Meeting report: 30th International Conference on Antiviral Research, in Atlanta, GA, USA

Vere Hodge, R Anthony

Ann Palmenberg described how RV-C had remained undetected for many years after the discovery of RV-A and RV-B and that this delay was due to RV-C using a different cellular receptor. I consider it optimistic to expect the inhibition or blocking of a host protein will give an antiviral therapy that is free from viral resistance problems. Although the target host protein may not be subject to change, the virus may well be able to use a 'back door escape route'. Priscilla Yang's team may find that is so for their antiviral approach. To my mind, the important result from her work is a good demonstration that antiviral compounds, which maybe not good enough for clinical use, are effective tools to learn more about viral replication. Her compounds have given more information about the dengue virus fusion process. I recall discussing with my friends from Roche at the 1999 ICAR (Jerusalem) the use of their HSV thymidine kinase inhibitors to investigate how an initially (immature) latently infected cell can mature to become a competent latently infected cell from which HSV can reactivate. Shortly afterwards, that work was closed down but the opportunity still remains. I ought to declare an interest in such an investigation into herpesvirus latency -famciclovir appears to act like a thymidine kinase inhibitor, preventing immature latently infected cells maturing 8 (and references therein).