Impact of delay on HIV-1 dynamics of fighting a virus with another virus.

In this paper, we propose a mathematical model for HIV-1 infection with intracellular delay. The model examines a viral-therapy for controlling infections through recombining HIV-1 virus with a genetically modified virus. For this model, the basic reproduction number R0 are identified and its threshold properties are discussed. When R0<1, the infection-free equilibrium E0 is globally asymptotically stable. When R0>1, E0 becomes unstable and there occurs the single-infection equilibrium Es, and E0 and Es exchange their stability at the transcritical point R0=1. If 1R1, Es loses its stability to the double-infection equilibrium Ed. There exist a constant R2 such that Ed is asymptotically stable if R1

Genomically recoded organisms expand biological functions.

We describe the construction and characterization of a genomically recoded organism (GRO). We replaced all known UAG stop codons in Escherichia coli MG1655 with synonymous UAA codons, which permitted the deletion of release factor 1 and reassignment of UAG translation function. This GRO exhibited improved properties for incorporation of nonstandard amino acids that expand the chemical diversity of proteins in vivo. The GRO also exhibited increased resistance to T7 bacteriophage, demonstrating that new genetic codes could enable increased viral resistance.