Drug resistance mutations in patients infected with HIV-2 living in Spain
Background In contrast with HIV-1, information about drug resistance in HIV-2 is scarce and mainly derived from small series of patients failing antiretroviral therapy. Methods The spectrum of changes in the reverse transcriptase (RT), protease (PR) and integrase (INT) genes was examined in HIV-2 in...
Saved in:
| Published in | Journal of antimicrobial chemotherapy Vol. 66; no. 7; pp. 1484 - 1488 |
|---|---|
| Main Authors | , , , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
Oxford
Oxford University Press
01.07.2011
Oxford Publishing Limited (England) |
| Subjects | |
| Online Access | Get full text |
| ISSN | 0305-7453 1460-2091 1460-2091 |
| DOI | 10.1093/jac/dkr164 |
Cover
| Abstract | Background
In contrast with HIV-1, information about drug resistance in HIV-2 is scarce and mainly derived from small series of patients failing antiretroviral therapy.
Methods
The spectrum of changes in the reverse transcriptase (RT), protease (PR) and integrase (INT) genes was examined in HIV-2 individuals enrolled in the HIV-2 Spanish register.
Results
From a total of 236 HIV-2-infected individuals registered in Spain from 1989 to June 2010, 53 PR, 44 RT and 8 INT sequences were obtained. Low plasma viraemia precluded collection of this information from most of the remaining cases. No major mutations associated with drug resistance in HIV-1 were recognized in 29 PR, 20 RT and 5 INT sequences from antiretroviral-naive HIV-2 individuals, although natural polymorphisms with potential effects on susceptibility to PR inhibitors were recognized at 10 positions (L10V/I, V32I, M36I, M46I, I47V, Q58E, A71V/I, G73A, V82I and L89I/V) and for nucleoside reverse transcriptase inhibitors at three positions (T69N, V75I and K219E). In 24 antiretroviral-experienced patients with virological failure the most frequent major RT resistance mutations were M184V (58%), Q151M (33%) and K65R (21%), which are rarely seen thymidine analogue mutations. In PR the most frequent major changes were V47A (17%), I54M (17%), I82F (13%), L90M (29%) and L99F (29%). Two of the three patients who failed on raltegravir had N155H in the INT region.
Conclusions
Drug resistance mutations in HIV-2 are selected at the same positions as in HIV-1, although with different frequency. Polymorphisms in the RT and PR associated with drug resistance in HIV-1 as compensatory changes are common in untreated HIV-2 subjects. These findings highlight the need for specific guidelines for interpreting genotypic resistance patterns in HIV-2 infection. |
|---|---|
| AbstractList | In contrast with HIV-1, information about drug resistance in HIV-2 is scarce and mainly derived from small series of patients failing antiretroviral therapy.
The spectrum of changes in the reverse transcriptase (RT), protease (PR) and integrase (INT) genes was examined in HIV-2 individuals enrolled in the HIV-2 Spanish register.
From a total of 236 HIV-2-infected individuals registered in Spain from 1989 to June 2010, 53 PR, 44 RT and 8 INT sequences were obtained. Low plasma viraemia precluded collection of this information from most of the remaining cases. No major mutations associated with drug resistance in HIV-1 were recognized in 29 PR, 20 RT and 5 INT sequences from antiretroviral-naive HIV-2 individuals, although natural polymorphisms with potential effects on susceptibility to PR inhibitors were recognized at 10 positions (L10V/I, V32I, M36I, M46I, I47V, Q58E, A71V/I, G73A, V82I and L89I/V) and for nucleoside reverse transcriptase inhibitors at three positions (T69N, V75I and K219E). In 24 antiretroviral-experienced patients with virological failure the most frequent major RT resistance mutations were M184V (58%), Q151M (33%) and K65R (21%), which are rarely seen thymidine analogue mutations. In PR the most frequent major changes were V47A (17%), I54M (17%), I82F (13%), L90M (29%) and L99F (29%). Two of the three patients who failed on raltegravir had N155H in the INT region.
