The calculated genetic barrier for antiretroviral drug resistance substitutions is largely similar for different HIV-1 subtypes

David A. Van De Vijver; Annemarie M.J. Wensing; Gioacchino Angarano; Birgitta Åsjö; Claudia Balotta; Enzo Boeri; Ricardo Camacho; Marie Laure Chaix; Dominique Costagliola; Andrea De Luca; Inge Derdelinckx; Zehava Grossman; Osamah Hamouda; Angelos Hatzakis; Robert Hemmer; Andy Hoepelman; Andrzej Horban; Klaus Korn; Claudia Kücherer; Thomas Leitner; Clive Loveday; Eilidh MacRae; Irina Maljkovic; Carmen De Mendoza; Laurence Meyer; Claus Nielsen; Eline L.M. Op De Coul; Vidar Ormaasen; Dimitris Paraskevis; Luc Perrin; Elisabeth Puchhammer-Stöckl; Lidia Ruiz; Mika Salminen; Jean Claude Schmit; Francois Schneider; Rob Schuurman; Vincent Soriano; Grzegorz Stanczak; Maja Stanojevic; Anne Mieke Vandamme; Kristel Van Laethem; Michela Violin; Karin Wilbe; Sabine Yerly; Maurizio Zazzi; Charles A.B. Boucher

doi:10.1097/01.qai.0000209899.05126.e4

The calculated genetic barrier for antiretroviral drug resistance substitutions is largely similar for different HIV-1 subtypes

David A. Van De Vijver
, Annemarie M.J. Wensing
, Gioacchino Angarano
, Birgitta Åsjö
, Claudia Balotta
, Enzo Boeri
, Ricardo Camacho
, Marie Laure Chaix
, Dominique Costagliola
, Andrea De Luca
, Inge Derdelinckx
, Zehava Grossman
, Osamah Hamouda
, Angelos Hatzakis
, Robert Hemmer
, Andy Hoepelman
, Andrzej Horban
, Klaus Korn
, Claudia Kücherer
, Thomas Leitner

Clive Loveday, Eilidh MacRae, Irina Maljkovic, Carmen De Mendoza, Laurence Meyer, Claus Nielsen, Eline L.M. Op De Coul, Vidar Ormaasen, Dimitris Paraskevis, Luc Perrin, Elisabeth Puchhammer-Stöckl, Lidia Ruiz, Mika Salminen, Jean Claude Schmit, Francois Schneider, Rob Schuurman, Vincent Soriano, Grzegorz Stanczak, Maja Stanojevic, Anne Mieke Vandamme, Kristel Van Laethem, Michela Violin, Karin Wilbe, Sabine Yerly, Maurizio Zazzi, Charles A.B. Boucher^*

^*Corresponding author for this work

Utrecht University
University of Foggia
Bergen University Medical School
University of Milan
Diagnostica e Ricerca San Raffaele
Hospital Egas Moniz
Institut Imagine
Institut national de la santé et de la recherche médicale
Catholic University
KU Leuven
Sheba Medical Center at Tel Hashomer
Robert Koch-Institut
National and Kapodistrian University of Athens
Center Hospitalier de Luxembourg
Hospital for Infectious Diseases
Friedrich-Alexander University Erlangen-Nürnberg
Los Alamos National Laboratory
International Clinical Virology Centre (Buckinghamshire)
Public Health Agency of Sweden
Hospital Universitario La Paz
Statens Serum Institut
National Institute of Public Health and the Environment
Oslo University Hospital-Ullevål
University Hospital of Geneva
University of Vienna
AIDS Research Institute
National Institute for Health and Welfare
University of Belgrade
University of Siena
Eijkman Winkler Institute

