Abstract
Background: One out of ten newly diagnosed patients in Europe was infected with a virus carrying a drug resistant mutation. We analysed the patterns over time for transmitted drug resistance mutations (TDRM) using data from the European Spread program.Methods: Clinical, epidemiological and virological data from 4317 patients newly diagnosed with HIV-1 infection between 2002 and 2007 were analysed. Patients were enrolled using a pre-defined sampling strategy.Results: The overall prevalence of TDRM in this period was 8.9% (95% CI: 8.1-9.8). Interestingly, significant changes over time in TDRM caused by the different drug classes were found. Whereas nucleoside resistance mutations remained constant at 5%, a significant decline in protease inhibitors resistance mutations was observed, from 3.9% in 2002 to 1.6% in 2007 (p = 0.001). In contrast, resistance to non-nucleoside reverse transcriptase inhibitors (NNRTIs) doubled from 2.0% in 2002 to 4.1% in 2007 (p = 0.004) with 58% of viral strains carrying a K103N mutation. Phylogenetic analysis showed that these temporal changes could not be explained by large clusters of TDRM.Conclusion: During the years 2002 to 2007 transmitted resistance to NNRTI has doubled to 4% in Europe. The frequent use of NNRTI in first-line regimens and the clinical impact of NNRTI mutations warrants continued monitoring.
| Original language | English |
|---|---|
| Article number | 407 |
| Journal | BMC Infectious Diseases |
| Volume | 14 |
| Issue number | 1 |
| DOIs | |
| Publication status | Published - 21 Jul 2014 |
Keywords
- Europe
- HIV-1
- Resistance
- Transmission
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In: BMC Infectious Diseases, Vol. 14, No. 1, 407, 21.07.2014.
Research output: Contribution to journal › Article › Research › peer-review
TY - JOUR
T1 - Increase in transmitted resistance to non-nucleoside reverse transcriptase inhibitors among newly diagnosed HIV-1 infections in Europe
AU - Frentz, Dineke
AU - Van de Vijver, David A.M.C.
AU - Abecasis, Ana B.
AU - Albert, Jan
AU - Hamouda, Osamah
AU - Jørgensen, Louise B.
AU - Kücherer, Claudia
AU - Struck, Daniel
AU - Schmit, Jean Claude
AU - Vercauteren, Jurgen
AU - Åsjö, Birgitta
AU - Balotta, Claudia
AU - Beshkov, Danail
AU - Camacho, Ricardo J.
AU - Clotet, Bonaventura
AU - Coughlan, Suzie
AU - Griskevicius, Algirdas
AU - Grossman, Zehava
AU - Horban, Andrzej
AU - Kolupajeva, Tatjana
AU - Korn, Klaus
AU - Kostrikis, Leontios G.
AU - Liitsola, Kirsi
AU - Linka, Marek
AU - Nielsen, Claus
AU - Otelea, Dan
AU - Paraskevis, Dimitrios
AU - Paredes, Roger
AU - Poljak, Mario
AU - Puchhammer-Stöckl, Elisabeth
AU - Sönnerborg, Anders
AU - Stanekova, Danica
AU - Stanojevic, Maja
AU - Van Wijngaerden, Eric
AU - Wensing, Annemarie M.J.
AU - Boucher, Charles A.B.
AU - Puchhammer-Stockl, E.
AU - Sarcletti, M.
AU - Schmied, B.
AU - Geit, M.
AU - Balluch, G.
AU - Vandamme, A. M.
AU - Vercauteren, J.
AU - Derdelinckx, I.
AU - Sasse, A.
AU - Bogaert, M.
AU - Ceunen, H.
AU - De Roo, A.
AU - De Wit, S.
AU - Echahidi, F.