Drug resistance mutations in HIV-2 are selected at the same positions as in HIV-1, although with different frequency. Polymorphisms in the RT and PR associated with drug resistance in HIV-1 as compensatory changes are common in untreated HIV-2 subjects. These findings highlight the need for specific guidelines for interpreting genotypic resistance patterns in HIV-2 infection. Background In contrast with HIV-1, information about drug resistance in HIV-2 is scarce and mainly derived from small series of patients failing antiretroviral therapy. Methods The spectrum of changes in the reverse transcriptase (RT), protease (PR) and integrase (INT) genes was examined in HIV-2 individuals enrolled in the HIV-2 Spanish register. Results From a total of 236 HIV-2-infected individuals registered in Spain from 1989 to June 2010, 53 PR, 44 RT and 8 INT sequences were obtained. Low plasma viraemia precluded collection of this information from most of the remaining cases. No major mutations associated with drug resistance in HIV-1 were recognized in 29 PR, 20 RT and 5 INT sequences from antiretroviral-naive HIV-2 individuals, although natural polymorphisms with potential effects on susceptibility to PR inhibitors were recognized at 10 positions (L10V/I, V32I, M36I, M46I, I47V, Q58E, A71V/I, G73A, V82I and L89I/V) and for nucleoside reverse transcriptase inhibitors at three positions (T69N, V75I and K219E). In 24 antiretroviral-experienced patients with virological failure the most frequent major RT resistance mutations were M184V (58%), Q151M (33%) and K65R (21%), which are rarely seen thymidine analogue mutations. In PR the most frequent major changes were V47A (17%), I54M (17%), I82F (13%), L90M (29%) and L99F (29%). Two of the three patients who failed on raltegravir had N155H in the INT region. Conclusions Drug resistance mutations in HIV-2 are selected at the same positions as in HIV-1, although with different frequency. Polymorphisms in the RT and PR associated with drug resistance in HIV-1 as compensatory changes are common in untreated HIV-2 subjects. These findings highlight the need for specific guidelines for interpreting genotypic resistance patterns in HIV-2 infection. In contrast with HIV-1, information about drug resistance in HIV-2 is scarce and mainly derived from small series of patients failing antiretroviral therapy. The spectrum of changes in the reverse transcriptase (RT), protease (PR) and integrase (INT) genes was examined in HIV-2 individuals enrolled in the HIV-2 Spanish register. From a total of 236 HIV-2-infected individuals registered in Spain from 1989 to June 2010, 53 PR, 44 RT and 8 INT sequences were obtained. Low plasma viraemia precluded collection of this information from most of the remaining cases. No major mutations associated with drug resistance in HIV-1 were recognized in 29 PR, 20 RT and 5 INT sequences from antiretroviral-naive HIV-2 individuals, although natural polymorphisms with potential effects on susceptibility to PR inhibitors were recognized at 10 positions (L10V/I, V32I, M36I, M46I, I47V, Q58E, A71V/I, G73A, V82I and L89I/V) and for nucleoside reverse transcriptase inhibitors at three positions (T69N, V75I and K219E). In 24 antiretroviral-experienced patients with virological failure the most frequent major RT resistance mutations were M184V (58%), Q151M (33%) and K65R (21%), which are rarely seen thymidine analogue mutations. In PR the most frequent major changes were V47A (17%), I54M (17%), I82F (13%), L90M (29%) and L99F (29%). Two of the three patients who failed on raltegravir had N155H in the INT region. Drug resistance mutations in HIV-2 are selected at the same positions as in HIV-1, although with different frequency. Polymorphisms