(Replying to PARENT post)
The scientists who discover these solutions are my heroes. They spend their lives tangled in these complexities and save actual lives with their work. That's admirable!
๐คkylehotchkiss๐9y๐ผ0๐จ๏ธ0
(Replying to PARENT post)
Just to check I understand this correctly, as a layman:
It stops HIV from progressing in the body, holding it at bay. Someone with HIV would need to take this medicine for the rest of their lives. It doesn't actually cure it. (not denying that holding it at bay is a significant step forward)
๐คTwirrim๐9y๐ผ0๐จ๏ธ0
(Replying to PARENT post)
The full paper is available on researchgate:
https://www.researchgate.net/publication/310327204_Identific...
๐คotm_shank๐9y๐ผ0๐จ๏ธ0
(Replying to PARENT post)
Reminds me of Shapely from William Gibson's Bridge Trilogy
"He was discovered by the AIDS industry when he had already been HIV-positive for twelve years. His strain of HIV was notpathogenic but was able to kill the lethal strain of HIV. By isolating his mutant strain of HIV it was possible to develop an AIDS vaccine."
๐คerrantspark๐9y๐ผ0๐จ๏ธ0
(Replying to PARENT post)
Thank you for this elegant summary!
๐คj_m_b๐9y๐ผ0๐จ๏ธ0
(Replying to PARENT post)
The article indicates that this could be used to create a vaccine. How would that work? So far as I understand the medicine for vaccines, they are used to train your immune system to create new antibodies by exposing it to the virus. What process would be used to train the immune system from an existing antibody?
๐คzamalek๐9y๐ผ0๐จ๏ธ0
(Replying to PARENT post)
Did the study indicate if the long-term nonprogressor on any anti-viral drugs?
I think the most interesting nonprogressors to look at are the ones who refuse treatment. Many of them die within 5 ~ 10 years, but the ones who don't could potentially have a natural resistance to HIV.
๐คdjsumdog๐9y๐ผ0๐จ๏ธ0
(Replying to PARENT post)
Great summary that can be understood without any technical knowledge about the topic. Thanks.
๐คerikb๐9y๐ผ0๐จ๏ธ0
(Replying to PARENT post)
Nice post, but there's an awful lot of anthropomorphizing there. As far as I know, viruses don't purposely mutate. Rather, their design has evolved to encourage beneficial (to them anyway) mutations.
๐คjudahmeek๐9y๐ผ0๐จ๏ธ0
(Replying to PARENT post)
Great summary! Is there any discussion of how these antibodies would affect transmission/communicability to others?
๐คastockwell๐9y๐ผ0๐จ๏ธ0
(Replying to PARENT post)
Can you recommend any introductory texts regarding protein complex binding dynamics?
๐คaswanson๐9y๐ผ0๐จ๏ธ0
(Replying to PARENT post)
In essence, an antibody called N6 was extracted from an HIV patient. The patient is a long-term nonprogressor who has had HIV for 21 years, but an exceptionally low viral load of <1000/mL and normal CD4 T-cell count. This indicates that his immune system has kept the virus at bay for all these years with essentially no ill effect.
HIV viruses have a surface protein complex called Env, which binds to the CD4 surface protein to gain entry to T-cells (part of the immune system). HIV cannot transmit without this protein complex, and so certain parts of the complex are very well conserved across different HIV strains.
N6 binds to this part of Env, in some sense "simulating" CD4. However, because it's just an antibody and not a cell, once Env is bound it cannot infect anything. This is what makes N6 a neutralizing antibody.
The thing that makes N6 special (more potent and more broadly applicable) is that it is able to avoid the parts of Env that HIV doesn't need for replication. Imagine Env as a wrench. The head of the wrench is a specific hex shape to mate with CD4 and can't change. Antibodies can grab on to the wrench handle to prevent infection. But the handle can change, and HIV regularly mutates this part to avoid being caught - adding side branches, changing the shape, and so forth. N6 is cleverly arranged so that it can strongly bind to the wrench without grabbing the handle too strongly - in other words, it tightly binds the head of the wrench like a person wrapping a thumb and index finger around it (this hand analogy appears in the paper). The result is that HIV has a much harder time getting out from under the antibody, since mutating itself to alter the head shape would also affect infectivity.
Now that larger HIV screening trials are done, and the technology has advanced to better detect such super-antibodies, more of these clever antibodies may be discovered. We may yet have a good shot at defeating this tricky virus!