MicrobiologyBytes

Bovine TB can spread in humans Bovine tuberculosis, caused by Mycobacterium bovis, can spread from person to person. A rare a cluster of six human cases, one fatal, has been identified in a group who visited the same Birmingham nightclub, but only one of the patients had been in contact with infected unpasteurised milk or cattle. DNA fingerprinting showed all six cases were identically linked, most probably by person-to-person spread. Estimates suggest only 1% of TB cases in the western world are caused by bovine TB – the rest are down to Mycobacterium tuberculosis.

Hepatitis C virus receptor Hepatitis C virus (HCV) is a leading cause of cirrhosis and liver cancer worldwide. A better understanding of the viral life cycle, including the mechanisms of entry into host cells, is needed to identify novel therapeutic targets. Although HCV entry requires the CD81 co-receptor, and other host molecules have been implicated, at least one factor critical to this process remains unknown. Claudin-1 (CLDN1), a tight junction component that is highly expressed in the liver, is essential for HCV entry. CLDN1 is required for HCV infection of human hepatoma cell lines and is the first factor to confer susceptibility to HCV when ectopically expressed in non-hepatic cells. Discrete residues within the first extracellular loop (EL1) of CLDN1, but not protein interaction motifs in intracellular domains, are critical for HCV entry. Antibodies directed against an epitope inserted in the CLDN1 EL1 block HCV infection. The kinetics of inhibition indicate that CLDN1 acts late in the entry process, after virus binding and interaction with the HCV co-receptor CD81. With CLDN1 we have identified a novel key factor for HCV entry and a new target for antiviral drug development. Claudin-1 is a hepatitis C virus co-receptor required for a late step in entry. Nature 446: 801-805 (12 April 2007)

Mixing it: why two antibiotics may be better than one The rapid evolution of bacterial drug resistance and the slowdown in development of new antibiotics is possibly the most worrying aspect of present-day microbiology. One possible answer is to develop effective multidrug combinations that it is much harder for pathogens to become resistant to than single drug treatments, but a paper just published in Nature shows how difficult this can be. Drug combinations can be classed as synergistic, additive or antagonistic, depending whether the combined effect of the drugs is larger than, equal to or smaller than the effect of their individual activities. In some cases the effect of certain drug combination is less than that of one of the drugs by itself. But the new paper shows that developing resistance to one drug can sometimes do invading bacteria more harm than good. Although the molecular mechanisms underlying drug interactions are complex, suppression between antibiotics is not uncommon. This work shows that picking the right drug combinations needs careful research. Antibiotic interactions that select against resistance. Nature 446: 668-671 (5 April 2007)

This entry was posted on Friday, April 13th, 2007 at 12:53 pm and is filed under Bacteria, Biology, Health, Medicine, Microbiology, Science, Tuberculosis, Virology. You can follow any responses to this entry through the RSS 2.0 feed. Both comments and pings are currently closed.