One of the ways by which viruses evade our immune system is mutation. They change parts of their genetic code, which results in small differences in the production of molecules that make up the 'body' of the virus. These changes often render the body 'blind' for the threat, because it is set to respond against predetermined molecular signatures. Scientists from MIT and Harvard have revealed that HIV, the virus that causes AIDS, undergoes several mutations in the first few weeks after infection. This may be the reason why HIV is so effective in destroying our bodily defences, and it is important information for vaccine development.
Mutations
After HIV enters the body, it undergoes several rapid mutations in order to evade immune cells that are out to destroy the virus. That is what the researchers discovered when they looked at the genetic code at different time points after infection. It appears that these rapid adaptations are required to keep the HIV infection steady, and allow for an efficient rate of reproduction, necessary for the pathogenic process in which the virus tries to maintain its presence in the body. It was already known that mutation poses one of the key successes for HIV, but a mechanism that reveals fast adaptations right after infection is new for us.
Response
It appears that HIV has ways for a rapid response against whatever it is that the immune system is throwing at it. The scientists found that whenever the immune system had raised a bunch of cells able to recognize certain molecular signatures present on the viral surface, known as an epitope, HIV was able to change it. It means that the virus holds an extremely effective mechanism to escape from the immune system, by adapting as soon as our defences cooked up a way to destroy the virus. Because viral destruction is impossible without raising cells able to recognize something as foreign, our immune system is effectively blind.
Vaccine
This mechanism helps us to develop an effective vaccine against HIV. Because of these rapid adaptations, a vaccine would surely be rendered ineffective after just a short period. It means we need to target parts of the virus that are unable to change. For example, HIV might have certain structures that cannot change because it would render the viral molecule to be ineffective in doing whatever job it is supposed to do, in turn impairing its ability to spread throughout the body.
Outlook
It is an interesting find that helps us to better understand the pathological mechanism behind HIV infection. The most relevant part is of course that it enables us to develop longer lasting vaccines. We might even be successful with that relatively soon. Scientists from Emory University recently published data from a study performed on primates. The vaccine developed against the monkey-infecting sibling of HIV promises long-lasting protection against the virus. Human trials are supposed to start soon.
Mutations
After HIV enters the body, it undergoes several rapid mutations in order to evade immune cells that are out to destroy the virus. That is what the researchers discovered when they looked at the genetic code at different time points after infection. It appears that these rapid adaptations are required to keep the HIV infection steady, and allow for an efficient rate of reproduction, necessary for the pathogenic process in which the virus tries to maintain its presence in the body. It was already known that mutation poses one of the key successes for HIV, but a mechanism that reveals fast adaptations right after infection is new for us.
The molecular mechanism by which HIV infects a cell. Specific surface markers enable entry into the cell, whereafter the cellular machinery is hijacked to copy its genetic code. |
It appears that HIV has ways for a rapid response against whatever it is that the immune system is throwing at it. The scientists found that whenever the immune system had raised a bunch of cells able to recognize certain molecular signatures present on the viral surface, known as an epitope, HIV was able to change it. It means that the virus holds an extremely effective mechanism to escape from the immune system, by adapting as soon as our defences cooked up a way to destroy the virus. Because viral destruction is impossible without raising cells able to recognize something as foreign, our immune system is effectively blind.
Vaccine
This mechanism helps us to develop an effective vaccine against HIV. Because of these rapid adaptations, a vaccine would surely be rendered ineffective after just a short period. It means we need to target parts of the virus that are unable to change. For example, HIV might have certain structures that cannot change because it would render the viral molecule to be ineffective in doing whatever job it is supposed to do, in turn impairing its ability to spread throughout the body.
Outlook
It is an interesting find that helps us to better understand the pathological mechanism behind HIV infection. The most relevant part is of course that it enables us to develop longer lasting vaccines. We might even be successful with that relatively soon. Scientists from Emory University recently published data from a study performed on primates. The vaccine developed against the monkey-infecting sibling of HIV promises long-lasting protection against the virus. Human trials are supposed to start soon.
"Then again using air travel it continued in its march to geographical saturation until it now resides in over 30 million bodies - in every corner of the globe. Think of those 30 million poor souls as independent laboratories, each producing uncountable reproductions and mutations daily - with only one goal.
ReplyDeleteQ: And what would that goal be?
MA: To break out.
Q: You mean to be more virulent, don't you?
MA: Yes, it has only one purpose, only one drive and only one effect - it kills human beings.
This bit of malevolent RNA has now colonized the planet earth and is working on a scale that you cannot imagine to move from host to host more efficiently. As it now exists, it is very difficult for it to pass from host to host. That being so, any mutation that allows it more access to a wider number of carriers will be highly beneficial to the organism and its relentless attack on our species.
Q: I can understand that. But it has not evolved in that arena yet, why do you believe that there is a likelihood of it becoming more transmittable?
MA: There are really not that many potential outcomes.
1. We find a way to kill it.
2. It continues to be a manageable chronic illness.
3. It becomes more virulent."
Mother Abigail
NOVEMBER 26, 2010
http://www.freerepublic.com/focus/bloggers/2820204/posts?q=1&;page=51#83