in the RT and PR associated with drug resistance in HIV-1 as compensatory changes are common in untreated HIV-2 subjects. These findings highlight the need for specific guidelines for interpreting genotypic resistance patterns in HIV-2 infection. In contrast with HIV-1, information about drug resistance in HIV-2 is scarce and mainly derived from small series of patients failing antiretroviral therapy.BACKGROUNDIn contrast with HIV-1, information about drug resistance in HIV-2 is scarce and mainly derived from small series of patients failing antiretroviral therapy.The spectrum of changes in the reverse transcriptase (RT), protease (PR) and integrase (INT) genes was examined in HIV-2 individuals enrolled in the HIV-2 Spanish register.METHODSThe spectrum of changes in the reverse transcriptase (RT), protease (PR) and integrase (INT) genes was examined in HIV-2 individuals enrolled in the HIV-2 Spanish register.From a total of 236 HIV-2-infected individuals registered in Spain from 1989 to June 2010, 53 PR, 44 RT and 8 INT sequences were obtained. Low plasma viraemia precluded collection of this information from most of the remaining cases. No major mutations associated with drug resistance in HIV-1 were recognized in 29 PR, 20 RT and 5 INT sequences from antiretroviral-naive HIV-2 individuals, although natural polymorphisms with potential effects on susceptibility to PR inhibitors were recognized at 10 positions (L10V/I, V32I, M36I, M46I, I47V, Q58E, A71V/I, G73A, V82I and L89I/V) and for nucleoside reverse transcriptase inhibitors at three positions (T69N, V75I and K219E). In 24 antiretroviral-experienced patients with virological failure the most frequent major RT resistance mutations were M184V (58%), Q151M (33%) and K65R (21%), which are rarely seen thymidine analogue mutations. In PR the most frequent major changes were V47A (17%), I54M (17%), I82F (13%), L90M (29%) and L99F (29%). Two of the three patients who failed on raltegravir had N155H in the INT region.RESULTSFrom a total of 236 HIV-2-infected individuals registered in Spain from 1989 to June 2010, 53 PR, 44 RT and 8 INT sequences were obtained. Low plasma viraemia precluded collection of this information from most of the remaining cases. No major mutations associated with drug resistance in HIV-1 were recognized in 29 PR, 20 RT and 5 INT sequences from antiretroviral-naive HIV-2 individuals, although natural polymorphisms with potential effects on susceptibility to PR inhibitors were recognized at 10 positions (L10V/I, V32I, M36I, M46I, I47V, Q58E, A71V/I, G73A, V82I and L89I/V) and for nucleoside reverse transcriptase inhibitors at three positions (T69N, V75I and K219E). In 24 antiretroviral-experienced patients with virological failure the most frequent major RT resistance mutations were M184V (58%), Q151M (33%) and K65R (21%), which are rarely seen thymidine analogue mutations. In PR the most frequent major changes were V47A (17%), I54M (17%), I82F (13%), L90M (29%) and L99F (29%). Two of the three patients who failed on raltegravir had N155H in the INT region.Drug resistance mutations in HIV-2 are selected at the same positions as in HIV-1, although with different frequency. Polymorphisms in the RT and PR associated with drug resistance in HIV-1 as compensatory changes are common in untreated HIV-2 subjects. These findings highlight the need for specific guidelines for interpreting genotypic resistance patterns in HIV-2 infection.CONCLUSIONSDrug resistance mutations in HIV-2 are selected at the same positions as in HIV-1, although with different frequency. Polymorphisms in the RT and PR associated with drug resistance in HIV-1 as compensatory changes are common in untreated HIV-2 