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Posted On: 07/03/2022 12:10:36 PM
Post# of 148984
When LRM is given to HIV patients, it prevents HIV from entering the CD-4 T Lymphocyte. It acts as an entry inhibitor. It does not keep it in a holding cell. It doesn't "go after' dormant HIV within CD-4 T Lymphocytes. All it does is prevent HIV from entering.
This Reservoir occurs not just in LRM treated patients, but in HAART treated patients as well. The HIV virus enters the CD 4 T Lymphocyte and then goes dormant for years and years. Finally, to emerge years later once HAART therapy is stopped or postponed. Thereby re-introducing the same disease process.
It is the virus' way of never being eradicated from a person's body once infected.
That is why they want to develop the HIV cure using AAV vector, Adeno Associated Virus Vector. Scott Kelly describes it here:
So if a patient has HIV, he has already developed antibodies to HIV. The body will try to reduce viral load on its own, but, in the end would be unsuccessful. The HIV virus will always win. Regardless, antibodies against it are in the patients memory. The HIV virus will go dormant while on HAART or LRM, but when the treatment stops, the HIV will re-emerge.
Now, it this patient receives the AAV vector treatment and the patient becomes capable of producing LRM within his own metabolism, if the HIV dormant virus, again becomes active and reproduces with in the CD-4T lymphocyte, and causes that cell to apoptosis, thereby spilling many HIV into the blood stream, it becomes impossible for those to enter any more CD-4 T lymphocytes because the body is now manufacturing its own LRM. And those free floating HIV progeny of the dormant HIV will be eliminated by the patient's antibodies and T memory cells.
It is possible, that with the patient's manufacture of LRM, this alone will suppress or prevent the dormant HIV from becoming activated, but if they do, their HIV progeny will be unsuccessful in entering any more cells due to the LRM already being produced by the patient's own metabolism, as encoded in their DNA by the AAV vector. So either the dormant HIV will remain dormant for life due to the presence of self manufactured LRM or if they decide to venture out and become active, they would then cause their host cell to apoptosis releasing their progeny into the blood leaving them susceptible to existing antibodies and T-memory cells and they also would be prevented from entering CD-4 T cells as well.
This Reservoir occurs not just in LRM treated patients, but in HAART treated patients as well. The HIV virus enters the CD 4 T Lymphocyte and then goes dormant for years and years. Finally, to emerge years later once HAART therapy is stopped or postponed. Thereby re-introducing the same disease process.
It is the virus' way of never being eradicated from a person's body once infected.
That is why they want to develop the HIV cure using AAV vector, Adeno Associated Virus Vector. Scott Kelly describes it here:
Quote:
Now, as Antonio mentioned, we do have some exciting news to announce regarding an NIH grant for HIV cure. We will be announcing this shortly, but OSHU has received ~$5 million grant from NIH to evaluate the role of LRM in HIV cure. The project director is Dr. Jonas Sacha. As you are aware, only 3 people have ever been cured of HIV and they received immune cells void of CCR5 receptor which is the same receptor that LRM blocks. What is unique about this grant, centers around the technology. We'll will be using a AAV vector (adeno associated virus vector), which delivers a gene encoded LRM into immune cells. Adenovirus is a promising vector platform due to safety and ability to stimulate immune responses in multiple species. This is essentially, a gene therapy designed to induce the body to produce LRM. If successful, this work could lead to a single injection that suppresses HIV replication long term without needing ART and this is one of the many projects we are working on to obtain non-dilutive capital financing of trials. We will keep you up to date as these progress.
So if a patient has HIV, he has already developed antibodies to HIV. The body will try to reduce viral load on its own, but, in the end would be unsuccessful. The HIV virus will always win. Regardless, antibodies against it are in the patients memory. The HIV virus will go dormant while on HAART or LRM, but when the treatment stops, the HIV will re-emerge.
Now, it this patient receives the AAV vector treatment and the patient becomes capable of producing LRM within his own metabolism, if the HIV dormant virus, again becomes active and reproduces with in the CD-4T lymphocyte, and causes that cell to apoptosis, thereby spilling many HIV into the blood stream, it becomes impossible for those to enter any more CD-4 T lymphocytes because the body is now manufacturing its own LRM. And those free floating HIV progeny of the dormant HIV will be eliminated by the patient's antibodies and T memory cells.
It is possible, that with the patient's manufacture of LRM, this alone will suppress or prevent the dormant HIV from becoming activated, but if they do, their HIV progeny will be unsuccessful in entering any more cells due to the LRM already being produced by the patient's own metabolism, as encoded in their DNA by the AAV vector. So either the dormant HIV will remain dormant for life due to the presence of self manufactured LRM or if they decide to venture out and become active, they would then cause their host cell to apoptosis releasing their progeny into the blood leaving them susceptible to existing antibodies and T-memory cells and they also would be prevented from entering CD-4 T cells as well.
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