Word: cd4
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...initial reaction was, Are you crazy?" recalls Sandy Vasan, a researcher at ADARC who, along with Ho and Huang, is now heading the ibalizumab studies. A clinician who sees patients, Vasan says, "It's really scary to want to put an antibody on CD4. You need CD4." (See "The Year in Health 2009: From...
Looking at the numbers, Ho saw more than just another member of the growing arsenal of ARV cocktails. Each of the ARVs focuses on thwarting just one of several different steps in HIV's infection process. Ibalizumab works at the critical juncture where the virus meets a healthy CD4 cell - a critical component of the immune system - essentially interposing itself between the two and preventing infection. If ibalizumab was so good at tamping down HIV in AIDS patients who were already infected, then maybe it could be tweaked to prevent AIDS in the first place. In other words, maybe...
What the ADARC scientists are struggling to achieve is a thorough understanding of how ibalizumab operates and how they can control those machinations. The CD4 cell is a bit like an immunological sentinel, endowed with the ability to recognize snippets of various pathogens, from common influenza to HIV, and mark them for destruction by other cells. Once attached to a CD4, HIV begins an intricate series of steps to gain entry into the cell. Ibalizumab is able to disrupt this intricate molecular choreography by binding to the CD4 and serving as an immunological snare. With the antibody stuck...
That's the beautifully elegant scenario that attracted Ho to the antibody, but the problem is that tying up CD4 this way may not be such a good idea. Taking so many of the body's essential defense cells out of commission means the patient may be left vulnerable to any number of other infectious agents - exactly the immunocompromised position that AIDS patients are trying to avoid. That was the fear that Ho's lab members expressed when he broached the idea...
...believes ibalizumab is more agile than that. CD4, it turns out, is like a marina with several docks; HIV berths in one, and ibalizumab in another, leaving the cell free to fight other pathogens. "If CD4's binding site to HIV is with its nose, then this antibody is binding to the back of CD4's neck," Ho says. That means the cell's ability to function as a pathogen troller is not impaired by being coupled to ibalizumab. "There is a solid scientific rationale for what they are attempting to do," says Harvard's Walker...