subjects. These findings highlight the need for specific guidelines for interpreting genotypic resistance patterns in HIV-2 infection. Background In contrast with HIV-1, information about drug resistance in HIV-2 is scarce and mainly derived from small series of patients failing antiretroviral therapy. Methods The spectrum of changes in the reverse transcriptase (RT), protease (PR) and integrase (INT) genes was examined in HIV-2 individuals enrolled in the HIV-2 Spanish register. Results From a total of 236 HIV-2-infected individuals registered in Spain from 1989 to June 2010, 53 PR, 44 RT and 8 INT sequences were obtained. Low plasma viraemia precluded collection of this information from most of the remaining cases. No major mutations associated with drug resistance in HIV-1 were recognized in 29 PR, 20 RT and 5 INT sequences from antiretroviral-naive HIV-2 individuals, although natural polymorphisms with potential effects on susceptibility to PR inhibitors were recognized at 10 positions (L10V/I, V32I, M36I, M46I, I47V, Q58E, A71V/I, G73A, V82I and L89I/V) and for nucleoside reverse transcriptase inhibitors at three positions (T69N, V75I and K219E). In 24 antiretroviral-experienced patients with virological failure the most frequent major RT resistance mutations were M184V (58%), Q151M (33%) and K65R (21%), which are rarely seen thymidine analogue mutations. In PR the most frequent major changes were V47A (17%), I54M (17%), I82F (13%), L90M (29%) and L99F (29%). Two of the three patients who failed on raltegravir had N155H in the INT region. Conclusions Drug resistance mutations in HIV-2 are selected at the same positions as in HIV-1, although with different frequency. Polymorphisms in the RT and PR associated with drug resistance in HIV-1 as compensatory changes are common in untreated HIV-2 subjects. These findings highlight the need for specific guidelines for interpreting genotypic resistance patterns in HIV-2 infection. |
| Author | Roc, Lourdes Aguilera, Antonio Soriano, Vincent Caballero, Estrella Benito, Rafael Rodríguez, Carmen Cabezas, Teresa Treviño, Ana Parra, Patricia de Mendoza, Carmen |
| Author_xml | – sequence: 1 givenname: Ana surname: Treviño fullname: Treviño, Ana organization: 1 Infectious Diseases Department, Hospital Carlos III, Madrid, Spain – sequence: 2 givenname: Carmen surname: de Mendoza fullname: de Mendoza, Carmen organization: 1 Infectious Diseases Department, Hospital Carlos III, Madrid, Spain – sequence: 3 givenname: Estrella surname: Caballero fullname: Caballero, Estrella organization: 2 Service of Microbiology, Hospital Vall d'Hebron, Barcelona, Spain – sequence: 4 givenname: Carmen surname: Rodríguez fullname: Rodríguez, Carmen organization: 3 Centro Sanitario Sandoval, Madrid, Spain – sequence: 5 givenname: Patricia surname: Parra fullname: Parra, Patricia organization: 1 Infectious Diseases Department, Hospital Carlos III, Madrid, Spain – sequence: 6 givenname: Rafael surname: Benito fullname: Benito, Rafael organization: 4 Service of Microbiology, Hospital Clínico Universitario Lozano Blesa, Zaragoza, Spain – sequence: 7 givenname: Teresa surname: Cabezas fullname: Cabezas, Teresa organization: 5 Service of Microbiology, Hospital de Poniente, Almería, Spain – sequence: 8 givenname: Lourdes surname: Roc fullname: Roc, Lourdes organization: 6 Service of Microbiology, Hospital Miguel Servet, Zaragoza, Spain – sequence: 9 givenname: Antonio surname: Aguilera fullname: Aguilera, Antonio organization: 7 Service of Microbiology, Hospital Conxo-CHUS, Santiago, Spain – sequence: 10 givenname: Vincent surname: Soriano fullname: Soriano, Vincent organization: 1 Infectious Diseases Department, Hospital Carlos III, Madrid, Spain |
