He was "cured" by a bone marrow transplant from a donor carrying the Delta-32 mutation, causing him to lack the CCR5 receptor, a cell-surface receptor present on antigen presenting cells of the immune system. This is not the only receptor that HIV can bind to and infect cells through, though. The CXCL4 receptor on activated T-cells is another target of the virus, and unless the donor is magically missing that one too, this guy still has HIV, and could spread it. He might more easily be able to fight the virus, especially in combination with typical HAART treatment (and considering his unique case, it's undoubted he would be receiving the therapy), but he is most definitely still HIV+, and the virus is still reproducing in his immune system, albeit without the help of using his APC's as a vector anymore.
It's not a cure, but it's a start."
A start is a damned good thing, at any rate, I think we can all agree.
especially in combination with typical HAART treatment (and considering his unique case, it's undoubted he would be receiving the therapy)
Nope. From AIDSMap:
The patient did not resume antiretroviral therapy after the transplant.
Nevertheless HIV remained undetectable by both viral load testing (RNA) and tests for viral DNA within cells, and HIV antibody levels declined to the point that the patient has no antibody reactivity to HIV core antibodies, and only very low levels of antibodies to the HIV envelope proteins.
And regarding the CXCR4 receptors: they're vulnerable, yes, but not attacked.
An additional indication that HIV is not present lies in the fact that the patient’s CD4 cells are vulnerable to infection with virus that targets the CXCR4 receptor. If any virus with this preference was still present, the researchers argue, it would be able to swiftly infect the large population of memory CD4 cells that has emerged.
From what I can get, this is because after all the immunosuppression therapy to keep him from rejecting the stem cell transplant, those new stem cells completely replaced all his old, infected CD4s.
The repopulation of CD4 cells was accompanied by the complete disappearance of host CD4 cells, and after two years the patient had the CD4 count of a healthy adult of the same age.
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"Okay, science time!
He was "cured" by a bone marrow transplant from a donor carrying the Delta-32 mutation, causing him to lack the CCR5 receptor, a cell-surface receptor present on antigen presenting cells of the immune system. This is not the only receptor that HIV can bind to and infect cells through, though. The CXCL4 receptor on activated T-cells is another target of the virus, and unless the donor is magically missing that one too, this guy still has HIV, and could spread it. He might more easily be able to fight the virus, especially in combination with typical HAART treatment (and considering his unique case, it's undoubted he would be receiving the therapy), but he is most definitely still HIV+, and the virus is still reproducing in his immune system, albeit without the help of using his APC's as a vector anymore.
It's not a cure, but it's a start."
A start is a damned good thing, at any rate, I think we can all agree.
Nope.
Nope. From AIDSMap:
The patient did not resume antiretroviral therapy after the transplant.
Nevertheless HIV remained undetectable by both viral load testing (RNA) and tests for viral DNA within cells, and HIV antibody levels declined to the point that the patient has no antibody reactivity to HIV core antibodies, and only very low levels of antibodies to the HIV envelope proteins.
And regarding the CXCR4 receptors: they're vulnerable, yes, but not attacked.
An additional indication that HIV is not present lies in the fact that the patient’s CD4 cells are vulnerable to infection with virus that targets the CXCR4 receptor. If any virus with this preference was still present, the researchers argue, it would be able to swiftly infect the large population of memory CD4 cells that has emerged.
From what I can get, this is because after all the immunosuppression therapy to keep him from rejecting the stem cell transplant, those new stem cells completely replaced all his old, infected CD4s.
The repopulation of CD4 cells was accompanied by the complete disappearance of host CD4 cells, and after two years the patient had the CD4 count of a healthy adult of the same age.