Question

Why are the mutations K65R and D113E, both causing drug resistance such a surprise, whereas, the mutations Q151M and Q151N are not such a surprise. Explain the reasoning behind this. The answer to this question is not found in the paper, but based on what you now understand about mutations in general

Answer 1

The Question is about drug resistance in HIV virus REVERSE TRANSCRIPTASE enzyme. The genetic material in HIV virus is RNA. To incorporate it's genetic material into host genetic material which is DNA ,it should be converted first into DNA from RNA.Reverse transcriptase do this work for virsuv

To tackle with HIV virus drugs have been synthesised against RT ENZYME .

Drugs binds to specific residues of the RT enzyme at specific sites.usualy drugs binds to the sites which are vital for enzyme activity i.e substrate binding site , polymerization site ,Rnase H site etc.

Mutation in the residues which are important for drug binding, can reduce binding of the drug to RT enzyme.

IN the above given mutation K65R (lysin to arginine) and D113E (aspartate to glutamate) are important sites for drug bind and mutation here will inhibit drug binding and HIV virus become resistant from the drug .

In mutation Q151M and Q151N ,binding assays has been done so far shows that these mutation doesnot halt drug binding ,drug binding inhibition canolny occur with mutation at other residues as well with this.