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Novel therapeutics with high effectiveness and mutation resistance are needed.
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The mechanisms of mutation-driven resistance are usually purposefully sought using genes for which a role in antibiotic resistance has already been described.
Drugs targeted against these residues may therefore fail to disrupt enzyme activity, and even if they did, mutations conferring resistance are likely to evolve.
Reversion may occur if the cost of the mutation conferring resistance is very high, but is unlikely if compensatory mutations have negated this cost.
Since most mutations that confer resistance are linked to an impairment of viral RC, this type of association was expected.
As many as 67 mutations conferring azole resistance are described up to now [13], [14], [15], [16], [17].
Mutations causing antibiotic resistance are often associated with a cost in the absence of antibiotics.
In those cases, probably only the most effective mutation conferring resistance is selected.
Tumours adapt; the genes and mutations responsible for this resistance are unknown.
Structural explanations for compound mutation-based resistance were obtained through molecular dynamics simulations.
Finally, the P. falciparum chloroquine resistance transporter gene (pfcrt) was identified, and mutations mediating resistance were characterized and confirmed clinically [ 56, 57].
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