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Questions About How HIV Meds Work -- and Might Work Better (Editor's Pick)

Jul 25, 2015

Hello sir, I had some questions after today's class. I know it will be dumb ones but here goes: 1. HIV virus has antigens made of glycoproteins and they change their shape via reverse transcriptase. So using only RTI drugs may not be the best option. But if we combine proteases with these drugs, is there any possibility of phagocytosis? 2. Will Interferon treatment along with the above measure(if possible) a good measure to eradicate them completely? 3. (Probably the dumbest) Can Interferons, Genetically Engineered opsonin with shape changing property and DNAase be specifically targeted into the affected cells? 4. Is there any way to create an artificial condition like that of our surroundings inside our body so that HIVs become inactive? (Based on the fact that they are the weakest virus outside human body) 5. Is there any Inhibitors to prevent the formation of Enzyme-Substrate complex of reverse transcriptase?

That's it. I am extremely proud to have got an opportunity to communicate with a great being like you, sir. I hope you'll clear my mind of these dumb doubts.... Sincerely, Ahammed Azhar

Response from Dr. Young

Hello Ahammed and thanks for posting.

Ah, enzymology. The stuff of my graduate thesis. :-)

1) I'm not sure the logic of your question, but currently recommended HIV therapies rely on two drug classes, RT inhibitors and a 3rd medication, of a 2nd class (non-nucleoside RT inhibitor, protease inhibitor or integrase inhibitor). These regimens work, not by enhancing phagocytosis, but rather by stopping viral replication.

2) Interferon therapies have been exhaustively evaluated for HIV in a range of clinical trials. None have demonstrated clinical benefit.

3) Not a dumb question; gene therapies have been, and continue to be explored as strategies to treat HIV. These range from modified HIV coreceptors to early phase glimpses of using CRISPR.

4) I'm not aware of these kind of strategies.

5) Nucleoside reverse transcriptase inhibitors bind to the active site of the RT, and do prevent formation of the E-S complex. Protease inhibitors appear to work similarly, by binding in the active site of the protease enzyme.

Keep thinking- they're not dumb thoughts. It's by going back over our basic assumptions and asking basic questions that we may uncover things assumed, but incorrect. In those undiscovered ideas may come the next big thing, or with luck, a cure.

Be well, BY



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