L90M mutation 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.
Infectious cell culture supernatant containing Alkhurma virus strain 8S1. This strain is preserved under Viral Storage Medium -80C and is Mycoplasma free. To confirm its identity the virus has been completely sequenced.
Infectious cell culture supernatant containing Alkhurma virus strain 3B1. This strain is preserved under Viral Storage Medium -80C and is Mycoplasma free. To confirm its identity the virus has been completely sequenced.
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.
HIV-1 variant, infectious recombinant virus with specific mutations in the protease gene as indicated. These mutations confer resistance to specific HIV protease inhibitors and have been reported for emerging virus in vivo.
HIV-1 variant, infectious recombinant virus with specific mutations in the protease gene as indicated. These mutations confer resistance to specific HIV protease inhibitors and have been reported for emerging virus in vivo.
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