The problem with broad spectrum anti-virals is that they are based on a very tight risk-benefit continuum. Viruses utilize the human cells' machinery to reproduce, so any anti-viral bears the distinct drawback of breaking the human cells' machinery. The more effective you are in stopping the virus from reproducing, the more you are breaking the cells themselves and therefore the more you will be killing the individual being treated. The alternative to this is to find viral life functions that are unique to viruses, and that usually means that they will be unique to a specific virus. Viruses that are similar are usually grouped together and can have similar or identical treatments, but different types of viruses (flu, rabies, yellow fever) are very different and there is not much that can be found that would be effective against all of them.
The peptide that is being used in this case is affecting the ability of the virus to attach to a cell. It does not however kill the virus. The attachment itself is very specific to HIV, and the only virus I know of that may be similar enough to be also inhibited would be the black plague. The black plague being fairly rare, I don't suspect that this drug will find much of a use outside of the HIV prevention field.
This could be very useful in conjunction with other AIDS treatments, but alone it probably would be more usefull in lowering the risk of initial infection rather than as a cure once the disease has taken hold.
Viruses are also difficult to combat because of their reproductive efficiency. This is why we have to use drug coctails to inhibit the development of AIDS in HIV patients. Its basically a numbers game, a game of odds. Lets say for simplicity's sake, that a mutation allowing the immunity to a specific drug in a virus is one in a million. That seems like we have pretty good chances, but if one offspring is immune, it can reinfect the entire body with the immune strain very quickly. With the number of viruses in a typical HIV patient exceeding many trillion, this will not work because the odds are 1 in a million, so 1 million tries will be successful out of 1 trillion. So then we use 2 drugs, and we can multiply our odds: 1 million x 1 million = 1 trillion. Now we have better odds, but it is still likely that a few viruses will develop immunity because we have only passed the 1 trillion to one odds, and we have a bit more than that number in viruses. Now when we have 3 drugs, we can increase our odds to 1 in 10^18, which seems to be high enough that the likelyhood of a virus becoming immune to all three drugs is pretty slim, as there probably wouldn't be nearly that many reproduced within a single human being. Now these numbers were chosen for ease of multiplication and may not be entirely accurate, but the general idea should be correct, and this is why we use 3 drug cocktails to combat HIV. Now I would assume that this math would also hold true for this new drug, so I would speculate that we would still need to use it in conjuction with other drugs.
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The problem with broad spectrum anti-virals is that they are based on a very tight risk-benefit continuum. Viruses utilize the human cells' machinery to reproduce, so any anti-viral bears the distinct drawback of breaking the human cells' machinery. The more effective you are in stopping the virus from reproducing, the more you are breaking the cells themselves and therefore the more you will be killing the individual being treated. The alternative to this is to find viral life functions that are unique to viruses, and that usually means that they will be unique to a specific virus. Viruses that are similar are usually grouped together and can have similar or identical treatments, but different types of viruses (flu, rabies, yellow fever) are very different and there is not much that can be found that would be effective against all of them.
The peptide that is being used in this case is affecting the ability of the virus to attach to a cell. It does not however kill the virus. The attachment itself is very specific to HIV, and the only virus I know of that may be similar enough to be also inhibited would be the black plague. The black plague being fairly rare, I don't suspect that this drug will find much of a use outside of the HIV prevention field.
This could be very useful in conjunction with other AIDS treatments, but alone it probably would be more usefull in lowering the risk of initial infection rather than as a cure once the disease has taken hold.
Viruses are also difficult to combat because of their reproductive efficiency. This is why we have to use drug coctails to inhibit the development of AIDS in HIV patients. Its basically a numbers game, a game of odds. Lets say for simplicity's sake, that a mutation allowing the immunity to a specific drug in a virus is one in a million. That seems like we have pretty good chances, but if one offspring is immune, it can reinfect the entire body with the immune strain very quickly. With the number of viruses in a typical HIV patient exceeding many trillion, this will not work because the odds are 1 in a million, so 1 million tries will be successful out of 1 trillion. So then we use 2 drugs, and we can multiply our odds: 1 million x 1 million = 1 trillion. Now we have better odds, but it is still likely that a few viruses will develop immunity because we have only passed the 1 trillion to one odds, and we have a bit more than that number in viruses. Now when we have 3 drugs, we can increase our odds to 1 in 10^18, which seems to be high enough that the likelyhood of a virus becoming immune to all three drugs is pretty slim, as there probably wouldn't be nearly that many reproduced within a single human being. Now these numbers were chosen for ease of multiplication and may not be entirely accurate, but the general idea should be correct, and this is why we use 3 drug cocktails to combat HIV. Now I would assume that this math would also hold true for this new drug, so I would speculate that we would still need to use it in conjuction with other drugs.