Amino acids 1-20 of the hepatitis C virus (HCV) core protein specifically inhibit HCV IRES- dependent translation in Hep G2 cells, and inhibit both HCV IRES- and cap-dependent translation in HuH7 and CV-1 cells.

A self-modulating mechanism by the hepatitis C virus (HCV) core protein has been suggested to influence the level of HCV replication, but current data on this subject are contradictory. We examined the effect of wild-type and mutated core protein on HCV IRES- and cap-dependent translation. The wild-type core protein was shown to inhibit both IRES- and cap-dependent translation in an in vitro system. This effect was duplicated in a dose-dependent manner with a synthetic peptide representing amino acids 1-20 of the HCV core protein. This peptide was able to bind to the HCV IRES as shown by a mobility shift assay. In contrast, a peptide derived from the hepatitis B virus (HBV) core protein that contained a similar proportion of basic residues was unable to inhibit translation or bind the HCV IRES. A recombinant vaccinia-HCV core virus was used to examine the effect of the HCV core protein on HCV IRES-dependent translation in cells and this was compared with the effects of an HBV core-recombinant vaccinia virus. In CV-1 and HuH7 cells, the HCV core protein inhibited translation directed by the IRES elements of HCV, encephalomyocarditis virus and classical swine fever virus as well as cap-dependent translation, whereas in HepG2 cells, only HCV IRES-dependent translation was affected. Thus, the ability of the HCV core protein to selectively inhibit HCV IRES-dependent translation is cell-specific. N-terminal truncated (aa 1-20) HCV core protein that was expressed from a novel recombinant vaccinia virus in cells abrogated the inhibitory phenotype of the core protein in vivo, consistent with the above in vitro data.

Climate change and biotic invasions: a case history of a tropical woody vine

The impacts of climate change in the potential distribution and relative abundance of a C3 shrubby vine, Cryptostegia grandiflora, were investigated using the CLIMEX modelling package. Based upon its current naturalised distribution, C. grandiflora appears to occupy only a small fraction of its potential distribution in Australia under current climatic conditions; mostly in apparently sub-optimal habitat. The potential distribution of C. grandiflora is sensitive towards changes in climate and atmospheric chemistry in the expected range of this century, particularly those that result in increased temperature and water use efficiency. Climate change is likely to increase the potential distribution and abundance of the plant, further increasing the area at risk of invasion, and threatening the viability of current control strategies markedly. By identifying areas at risk of invasion, and vulnerabilities of control strategies, this analysis demonstrates the utility of climate models for providing information suitable to help formulate large-scale, long-term strategic plans for controlling biotic invasions. The effects of climate change upon the potential distribution of C. grandiflora are sufficiently great that strategic control plans for biotic invasions should routinely include their consideration. Whilst the effect of climate change upon the efficacy of introduced biological control agents remain unknown, their possible effect in the potential distribution of C. grandiflora will likely depend not only upon their effects on the population dynamics of C. grandiflora, but also on the gradient of climatic suitability adjacent to each segment of the range boundary.