Virus was produced from plasmid-based DNA segments of a common Wuhan strain. The S-gene was site-specifically replaced with a cloned BA.5-based S-gene sequence.
Virus has been produced from plasmid-based DNA segments of a common Wuhan strain. The S-gene was site-specifically replaced with a cloned BA.2-based S-gene sequence.
Virus was produced from plasmid-based DNA segments of a common Wuhan strain. The S-gene was site-specifically replaced with a cloned BA.1-based S-gene sequence.
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
HIV-1 variant, infectious recombinant virus with specific mutations in the RT gene as indicated. These mutations confer resistance to specific HIV RT inhibitors and have been reported for emerging virus in vivo.
HIV-1 variant, infectious recombinant virus with specific mutations in the RT gene as indicated. These mutations confer resistance to specific HIV RT inhibitors and have been reported for emerging virus in vivo.
HIV-1 variant, infectious recombinant virus with specific mutations in the RT gene as indicated. These mutations confer resistance to specific HIV RT inhibitors and have been reported for emerging virus in vivo.
This recombinant HIV-1 variant contains a common polymorphism, which has been described as increasing viral replication in the presence of fitness-reducing Pr mutations