| BackLink | http://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=24289212$$DView record in Pascal Francis https://www.ncbi.nlm.nih.gov/pubmed/21558334$$D View this record in MEDLINE/PubMed |
| BookMark | eNqF0d9rFDEQB_AgFXutvvgHyCKIIKyd_Nhs8liqbQ8KffDHa5jNZmvOveyaZBX_e3PcFaGIfco8fGaYfOeEHIUpOEJeUnhPQfOzDdqz_nukUjwhKyok1Aw0PSIr4NDUrWj4MTlJaQMAspHqGTlmtGkU52JF1h_icldFl3zKGKyrtkvG7KeQKh-quZQu5F09OJtdX_3y-Vt1vf5as2r0P32427FPM_rwnDwdcEzuxeE9JV8uP36-uK5vbq_WF-c3tRWC5loO2AqQ2OtGI0hokSrX8a5tWecsSmxROFCy763uetYj7xpgQ9kYukZqx0_J2_3cOU4_Fpey2fpk3ThicNOSjAbGpaQgHpVKARXAlCry9QO5mZYYyjeMamURUuiCXh3Q0m1db-botxh_m_swC3hzAJgsjkMsgfr01wmmNKOsONg7G6eUohuM9fvQc0Q_Ggpmd1dT7mr2dy0t7x603E_9Jz7sMS3z_9wfS9eu6w |
| CODEN | JACHDX |
| CitedBy_id | crossref_primary_10_1021_acsinfecdis_9b00512 crossref_primary_10_1074_jbc_RA117_000177 crossref_primary_10_1186_s12977_015_0146_8 crossref_primary_10_1089_aid_2013_0153 crossref_primary_10_1099_vir_0_038638_0 crossref_primary_10_1097_QCO_0b013e32835a1de7 crossref_primary_10_1128_JVI_06597_11 crossref_primary_10_2217_fvl_2017_0037 crossref_primary_10_1093_infdis_jiaa026 crossref_primary_10_1093_jac_dkz007 crossref_primary_10_1093_jac_dkx090 crossref_primary_10_1128_AAC_00744_17 crossref_primary_10_1097_QAI_0b013e31826327c4 crossref_primary_10_1097_MD_0000000000014313 crossref_primary_10_1097_QAD_0b013e32834cdb89 crossref_primary_10_1371_journal_pone_0092747 crossref_primary_10_1097_QAD_0000000000001485 crossref_primary_10_3390_pathogens10111377 crossref_primary_10_1016_j_jcv_2015_01_001 crossref_primary_10_1186_s12981_020_0259_6 crossref_primary_10_3390_ijms24065905 crossref_primary_10_1016_j_virol_2016_02_008 crossref_primary_10_1128_AAC_01326_15 |
| Cites_doi | 10.1128/JCM.38.4.1370-1374.2000 10.1002/jmv.20174 10.1128/JCM.42.2.570-577.2004 10.1111/j.1747-0285.2008.00647.x 10.1177/135965350400900112 10.1089/088922204322996590 10.1099/0022-1317-83-6-1253 10.1128/AAC.00870-06 10.1056/NEJMoa013552 10.1177/135965350400900422 10.1016/0042-6822(91)90038-D 10.1086/599107 10.1128/AAC.00154-09 10.1093/nar/gkp455 10.1128/AAC.01284-07 10.1016/j.pbiomolbio.2004.07.005 10.1093/jac/dkl034 10.1016/j.jcv.2009.06.020 10.1097/QAD.0b013e3282f51203 10.1086/496982 10.1086/596504 10.1177/135965350400900115 10.1093/jac/dkn335 10.1097/01.aids.0000196171.35056.6c |
| ContentType | Journal Article |
| Contributor | Lopez-Dieguez, M Ramos, J M Rodríguez-Iglesias, M Tuset, T Regueiro, B García, R Pérez, S Pérez-Trallero, E García, J García, I Tuset, C Capote, F Escudero, D Pumarola, T López-Aldeguer, J Treviño, A Del Romero, J Cortizo, S Domingo, P Eiros, J M Cilla, G Calderón, E Hernandez-Betancor, A Molina, I Gutiérrez, M M Rodríguez, C Niubó, J Trigo, M Miró, J M Fernandez, J M Viciana, I Force, L Paz, I López Lirola, A M Raya, C Soriano, V Roc, L Caballero, E Diz, J Pujol, E Marcaida, G Fernández-Pereira, L Torres, A Benito, R Gorgolas, M Alvarez, P García-Campello, M Lozano, A Rodríguez, J C González-Praetorius, A Gutiérrez, M Mena, A Pérez, J L de Mendoza, C Medrano, F J Veloso, S Peñaranda, M Martinez Sapiña, A Montejo, J M Gutiérrez, F Cabezas, T Dronda, F Cifuentes, C Aguilera, A Sola, J Gaspar, G Rodríguez-Calviño, J J Leal, M Moreno, S Gómez-Hernando, C Gómez Sirvent, J L Ortiz de Lejarazu, R Vallejo, A Borrás, M Martín, A M Guelar, A Parra, P |