Research output: Contribution to journal › Article › Academic › peer-review

90 Citations (Scopus)

Abstract

Background: The genetic barrier, defined as the number of mutations required to overcome drug-selective pressure, is an important factor for the development of HIV drug resistance. Because of high variability between subtypes, particular HIV-1 subtypes could have different genetic barriers for drug resistance substitutions. This study compared the genetic barrier between subtypes using some 2000 HIV-1 sequences (>600 of non-B subtype) isolated from antiretroviral-naive patients in Europe. Methods: The genetic barrier was calculated as the sum of transitions (scored as 1) and/or transversions (2.5) required for evolution to any major drug resistance substitution. In addition, the number of minor protease substitutions was determined for every subtype. Results: Few dissimilarities were found. An increased genetic barrier was calculated for I82A (subtypes C and G), V108I (subtype G), V118I (subtype G), Q151M (subtypes D and F), L210W (subtypes C, F, G, and CRF02_AG), and P225H (subtype A) (P < 0.001 compared with subtype B). A decreased genetic barrier was found for I82T (subtypes C and G) and V106M (subtype C) (P < 0.001 vs subtype B). Conversely, minor protease substitutions differed extensively between subtypes. Conclusions: Based on the calculated genetic barrier, the rate of drug resistance development may be similar for different HIV-1 subtypes. Because of differences in minor protease substitutions, protease inhibitor resistance could be enhanced in particular subtypes once the relevant major substitutions are selected.

Original language	English
Pages (from-to)	352-360
Number of pages	9
Journal	Journal of Acquired Immune Deficiency Syndromes (1999)
Volume	41
Issue number	3
DOIs	https://doi.org/10.1097/01.qai.0000209899.05126.e4
Publication status	Published - Mar 2006
Externally published	Yes

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SDG 3 Good Health and Well-being

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10.1097/01.qai.0000209899.05126.e4

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Van De Vijver, D. A., Wensing, A. M. J., Angarano, G., Åsjö, B., Balotta, C., Boeri, E., Camacho, R., Chaix, M. L., Costagliola, D., De Luca, A., Derdelinckx, I., Grossman, Z., Hamouda, O., Hatzakis, A., Hemmer, R., Hoepelman, A., Horban, A., Korn, K., Kücherer, C., ... Boucher, C. A. B. (2006). The calculated genetic barrier for antiretroviral drug resistance substitutions is largely similar for different HIV-1 subtypes. Journal of Acquired Immune Deficiency Syndromes (1999), 41(3), 352-360. https://doi.org/10.1097/01.qai.0000209899.05126.e4

@article{39461605b8d440168feadf920f29d5d9,

title = "The calculated genetic barrier for antiretroviral drug resistance substitutions is largely similar for different HIV-1 subtypes",

abstract = "Background: The genetic barrier, defined as the number of mutations required to overcome drug-selective pressure, is an important factor for the development of HIV drug resistance. Because of high variability between subtypes, particular HIV-1 subtypes could have different genetic barriers for drug resistance substitutions. This study compared the genetic barrier between subtypes using some 2000 HIV-1 sequences (>600 of non-B subtype) isolated from antiretroviral-naive patients in Europe. Methods: The genetic barrier was calculated as the sum of transitions (scored as 1) and/or transversions (2.5) required for evolution to any major drug resistance substitution. In addition, the number of minor protease substitutions was determined for every subtype. Results: Few dissimilarities were found. An increased genetic barrier was calculated for I82A (subtypes C and G), V108I (subtype G), V118I (subtype G), Q151M (subtypes D and F), L210W (subtypes C, F, G, and CRF02\_AG), and P225H (subtype A) (P < 0.001 compared with subtype B). A decreased genetic barrier was found for I82T (subtypes C and G) and V106M (subtype C) (P < 0.001 vs subtype B). Conversely, minor protease substitutions differed extensively between subtypes. Conclusions: Based on the calculated genetic barrier, the rate of drug resistance development may be similar for different HIV-1 subtypes. Because of differences in minor protease substitutions, protease inhibitor resistance could be enhanced in particular subtypes once the relevant major substitutions are selected.",