AU - on behalf of the SPREAD-programme
N1 - Funding Information: The following are the GenBank accession numbers for all of the sequences used in this analysis: AJ971091, AJ971093, AJ971096, AJ971102, AJ971103, AJ971106, AJ971107, AJ971109, AJ971110, AJ971113, AJ971114, AJ971117, AJ971122, AJ971128, AJ971133, AJ971140, AJ971143, AJ971144, AJ971268, AJ971271, AJ971274, AJ971276–AJ971281, AJ971283, AJ971285–AJ971287, AJ971289, AM113750, AY694290, AY694313, AY694317, AY694318, AY694321, AY694322, AY694324, AY694328–AY694330, AY694338, AY694339, AY694343–AY694345, AY694350, AY694353, AY694361, AY694362, AY694377, AY694382, AY938435/ AY940218, AY938437/AY940236, AY938439/AY940229, AY938440/AY940230, Y938441/AY940315, AY938442/AY940257, AY938443/AY940259, AY938444/ AY940243, AY938445/AY940238, AY938446/AY940238, AY938447/AY940237, AY938448/AY940239, AY938449/AY940240, AY938450/AY940245, Y938451/ AY940246, AY938452/AY940224, AY938453/AY940264, AY938454/AY940247, AY938455/AY940248, AY938456/AY940222, AY938458/AY940262, AY938459/AY940253, AY938460/AY940219, AY938461/AY940220, AY938463/ AY940244, AY938464/AY940216, AY938465/AY940215, AY938470/AY940252, AY938471/AY940254, AY938472/AY940232, AY938473/AY940235, AY938474/ AY940225, AY938475/AY940277, AY938476/AY940296, AY938477/AY940282, AY938482/AY940273, AY938484/AY940276, AY938487/AY940293, AY938488/AY940283, AY938489/ AY940280, AY938490/AY940275, AY938492/AY940272, AY938498/AY940297, AY938499/AY940249, AY938500/AY940270, AY938501/AY940298, AY938502/ AY940251, AY938503/AY940302, AY938504/AY940217, AY938507/AY940279, AY938508/AY940291, AY938509/AY940274, AY938510/AY940271, AY938511/ AY940301, AY938512/AY940234, AY938513/AY940263, AY938514/AY940265, AY938515/AY940267, AY938516/AY940268, AY938517/AY940260, AY938519/ AY940266, AY938520/AY940250, AY938521/AY940304, AY938522/AY940307, AY938523/AY940305, AY938524/AY940306, AY938525/AY940226, AY938526/ AY940311, AY938527/AY940312, Y938528/AY940313, AY938530/AY940294, AY938531/AY940255, Y938532/AY940233, AY938533/AY940269, DQ974841, DQ974844, DQ974845, DQ974847, DQ974848, DQ974850, DQ974853, DQ974854, DQ974857, DQ974858, DQ974863–DQ974865, DQ974867–DQ974873, DQ974875–DQ974877, DQ974880–DQ974882, DQ974887, DQ974890, DQ974892, DQ974893, DQ974895–DQ974897, DQ974899, DQ974902–DQ974906, DQ974908, DQ974910–DQ974912, DQ974922–DQ974924, DQ974927–DQ974929, DQ974931, DQ974932, DQ974941, DQ974944–DQ974947, DQ974951–DQ974953, DQ974955_DQ974963, DQ974965, DQ974966, DQ974968, DQ974982–DQ974991, DQ974996–DQ974998, DQ975003, DQ975011–DQ975015, DQ975018–DQ975021, DQ975024, DQ975032, DQ975034–DQ975036, DQ975044, DQ975136, DQ975139, DQ975140–DQ975147, DQ975156–DQ975159, DQ975161–DQ975163, DQ975165, DQ975169, DQ975172, DQ975173, DQ975187, EU248291–EU248297, EU248299, EU248300, EU248302, EU248303, EU248305–EU248307, EU248309, EU248310, EU248312, EU248314, EU248315, EU248317, EU248320–EU248323, EU248325, EU248327, EU248329, EU248331–EU248337, EU248340, EU248341, EU248343–EU248345, EU248347–EU248360, EU248363–EU248365, EU248368, EU248371– EU248373, EU248376–EU248378, EU248382, EU248383, EU248385–EU248387, EU248389, EU248392, EU248393, EU248396, EU248399, EU248400, EU248401, EU248403, EU248404, EU248406–EU248408, EU248410–EU248412, EU248415– EU248419, EU248421–EU248426, EU248428, EU248431, EU248432, EU248435, EU248439, EU248440–EU248444, EU248446, EU248448, EU248449, EU248451, EU248453, EU248455–EU248457, EU248459–EU248461, EU248463–EU248466, EU248468–EU248474, EU248476, EU248477, EU248479, EU248480, EU248483, EU248485, EU248487–EU248490, EU248492, EU248494–EU248498, EU248500–EU248505, EU248507, EU248509, EU248512, EU248515, EU248517–EU248521, EU248523, EU248526–EU248569, EU248571–EU248582, EU248584–EU248588, EU673374–EU673397, FJ030767, FJ030769, FJ030771, FJ030772, FJ185113– FJ185120, FJ185122, FJ185124, FJ185125, FJ185127, GQ398826–GQ401023, JX299533-JX301162. The work has been partially funded by the European Commission (grant QLK2-CT-2001-01344, fifth framework; grant LSHP-CT-2006-518211, sixth framework, grant DynaNets no. 233847), seventh framework; Belgian AIDS Reference Laboratory Fund, Belgian Fonds voor Wetenschappelijk Onderzoek (grant G.0611.09); Interuniversitaire