| Contributor_xml | – sequence: 1 givenname: C surname: Rodríguez fullname: Rodríguez, C – sequence: 2 givenname: J surname: Del Romero fullname: Del Romero, J – sequence: 3 givenname: C surname: Tuset fullname: Tuset, C – sequence: 4 givenname: G surname: Marcaida fullname: Marcaida, G – sequence: 5 givenname: T surname: Tuset fullname: Tuset, T – sequence: 6 givenname: E surname: Caballero fullname: Caballero, E – sequence: 7 givenname: I surname: Molina fullname: Molina, I – sequence: 8 givenname: A surname: Aguilera fullname: Aguilera, A – sequence: 9 givenname: J J surname: Rodríguez-Calviño fullname: Rodríguez-Calviño, J J – sequence: 10 givenname: S surname: Cortizo fullname: Cortizo, S – sequence: 11 givenname: B surname: Regueiro fullname: Regueiro, B – sequence: 12 givenname: R surname: Benito fullname: Benito, R – sequence: 13 givenname: M surname: Borrás fullname: Borrás, M – sequence: 14 givenname: R surname: Ortiz de Lejarazu fullname: Ortiz de Lejarazu, R – sequence: 15 givenname: J M surname: Eiros fullname: Eiros, J M – sequence: 16 givenname: J M surname: Miró fullname: Miró, J M – sequence: 17 givenname: M surname: Lopez-Dieguez fullname: Lopez-Dieguez, M – sequence: 18 givenname: M M surname: Gutiérrez fullname: Gutiérrez, M M – sequence: 19 givenname: T surname: Pumarola fullname: Pumarola, T – sequence: 20 givenname: J surname: García fullname: García, J – sequence: 21 givenname: I surname: Paz fullname: Paz, I – sequence: 22 givenname: E surname: Calderón fullname: Calderón, E – sequence: 23 givenname: F J surname: Medrano fullname: Medrano, F J – sequence: 24 givenname: M surname: Leal fullname: Leal, M – sequence: 25 givenname: F surname: Capote fullname: Capote, F – sequence: 26 givenname: A surname: Vallejo fullname: Vallejo, A – sequence: 27 givenname: F surname: Dronda fullname: Dronda, F – sequence: 28 givenname: S surname: Moreno fullname: Moreno, S – sequence: 29 givenname: D surname: Escudero fullname: Escudero, D – sequence: 30 givenname: E surname: Pujol fullname: Pujol, E – sequence: 31 givenname: M surname: Trigo fullname: Trigo, M – sequence: 32 givenname: J surname: Diz fullname: Diz, J – sequence: 33 givenname: P surname: Alvarez fullname: Alvarez, P – sequence: 34 givenname: M surname: García-Campello fullname: García-Campello, M – sequence: 35 givenname: M surname: Rodríguez-Iglesias fullname: Rodríguez-Iglesias, M – sequence: 36 givenname: A M surname: Martín fullname: Martín, A M – sequence: 37 givenname: A surname: Hernandez-Betancor fullname: Hernandez-Betancor, A – sequence: 38 givenname: J M surname: Ramos fullname: Ramos, J M – sequence: 39 givenname: J C surname: Rodríguez fullname: Rodríguez, J C – sequence: 40 givenname: F surname: Gutiérrez fullname: Gutiérrez, F – sequence: 41 givenname: C surname: Gómez-Hernando fullname: Gómez-Hernando, C – sequence: 42 givenname: A surname: Guelar fullname: Guelar, A – sequence: 43 givenname: G surname: Cilla fullname: Cilla, G – sequence: 44 givenname: E surname: Pérez-Trallero fullname: Pérez-Trallero, E – sequence: 45 givenname: J surname: López-Aldeguer fullname: López-Aldeguer, J – sequence: 46 givenname: J surname: Sola fullname: Sola, J – sequence: 47 givenname: L surname: Fernández-Pereira fullname: Fernández-Pereira, L – sequence: 48 givenname: J surname: Niubó fullname: Niubó, J – sequence: 49 givenname: S surname: Veloso fullname: Veloso, S – sequence: 50 givenname: A surname: Torres fullname: Torres, A – sequence: 51 givenname: A M surname: López Lirola fullname: López Lirola, A M – sequence: 52 givenname: J L surname: Gómez Sirvent fullname: Gómez Sirvent, J L – sequence: 53 givenname: L surname: Force fullname: Force, L – sequence: 54 givenname: C surname: Cifuentes fullname: Cifuentes, C – sequence: 55 givenname: S surname: Pérez fullname: Pérez, S – sequence: 56 givenname: C surname: Raya fullname: Raya, C – sequence: 57 givenname: A surname: González-Praetorius fullname: González-Praetorius, A – sequence: 58 givenname: A surname: Mena fullname: Mena, A – sequence: 59 givenname: J L surname: Pérez fullname: Pérez, J L – sequence: 60 givenname: M surname: Peñaranda fullname: