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. 2010 Jan 28;2(2):372–394. doi: 10.3390/v2020372

Table 2.

PFA-resistant mutants of HIV-1 RT.

Location in RT structure How isolated? Mutations AZT sensitivity Excision activity in vitro
dNTP binding site Site-directed mutagenesis or bacterial library mutagenesis D113G/E, A114S/G, Y115N/H, Q151H [66,70]
R72A [71]
Hypersensitivity shown for D113E & A114S [70] Reduced for A114S [72]
From patients treated with NRTIs K65R [7376] Suppression of AZT resistance [37,7780] Reduced for K65R [37,78]
Palm domain between the fingers domain and the template strand From PFA-treated patients W88S, W88G, Q161L, H208Y [68] Suppression of AZT resistance shown for W88G and Q161L [37]
No effect for W88S [37]
Reduced for W88G and Q161L [37]
Not reduced for W88S [37]
Serial passage of HIV-1 in culture Q161L/H208Y [68]
E89K, L92I, S156A [67]
W88G, S117T, F160Y, M164I [76]
Suppression of AZT resistance shown for W88G, E89K, Q161L/H208Y, S117T, and M164I [37,6769] Reduced for W88G, E89K, Q161L/H208Y, S117T, and M164I [37]
Site-directed or random mutagenesis K154E, Y183S, G190R [66,70,81]
E89G/T/A/D/V[82,83] V90A [84]
AZT sensitivity not determined in infectivity assays Not done