EVAg

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.

full length plasmid clone of proviral HIV-1; construct produces infectious HIV-1 upon transfection into eukaryotic cells

Plasmid containing an NL4-3 based HIV-1 genome with a big deletion between SalI site (5785) and XhoI site (8887), leading to a deletion of the viral genes vpu,env, tat, rev. Also the "rev-response-element" RRE is missing, leading to a lack of expression also of the gag-pol genes

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.

recombinant HIV-1 virus derived from pNL4-3 carrying (instead of the HIV-1 protease) the protease gene of HIV-2 (ROD14)

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.)