Peñaranda, M – sequence: 61 givenname: J M surname: Montejo fullname: Montejo, J M – sequence: 62 givenname: M surname: Gutiérrez fullname: Gutiérrez, M – sequence: 63 givenname: P surname: Domingo fullname: Domingo, P – sequence: 64 givenname: L surname: Roc fullname: Roc, L – sequence: 65 givenname: A surname: Martinez Sapiña fullname: Martinez Sapiña, A – sequence: 66 givenname: I surname: Viciana fullname: Viciana, I – sequence: 67 givenname: T surname: Cabezas fullname: Cabezas, T – sequence: 68 givenname: A surname: Lozano fullname: Lozano, A – sequence: 69 givenname: J M surname: Fernandez fullname: Fernandez, J M – sequence: 70 givenname: I surname: García fullname: García, I – sequence: 71 givenname: G surname: Gaspar fullname: Gaspar, G – sequence: 72 givenname: R surname: García fullname: García, R – sequence: 73 givenname: M surname: Gorgolas fullname: Gorgolas, M – sequence: 74 givenname: A surname: Treviño fullname: Treviño, A – sequence: 75 givenname: P surname: Parra fullname: Parra, P – sequence: 76 givenname: C surname: de Mendoza fullname: de Mendoza, C – sequence: 77 givenname: V surname: Soriano fullname: Soriano, V |
| Copyright | The Author 2011. Published by Oxford University Press on behalf of the British Society for Antimicrobial Chemotherapy. All rights reserved. For Permissions, please e-mail: journals.permissions@oup.com 2011 2015 INIST-CNRS Copyright Oxford Publishing Limited(England) Jul 2011 |
| Copyright_xml | – notice: The Author 2011. Published by Oxford University Press on behalf of the British Society for Antimicrobial Chemotherapy. All rights reserved. For Permissions, please e-mail: journals.permissions@oup.com 2011 – notice: 2015 INIST-CNRS – notice: Copyright Oxford Publishing Limited(England) Jul 2011 |
| CorporateAuthor | on behalf of the HIV-2 Spanish Study Group HIV-2 Spanish Study Group |
| CorporateAuthor_xml | – name: on behalf of the HIV-2 Spanish Study Group – name: HIV-2 Spanish Study Group |
| DBID | AAYXX CITATION IQODW CGR CUY CVF ECM EIF NPM 7QL 7QO 7T7 7U7 7U9 8FD C1K FR3 H94 K9. M7N NAPCQ P64 7X8 |
| DOI | 10.1093/jac/dkr164 |
| DatabaseName | CrossRef Pascal-Francis Medline MEDLINE MEDLINE (Ovid) MEDLINE MEDLINE PubMed Bacteriology Abstracts (Microbiology B) Biotechnology Research Abstracts Industrial and Applied Microbiology Abstracts (Microbiology A) Toxicology Abstracts Virology and AIDS Abstracts Technology Research Database Environmental Sciences and Pollution Management Engineering Research Database AIDS and Cancer Research Abstracts ProQuest Health & Medical Complete (Alumni) Algology Mycology and Protozoology Abstracts (Microbiology C) Nursing & Allied Health Premium Biotechnology and BioEngineering Abstracts MEDLINE - Academic |
| DatabaseTitle | CrossRef MEDLINE Medline Complete MEDLINE with Full Text PubMed MEDLINE (Ovid) Virology and AIDS Abstracts Technology Research Database Toxicology Abstracts ProQuest Health & Medical Complete (Alumni) Biotechnology and BioEngineering Abstracts Environmental Sciences and Pollution Management Nursing & Allied Health Premium Biotechnology Research Abstracts Bacteriology Abstracts (Microbiology B) Algology Mycology and Protozoology Abstracts (Microbiology C) AIDS and Cancer Research Abstracts Engineering Research Database Industrial and Applied Microbiology Abstracts (Microbiology A) MEDLINE - Academic |
| DatabaseTitleList | MEDLINE Virology and AIDS Abstracts MEDLINE - Academic Engineering Research Database |
| Database_xml | – sequence: 1 dbid: NPM name: PubMed url: https://proxy.k.utb.cz/login?url=http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed sourceTypes: Index Database – sequence: 2 dbid: EIF name: MEDLINE url: https://proxy.k.utb.cz/login?url=https://www.webofscience.com/wos/medline/basic-search sourceTypes: Index Database |