author = "\{Van De Vijver\}, \{David A.\} and Wensing, \{Annemarie M.J.\} and Gioacchino Angarano and Birgitta {\AA}sj{\"o} and Claudia Balotta and Enzo Boeri and Ricardo Camacho and Chaix, \{Marie Laure\} and Dominique Costagliola and \{De Luca\}, Andrea and Inge Derdelinckx and Zehava Grossman and Osamah Hamouda and Angelos Hatzakis and Robert Hemmer and Andy Hoepelman and Andrzej Horban and Klaus Korn and Claudia K{\"u}cherer and Thomas Leitner and Clive Loveday and Eilidh MacRae and Irina Maljkovic and \{De Mendoza\}, Carmen and Laurence Meyer and Claus Nielsen and \{Op De Coul\}, \{Eline L.M.\} and Vidar Ormaasen and Dimitris Paraskevis and Luc Perrin and Elisabeth Puchhammer-St{\"o}ckl and Lidia Ruiz and Mika Salminen and Schmit, \{Jean Claude\} and Francois Schneider and Rob Schuurman and Vincent Soriano and Grzegorz Stanczak and Maja Stanojevic and Vandamme, \{Anne Mieke\} and \{Van Laethem\}, Kristel and Michela Violin and Karin Wilbe and Sabine Yerly and Maurizio Zazzi and Boucher, \{Charles A.B.\}",

year = "2006",

month = mar,

doi = "10.1097/01.qai.0000209899.05126.e4",

language = "English",

volume = "41",

pages = "352--360",

number = "3",

}

Van De Vijver, DA, Wensing, AMJ, Angarano, G, Åsjö, B, Balotta, C, Boeri, E, Camacho, R, Chaix, ML, Costagliola, D, De Luca, A, Derdelinckx, I, Grossman, Z, Hamouda, O, Hatzakis, A, Hemmer, R, Hoepelman, A, Horban, A, Korn, K, Kücherer, C, Leitner, T, Loveday, C, MacRae, E, Maljkovic, I, De Mendoza, C, Meyer, L, Nielsen, C, Op De Coul, ELM, Ormaasen, V, Paraskevis, D, Perrin, L, Puchhammer-Stöckl, E, Ruiz, L, Salminen, M, Schmit, JC, Schneider, F, Schuurman, R, Soriano, V, Stanczak, G, Stanojevic, M, Vandamme, AM, Van Laethem, K, Violin, M, Wilbe, K, Yerly, S, Zazzi, M & Boucher, CAB 2006, 'The calculated genetic barrier for antiretroviral drug resistance substitutions is largely similar for different HIV-1 subtypes', Journal of Acquired Immune Deficiency Syndromes (1999), vol. 41, no. 3, pp. 352-360. https://doi.org/10.1097/01.qai.0000209899.05126.e4

The calculated genetic barrier for antiretroviral drug resistance substitutions is largely similar for different HIV-1 subtypes. / Van De Vijver, David A.; Wensing, Annemarie M.J.; Angarano, Gioacchino et al.
In: Journal of Acquired Immune Deficiency Syndromes (1999), Vol. 41, No. 3, 03.2006, p. 352-360.

Research output: Contribution to journal › Article › Academic › peer-review

TY - JOUR

T1 - The calculated genetic barrier for antiretroviral drug resistance substitutions is largely similar for different HIV-1 subtypes

AU - Van De Vijver, David A.

AU - Wensing, Annemarie M.J.

AU - Angarano, Gioacchino

AU - Åsjö, Birgitta

AU - Balotta, Claudia

AU - Boeri, Enzo

AU - Camacho, Ricardo

AU - Chaix, Marie Laure

AU - Costagliola, Dominique

AU - De Luca, Andrea

AU - Derdelinckx, Inge

AU - Grossman, Zehava

AU - Hamouda, Osamah

AU - Hatzakis, Angelos

AU - Hemmer, Robert

AU - Hoepelman, Andy

AU - Horban, Andrzej

AU - Korn, Klaus

AU - Kücherer, Claudia

AU - Leitner, Thomas

AU - Loveday, Clive

AU - MacRae, Eilidh

AU - Maljkovic, Irina

AU - De Mendoza, Carmen

AU - Meyer, Laurence

AU - Nielsen, Claus

AU - Op De Coul, Eline L.M.

