is still the way.