EVAg

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 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.

Plasmid contains the entire genome of HIV-1 with specific mutations in the protease gene, which can confer drug resistance to specific HIV-1 PR inhibitors. The respective mutations have been reported in viruses from HIV-infected individuals on PR inhibitors with virologic therapy failure.

Plasmid contains the entire genome of HIV-1 with specific mutations in the protease gene, which can confer drug resistance to specific HIV-1 PR inhibitors. The respective mutations have been reported in viruses from HIV-infected individuals on PR inhibitors with virologic therapy failure.

Plasmid contains the entire genome of HIV-1 with specific mutations in the protease gene, which can confer drug resistance to specific HIV-1 PR inhibitors. The respective mutations have been reported in viruses from HIV-infected individuals on PR inhibitors with virologic therapy failure.

Plasmid contains the entire genome of HIV-1 with specific mutations in the protease gene, which can confer drug resistance to specific HIV-1 PR inhibitors. The respective mutations have been reported in viruses from HIV-infected individuals on PR inhibitors with virologic therapy failure.

Plasmid contains the entire genome of HIV-1 with specific mutations in the protease gene, which can confer drug resistance to specific HIV-1 PR inhibitors. The respective mutations have been reported in viruses from HIV-infected individuals on PR inhibitors with virologic therapy failure.

Plasmid contains the entire genome of HIV-1 with specific mutations in the protease gene, which can confer drug resistance to specific HIV-1 PR inhibitors. The respective mutations have been reported in viruses from HIV-infected individuals on PR inhibitors with virologic therapy failure.

Plasmid contains the entire genome of HIV-1 with specific mutations in the protease gene, which can confer drug resistance to specific HIV-1 PR inhibitors. The respective mutations have been reported in viruses from HIV-infected individuals on PR inhibitors with virologic therapy failure.

Plasmid contains the entire genome of HIV-1 with specific mutations in the protease gene, which can confer drug resistance to specific HIV-1 PR inhibitors. The respective mutations have been reported in viruses from HIV-infected individuals on PR inhibitors with virologic therapy failure.

Protease mutant with discrete mutations relevant for drug resistance to protease inhibitors

Protease mutant with the indicated discrete mutations relevant for drug resistance to protease inhibitors

HIV-1, drug resistant point mutant of protease, selected by specific HIV protease inhibitors.

HIV-1, drug resistant point mutant of protease, selected by specific HIV protease inhibitors in vivo

HIV-1 variant, infectious recombinant virus with specific mutations in the protease gene as indicated.

HIV-1 variant, infectious recombinant virus with specific mutations in the protease gene as indicated.

HIV-1, drug resistant point mutant of protease, reported to be specifically selected by the HIV protease inhibitor atazanavir in vivo

Plasmid contains the entire genome of HIV-1 with specific mutations in the viral protease gene, which can confer drug resistance to specific HIV-1 protease inhibitors. The respective mutations have been reported in viruses from HIV-infected individuals on protease inhibitors with virologic therapy failure.

Recombinant HIV-1 plasmid (derived from pNL4-3) with the indicated mutations in the protease gene, which have been reported in the context of clinical drug resistance to HIV protease inhibitors.

Recombinant HIV-1 virus with the indicated mutations in the protease gene. Mutations have been reported from drug resistant viral variants emerging in vivo, e.g. after treatment with the HIV protease inhibitor saquinavir

full length plasmid clone of proviral HIV-1; construct produces defective HIV-1 upon transfection into eukaryotic cells (frame-shift in gag); based on NL-BX

Plasmid contains the entire genome of HIV-1 (NL4-3) with the respective specific mutations in the protease gene. These may confer drug resistance to specific HIV protease inhibitors and have been identified in clinical specimens from individuals with therapeutic failure.

full length plasmid clone of proviral HIV-1; construct produces HIV-1 proteins upon transfection into eukaryotic cells but is non-infectious due to a protease-inactivating mutation in the catalytic centre of the protein (D25N); virus is based on NL-BX

full length plasmid clone of proviral HIV-1; construct produces fully infectious HIV-1 upon transfection into eukaryotic cells; based on NL-BX

full length plasmid clone of proviral HIV-1; construct produces fully infectious HIV-1 upon transfection into eukaryotic cells; based on NL-BX