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J Virol, June 1998, p. 5099-5107, Vol. 72, No. 6
0022-538X/98/$04.00+0
Copyright © 1998, American Society for Microbiology. All rights reserved.

Evolution of Syncytium-Inducing and Non-Syncytium-Inducing Biological Virus Clones in Relation to Replication Kinetics during the Course of Human Immunodeficiency Virus Type 1 Infection

Angélique B. van 't Wout,1,dagger Hetty Blaak,1 Leonie J. Ran,1 Margreet Brouwer,1 Carla Kuiken,2 and Hanneke Schuitemaker1,*

Department of Clinical Viro-Immunology, Central Laboratory of The Netherlands Red Cross Blood Transfusion Service and Laboratory of Experimental and Clinical Immunology, University of Amsterdam, Academic Medical Centre, Amsterdam, The Netherlands,1 and HIV Database and Analysis Group, Los Alamos National Laboratory, Los Alamos, New Mexico2

Received 6 November 1997/Accepted 23 February 1998

To investigate the temporal relationship between human immunodeficiency virus type 1 (HIV-1) replicative capacity and syncytium-inducing (SI) phenotype, biological and genetic characteristics of longitudinally obtained virus clones from two HIV-1-infected individuals who developed SI variants were studied. In one individual, the emergence of rapidly replicating SI and non-syncytium-inducing (NSI) variants was accompanied by a loss of the slowly replicating NSI variants. In the other subject, NSI variants were always slowly replicating, while the coexisting SI variants showed an increase in the rate of replication. Irrespective their replicative capacity, the NSI variants remained present throughout the infection in both individuals. Phylogenetic analysis of the V3 region showed early branching of the SI variants from the NSI tree. Successful SI conversion seemed a unique event since no SI variants were found among later-stage NSI variants. This was also confirmed by the increasing evolutionary distance between the two subpopulations. At any time point during the course of the infection, the variation within the coexisting SI and NSI populations did not exceed 2%, indicating continuous competition within each viral subpopulation.

* Corresponding author. Mailing address: Department of Clinical Viro-Immunology, Central Laboratory of The Netherlands Red Cross Blood Transfusion Service, Plesmanlaan 125, 1066 CX Amsterdam, The Netherlands. Phone: 31 20 512 3317. Fax: 31 20 512 3310. E-mail: J_Schuitemaker{at}CLB.nl.

dagger Present address: Department of Microbiology, University of Washington, Seattle, WA 98195-7740.

J Virol, June 1998, p. 5099-5107, Vol. 72, No. 6
0022-538X/98/$04.00+0
Copyright © 1998, American Society for Microbiology. All rights reserved.


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