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.
Infectious supernatant containing LCMV strain Clone 13 with a point mutation at glycoprotein Aa38 (phenylalanine to leucine), resulting in a loss of binding of the otherwise immunodominant and here mutated H-2Db-presente
Infectious supernatant containing LCMV strain Clone 13 with a point mutation at glycoprotein Aa280 (asparagine to aspartic acid), resulting in a loss of binding of the otherwise immunodominant and here mutated H-2Db-pres
Infectious supernatant containing LCMV strain Clone 13 with a point mutation at nucleoprotein Aa400 (asparagine to serine), resulting in a loss of binding of the otherwise immunodominant and here mutated H-2Db-presented
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.
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.
full length proviral HIV-1 genome with a TAG stop codon inserted after position 8368 in gp41 (NL4-3), truncating the intracellular domain of gp41; (a stop codon at analogous position have been reported in early reports of SIV propagation in vitro.)
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.