Attractiepolen (Belgium; grant P6/41); Cyprus Research Promotion Foundation (grant Health/0104/22); Danish AIDS Foundation; Ministry of Health (Germany; grant 1502-686-18); Ministry of Education and Research (Germany; grant 01KI501); Fifth National Program on HIV/AIDS, Istituto Superiore di Sanità (Italy; grants N 40F.56 and 20D.1.6); Fondation Recherche sur le SiDA; Ministry of Health (Luxembourg); Swedish Research Council; Swedish Civil Contingencies Agency; CHAIN, Collaborative HIV and Anti-HIV Drug Resistance Network’, Integrated Project no. 223131, funded by the European Commission Framework 7 Program; Ministry of Education and Science (Republic of Serbia; grant 175024). ABA is supported by Fundação para a Ciência e Tecnologia (grant no. SFRH/BPD/65605/2009). Results of this paper have been presented at the 9th European Workshop on HIV & Hepatitis-Treatment Strategies & Antiviral Drug Resistance, Cyprus. SPREAD (Strategy to Control the Spread of HIV-1) investigators are listed after the text. Publisher Copyright: © 2014 Frentz et al.; licensee BioMed Central Ltd.
PY - 2014/7/21
Y1 - 2014/7/21
N2 - Background: One out of ten newly diagnosed patients in Europe was infected with a virus carrying a drug resistant mutation. We analysed the patterns over time for transmitted drug resistance mutations (TDRM) using data from the European Spread program.Methods: Clinical, epidemiological and virological data from 4317 patients newly diagnosed with HIV-1 infection between 2002 and 2007 were analysed. Patients were enrolled using a pre-defined sampling strategy.Results: The overall prevalence of TDRM in this period was 8.9% (95% CI: 8.1-9.8). Interestingly, significant changes over time in TDRM caused by the different drug classes were found. Whereas nucleoside resistance mutations remained constant at 5%, a significant decline in protease inhibitors resistance mutations was observed, from 3.9% in 2002 to 1.6% in 2007 (p = 0.001). In contrast, resistance to non-nucleoside reverse transcriptase inhibitors (NNRTIs) doubled from 2.0% in 2002 to 4.1% in 2007 (p = 0.004) with 58% of viral strains carrying a K103N mutation. Phylogenetic analysis showed that these temporal changes could not be explained by large clusters of TDRM.Conclusion: During the years 2002 to 2007 transmitted resistance to NNRTI has doubled to 4% in Europe. The frequent use of NNRTI in first-line regimens and the clinical impact of NNRTI mutations warrants continued monitoring.
AB - Background: One out of ten newly diagnosed patients in Europe was infected with a virus carrying a drug resistant mutation. We analysed the patterns over time for transmitted drug resistance mutations (TDRM) using data from the European Spread program.Methods: Clinical, epidemiological and virological data from 4317 patients newly diagnosed with HIV-1 infection between 2002 and 2007 were analysed. Patients were enrolled using a pre-defined sampling strategy.Results: The overall prevalence of TDRM in this period was 8.9% (95% CI: 8.1-9.8). Interestingly, significant changes over time in TDRM caused by the different drug classes were found. Whereas nucleoside resistance mutations remained constant at 5%, a significant decline in protease inhibitors resistance mutations was observed, from 3.9% in 2002 to 1.6% in 2007 (p = 0.001). In contrast, resistance to non-nucleoside reverse transcriptase inhibitors (NNRTIs) doubled from 2.0% in 2002 to 4.1% in 2007 (p = 0.004) with 58% of viral strains carrying a K103N mutation. Phylogenetic analysis showed that these temporal changes could not be explained by large clusters of TDRM.Conclusion: During the years 2002 to 2007 transmitted resistance to NNRTI has doubled to 4% in Europe. The frequent use of NNRTI in first-line regimens and the clinical impact of NNRTI mutations warrants continued monitoring.
KW - Europe
KW - HIV-1
KW - Resistance
KW - Transmission
UR - http://www.scopus.com/inward/record.url?scp=84904448066&partnerID=8YFLogxK
U2 - 10.1186/1471-2334-14-407
DO - 10.1186/1471-2334-14-407
M3 - Article
C2 - 25047543
AN - SCOPUS:84904448066
SN - 1471-2334
VL - 14
JO - BMC Infectious Diseases
JF - BMC Infectious Diseases
IS - 1
M1 - 407
ER -