AU - Ormaasen, Vidar

AU - Paraskevis, Dimitris

AU - Perrin, Luc

AU - Puchhammer-Stöckl, Elisabeth

AU - Ruiz, Lidia

AU - Salminen, Mika

AU - Schmit, Jean Claude

AU - Schneider, Francois

AU - Schuurman, Rob

AU - Soriano, Vincent

AU - Stanczak, Grzegorz

AU - Stanojevic, Maja

AU - Vandamme, Anne Mieke

AU - Van Laethem, Kristel

AU - Violin, Michela

AU - Wilbe, Karin

AU - Yerly, Sabine

AU - Zazzi, Maurizio

AU - Boucher, Charles A.B.

PY - 2006/3

Y1 - 2006/3

N2 - Background: The genetic barrier, defined as the number of mutations required to overcome drug-selective pressure, is an important factor for the development of HIV drug resistance. Because of high variability between subtypes, particular HIV-1 subtypes could have different genetic barriers for drug resistance substitutions. This study compared the genetic barrier between subtypes using some 2000 HIV-1 sequences (>600 of non-B subtype) isolated from antiretroviral-naive patients in Europe. Methods: The genetic barrier was calculated as the sum of transitions (scored as 1) and/or transversions (2.5) required for evolution to any major drug resistance substitution. In addition, the number of minor protease substitutions was determined for every subtype. Results: Few dissimilarities were found. An increased genetic barrier was calculated for I82A (subtypes C and G), V108I (subtype G), V118I (subtype G), Q151M (subtypes D and F), L210W (subtypes C, F, G, and CRF02_AG), and P225H (subtype A) (P < 0.001 compared with subtype B). A decreased genetic barrier was found for I82T (subtypes C and G) and V106M (subtype C) (P < 0.001 vs subtype B). Conversely, minor protease substitutions differed extensively between subtypes. Conclusions: Based on the calculated genetic barrier, the rate of drug resistance development may be similar for different HIV-1 subtypes. Because of differences in minor protease substitutions, protease inhibitor resistance could be enhanced in particular subtypes once the relevant major substitutions are selected.

AB - Background: The genetic barrier, defined as the number of mutations required to overcome drug-selective pressure, is an important factor for the development of HIV drug resistance. Because of high variability between subtypes, particular HIV-1 subtypes could have different genetic barriers for drug resistance substitutions. This study compared the genetic barrier between subtypes using some 2000 HIV-1 sequences (>600 of non-B subtype) isolated from antiretroviral-naive patients in Europe. Methods: The genetic barrier was calculated as the sum of transitions (scored as 1) and/or transversions (2.5) required for evolution to any major drug resistance substitution. In addition, the number of minor protease substitutions was determined for every subtype. Results: Few dissimilarities were found. An increased genetic barrier was calculated for I82A (subtypes C and G), V108I (subtype G), V118I (subtype G), Q151M (subtypes D and F), L210W (subtypes C, F, G, and CRF02_AG), and P225H (subtype A) (P < 0.001 compared with subtype B). A decreased genetic barrier was found for I82T (subtypes C and G) and V106M (subtype C) (P < 0.001 vs subtype B). Conversely, minor protease substitutions differed extensively between subtypes. Conclusions: Based on the calculated genetic barrier, the rate of drug resistance development may be similar for different HIV-1 subtypes. Because of differences in minor protease substitutions, protease inhibitor resistance could be enhanced in particular subtypes once the relevant major substitutions are selected.

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DO - 10.1097/01.qai.0000209899.05126.e4

M3 - Article

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AN - SCOPUS:33645098601

SN - 1525-4135

VL - 41

SP - 352

EP - 360

JO - Journal of Acquired Immune Deficiency Syndromes (1999)

JF - Journal of Acquired Immune Deficiency Syndromes (1999)

IS - 3

ER -

The calculated genetic barrier for antiretroviral drug resistance substitutions is largely similar for different HIV-1 subtypes

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