Plasmid contains the entire genome of HIV-1 with a specific mutation in the protease gene, which has been described as a polymorphic mutation. It is unclear, whether it can confer drug resistance to specific HIV-1 PR inhibitors directly. It has been shown in cell culture that the presence of the 63P change leads to higher "replicative fitness" of the virus. The respective mutations have been reported in viruses from HIV-infected individuals on PR inhibitors with virologic therapy failure.
Gp41 recombinant, carrying the "MIF" motif, typical for subtype AE, in the fusion domain of the subtype B prototype NL4-3 - for studying the fusion function.
Plasmid contains the entire genome of HIV-1 with specific mutations in the reverse transcriptase gene, which can confer drug resistance to specific HIV-1 inhibitors. The respective mutations have been reported in viruses from HIV-infected individuals on reverse transcriptase inhibitors with virologic therapy failure.
Plasmid contains the entire genome of HIV-1 with specific mutations in the reverse transcriptase gene, which can confer drug resistance to specific HIV-1 inhibitors. The respective mutations have been reported in viruses from HIV-infected individuals on reverse transcriptase inhibitors with virologic therapy failure.
proviral HIV-1 clone with an inserted TAATGA double stop codon in the endodomain of gp41 after position 8368 (NL4-3); (a stop codon at analogous position have been reported in early reports of SIV propagation in vitro.)
Deletion mutant of HIV-1 with a deleted env gene; RRE reintroduced for the expression of HIV-1 Gag. The genes vpr, env, tat, rev, vpu, nef are not expressed.
Mutant of HIV-1 with deletions between SphI and SalI of pNL4-3, resulting in a frameshift in the gag gene; TAG stop codon inserted in gp41, truncating the endodomain