This Article Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Reprints and Permissions Copyright Information Books from ASM Press MicrobeWorld Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by van Opijnen, T. Articles by Berkhout, B. Search for Related Content PubMed PubMed Citation Articles by van Opijnen, T. Articles by Berkhout, B.

 Previous Article  |  Next Article 

Journal of Virology, April 2004, p. 3675-3683, Vol. 78, No. 7
0022-538X/04/$08.00+0     DOI: 10.1128/JVI.78.7.3675-3683.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.

Human Immunodeficiency Virus Type 1 Subtypes Have a Distinct Long Terminal Repeat That Determines the Replication Rate in a Host-Cell-Specific Manner

Department of Human Retrovirology, Academic Medical Center, University of Amsterdam, 1105 AZ Amsterdam,¹ Section Population Biology, Institute for Biodiversity and Ecosystem Dynamics, University of Amsterdam, 1098 SM Amsterdam, The Netherlands,² HIV Laboratory, Department of Infectious Disease Epidemiology, National Public Health Institute, 00300 Helsinki, Finland³

Received 19 November 2003/ Accepted 23 November 2003

The long terminal repeat (LTR) transcriptional promoters of different human immunodeficiency virus (HIV) type 1 subtypes were inserted into the LAI molecular clone of subtype B. The viral genotypes represent seven subtypes (A, B, C, D, E, F, and G) and one circulating recombinant form (AG). We performed replication studies with this isogenic set of viruses across six cellular environments. This approach revealed strong cellular environment effects, but the method was not sensitive enough to detect small differences in the replication rate between the subtypes. By conducting pairwise competition experiments between the virus variants in six cellular environments, we could demonstrate significant differences in the replication rates of the subtypes and that LTR-determined viral fitness depends both on the host cell type and the activation state of the cell. In addition, we determined the degree of conservation of the transcription factor-binding sites (TFBS) in the different-subtype LTRs by analyzing sequences from the HIV sequence database. The sequence analyses revealed subtype-specific conservation of certain TFBS. The results indicate that one should consider the possibility of subtype-specific viral replication rates in vivo, which are strongly influenced by the host environment. We argue that the multidimensional host environment may have shaped the genetic structures of the subtype LTRs.

This article has been cited by other articles:

• Dykes, C., Demeter, L. M. (2007). Clinical Significance of Human Immunodeficiency Virus Type 1 Replication Fitness. Clin. Microbiol. Rev. 20: 550-578 [Abstract] [Full Text]  
• Oskarsson, T., Hreggvidsdottir, H. S., Agnarsdottir, G., Matthiasdottir, S., Ogmundsdottir, M. H., Jonsson, S. R., Georgsson, G., Ingvarsson, S., Andresson, O. S., Andresdottir, V. (2007). Duplicated Sequence Motif in the Long Terminal Repeat of Maedi-Visna Virus Extends Cell Tropism and Is Associated with Neurovirulence. J. Virol. 81: 4052-4057 [Abstract] [Full Text]  
• van Opijnen, T., Boerlijst, M. C., Berkhout, B. (2006). Effects of random mutations in the human immunodeficiency virus type 1 transcriptional promoter on viral fitness in different host cell environments.. J. Virol. 80: 6678-6685 [Abstract] [Full Text]  
• Hidalgo-Estevez, A. M., Gonzalez, E., Punzon, C., Fresno, M. (2006). Human immunodeficiency virus type 1 Tat increases cooperation between AP-1 and NFAT transcription factors in T cells. J. Gen. Virol. 87: 1603-1612 [Abstract] [Full Text]  
• Rizzi, C., Crippa, M. P., Jeeninga, R. E., Berkhout, B., Blasi, F., Poli, G., Alfano, M. (2006). Pertussis Toxin B-Oligomer Suppresses IL-6 Induced HIV-1 and Chemokine Expression in Chronically Infected U1 Cells via Inhibition of Activator Protein 1. J. Immunol. 176: 999-1006 [Abstract] [Full Text]  
• Desfosses, Y., Solis, M., Sun, Q., Grandvaux, N., Van Lint, C., Burny, A., Gatignol, A., Wainberg, M. A., Lin, R., Hiscott, J. (2005). Regulation of Human Immunodeficiency Virus Type 1 Gene Expression by Clade-Specific Tat Proteins. J. Virol. 79: 9180-9191 [Abstract] [Full Text]  
• Marozsan, A. J., Moore, D. M., Lobritz, M. A., Fraundorf, E., Abraha, A., Reeves, J. D., Arts, E. J. (2005). Differences in the Fitness of Two Diverse Wild-Type Human Immunodeficiency Virus Type 1 Isolates Are Related to the Efficiency of Cell Binding and Entry. J. Virol. 79: 7121-7134 [Abstract] [Full Text]  
• Lemieux, A.-M., Pare, M.-E., Audet, B., Legault, E., Lefort, S., Boucher, N., Landry, S., van Opijnen, T., Berkhout, B., Naghavi, M. H., Tremblay, M. J., Barbeau, B. (2004). T-cell Activation Leads to Poor Activation of the HIV-1 Clade E Long Terminal Repeat and Weak Association of Nuclear Factor-{kappa}B and NFAT with Its Enhancer Region. J. Biol. Chem. 279: 52949-52960 [Abstract] [Full Text]  
• van Opijnen, T., Kamoschinski, J., Jeeninga, R. E., Berkhout, B. (2004). The Human Immunodeficiency Virus Type 1 Promoter Contains a CATA Box Instead of a TATA Box for Optimal Transcription and Replication. J. Virol. 78: 6883-6890 [Abstract] [Full Text]