Notice: Users may be experiencing issues with displaying some pages on stanfordhealthcare.org. We are working closely with our technical teams to resolve the issue as quickly as possible. Thank you for your patience.
 

Learn about the flu shot, COVID-19 vaccine, and our masking policy »

Stanford Health Care

Association of a novel human immunodeficiency virus type 1 protease substrate cleft mutation, L23I, with protease inhibitor therapy and in vitro drug resistance ANTIMICROBIAL AGENTS AND CHEMOTHERAPY Johnston, E., Winters, M. A., Rhee, S. Y., Merigan, T. C., Schiffer, C. A., Shafer, R. W. 2004; 48 (12): 4864-4868

Abstract

We observed a previously uncharacterized mutation in the protease substrate cleft, L23I, in 31 of 4,303 persons undergoing human immunodeficiency virus type 1 genotypic resistance testing. In combination with V82I, L23I was associated with a sevenfold reduction in nelfinavir susceptibility and a decrease in replication capacity. In combination with other drug resistance mutations, L23I was associated with multidrug resistance and a compensatory increase in replication capacity.

View details for DOI 10.1128/AAC.48.12.4864-4868.2004

View details for Web of Science ID 000225474500052

View details for PubMedID 15561868

View details for PubMedCentralID PMC529213