Structural Mechanism for Rifampicin Inhibition of Bacterial RNA Polymerase

The emergence of resistance to antibacterial agents is a pressing concern for human health New drugs to combat this problem are therefore in great demand, but as past experience indicates, the time for resistance to new drugs to develop is often short Conventionally, antibacterial drugs have been developed on the basis of their ability to inhibit bacterial multiplication, and this remains at the core of most approaches to discover new antibacterial drugs Here, we focus primarily on an alternative novel strategy for antibacterial drug development that could potentially alleviate the current situation of drug resistance — targeting non-multiplying latent bacteria, which prolong the duration of antimicrobial chemotherapy and so might increase the rate of development of resistance

The future challenges facing the development of new antimicrobial drugs

A new T7-specific RNA polymerase is found in T7 phage-infected cells It is the product of T7 gene I and is physically and biochemically distinct from the host cell RNA polymerase The synthesis of T7 RNA polymerase provides a direct explanation for the pleiotropic control of late T7 functions exerted by gene I

New RNA polymerase from Escherichia coli infected with bacteriophage T7.

Fritz Knusel

Papers

Interaction of rifamycin with bacterial RNA polymerase.

Action of rifamycins on RNA polymerase.

Action of rifamycin on RNA-polymerase from sensitive and resistant bacteria.