G-1 Appeal Activity in the Public Assistance Programs, December 2005

Appeal Activity in the Public Assistance Programs - December 2005

G-1 Appeal Activity in the Public Assistance Programs, January 2006

Appeal Activity in the Public Assistance Programs, January 2006

G-1 Appeal Activity in the Public Assistance Programs, February 2006

Appeal Activity in the Public Assistance Programs, February 2006

G-1 Appeal Activity in the Public Assistance Programs, March 2006

G-1 - March 2006 - Appeal Activity in the Public Assistance Programs

Carte de la Grèce ancienne pour servir à l'histoire des Juifs de Mr. Prideaux / G. par L. Borde

Échelle(s) : [1:2 900 000 environ], Echelle, Stades grecs a 600 au D. [600 = 3,8 cm]

G-1 Appeal Activity in the Public Assistance Programs, April 2006

Appeal Activity in the Public Assistance Programs April 2006

HIV-1 protease mutation 82M contributes to phenotypic resistance to protease inhibitors in subtype G.

OBJECTIVES: The purpose of this study was the qualitative and quantitative assessment of the in vitro effect of HIV-1 protease (PR) mutation 82M on replication capacity and susceptibility to the eight clinically available PR inhibitors (PIs).¦METHODS: The 82M substitution was introduced by site-directed mutagenesis in wild-type subtype B and G strains, as well as reverted back to wild-type in a therapy-failing strain. The recombinant viruses were evaluated for their replication capacity and susceptibility to PIs.¦RESULTS: The single 82M mutation within a wild-type subtype B or G background did not result in drug resistance. However, the in vitro effect of single PR mutations on PI susceptibility is not always distinguishable from wild-type virus, and particular background mutations and polymorphisms are required to detect significant differences in the drug susceptibility profile. Consequently, reverting the 82M mutation back to wild-type (82I) in a subtype G isolate from a patient that failed therapy with multiple other PR mutations did result in significant increases in susceptibility towards indinavir and lopinavir and minor increases in susceptibility towards amprenavir and atazanavir. The presence of the 82M mutation also slightly decreased viral replication, whether it was in the genetic background of subtype B or subtype G.¦CONCLUSIONS: Our results suggest that 82M has an impact on PI susceptibility and that this effect is not due to a compensatory effect on the replication capacity. Because 82M is not observed as a polymorphism in any subtype, these observations support the inclusion of 82M in drug resistance interpretation systems and PI mutation lists.

G-1, Appeal Activity in the Public Assistance Programs, May 2006

G-1, Appeal Activity in the Public Assistance Programs, May 2006

G-1 Appeal Activity in the Public Assistance Programs, February 2005

Appeal activity in the Public Assistance Programs