| DeliveryMethod | fulltext_linktorsrc |
| Discipline | Medicine Pharmacy, Therapeutics, & Pharmacology |
| EISSN | 1460-2091 |
| EndPage | 1488 |
| ExternalDocumentID | 2398455971 21558334 24289212 10_1093_jac_dkr164 10.1093/jac/dkr164 |
| Genre | Research Support, Non-U.S. Gov't Journal Article Feature |
| GeographicLocations | Europe Spain |
| GeographicLocations_xml | – name: Spain |
| GroupedDBID | --- -E4 .2P .GJ .I3 .XZ .ZR 0R~ 18M 1TH 29J 2WC 3O- 4.4 482 48X 53G 5GY 5RE 5VS 5WA 5WD 6.Y 70D AABZA AACZT AAJKP AAJQQ AAMVS AAOGV AAPGJ AAPNW AAPQZ AAPXW AARHZ AASNB AAUAY AAUQX AAVAP AAWDT AAWTL ABEUO ABIXL ABJNI ABKDP ABLJU ABNHQ ABNKS ABPTD ABQLI ABQNK ABQTQ ABSAR ABSMQ ABWST ABXVV ABZBJ ACCCW ACFRR ACGFO ACGFS ACIWK ACMRT ACPQN ACPRK ACUFI ACUTJ ACUTO ACYHN ACZBC ADBBV ADEYI ADEZT ADGZP ADHKW ADHZD ADIPN ADJQC ADOCK ADQBN ADRIX ADRTK ADVEK ADYVW ADZXQ AEGPL AEJOX AEKPW AEKSI AEMDU AENEX AENZO AEPUE AETBJ AEWNT AFFNX AFFZL AFIYH AFOFC AFRAH AFSHK AFXAL AFXEN AFYAG AGINJ AGKEF AGKRT AGMDO AGQXC AGSYK AGUTN AHMBA AHXPO AI. AIAGR AIJHB AJEEA ALMA_UNASSIGNED_HOLDINGS ALUQC APIBT APJGH APWMN AQDSO AQKUS ASPBG ATGXG ATTQO AVNTJ AVWKF AXUDD AZFZN BAWUL BAYMD BCRHZ BEYMZ BHONS BTRTY BVRKM BZKNY C45 CAG CDBKE COF CS3 CZ4 DAKXR DIK DILTD DU5 D~K E3Z EBS ECGQY EE~ EIHJH EJD EMOBN ENERS F5P F9B FECEO FEDTE FLUFQ FOEOM FOTVD FQBLK GAUVT GJXCC GX1 H13 H5~ HAR HH5 HVGLF HW0 HZ~ IOX J21 J5H JXSIZ KAQDR KBUDW KOP KQ8 KSI KSN L7B M-Z M49 MBLQV MHKGH ML0 N9A NGC NOMLY NOYVH NTWIH NU- NVLIB O0~ O9- OAUYM OAWHX OBS OCZFY ODMLO OJQWA OJZSN OK1 OPAEJ OVD OWPYF O~Y P2P PAFKI PB- PEELM PQQKQ Q1. Q5Y QBD R44 RD5 RHF RNI ROL ROX ROZ RUSNO RW1 RXO RZF RZO TCURE TEORI TJX TMA TR2 UCJ VH1 W8F WOQ X7H Y6R YAYTL YKOAZ YXANX ZGI ZKX ZXP ~91 ~A~ AAYXX ABDFA ABEJV ABGNP ABPQP ABVGC ADNBA AEMQT AGORE AHMMS AJBYB AJNCP ALXQX CITATION ABNGD ACUKT ACVCV ADMTO AEHUL AFFQV AGQPQ AHGBF AJDVS IQODW OBFPC CGR CUY CVF ECM EIF NPM 7QL 7QO 7T7 7U7 7U9 8FD C1K FR3 H94 K9. M7N NAPCQ P64 7X8 |
| ID | FETCH-LOGICAL-c441t-6fa7406ad959a0607a18eb3b772beca6a7a4e086ddc9bd2da3b502f2150b569e3 |
| ISSN | 0305-7453 1460-2091 |
| IngestDate | Sat Sep 27 17:57:09 EDT 2025 Sun Sep 28 06:46:05 EDT 2025 Mon Jun 30 16:45:14 EDT 2025 Mon Jul 21 05:54:34 EDT 2025 Mon Jul 21 09:15:38 EDT 2025 Tue Jul 01 03:16:46 EDT 2025 Thu Apr 24 23:02:24 EDT 2025 Wed Aug 28 03:24:40 EDT 2024 |
| IsDoiOpenAccess | false |
| IsOpenAccess | true |
| IsPeerReviewed | true |
| IsScholarly | true |
| Issue | 7 |
| Keywords | protease reverse transcriptase integrase Human Immunopathology Treatment resistance RNA-directed DNA polymerase Enzyme Transferases Reverse transcription Patient AIDS Immune deficiency Infection Peptidases Nucleotidyltransferases Viral disease Hydrolases Genetics Mutation |
| Language | English |
| License | CC BY 4.0 |
| LinkModel | OpenURL |
| MergedId | FETCHMERGED-LOGICAL-c441t-6fa7406ad959a0607a18eb3b772beca6a7a4e086ddc9bd2da3b502f2150b569e3 |
| Notes | SourceType-Scholarly Journals-1 ObjectType-Feature-1 content type line 14 ObjectType-Article-1 ObjectType-Feature-2 content type line 23 ObjectType-Article-2 |
| OpenAccessLink | https://academic.oup.com/jac/article-pdf/66/7/1484/2353885/dkr164.pdf |
| PMID | 21558334 |
| PQID | 876288649 |
| PQPubID | 32192 |
| PageCount | 5 |
| ParticipantIDs | proquest_miscellaneous_902366104 proquest_miscellaneous_880140288 proquest_journals_876288649 pubmed_primary_21558334 pascalfrancis_primary_24289212 crossref_citationtrail_10_1093_jac_dkr164 crossref_primary_10_1093_jac_dkr164 oup_primary_10_1093_jac_dkr164 |
| ProviderPackageCode | CITATION AAYXX |
| PublicationCentury | 2000 |
| PublicationDate | 2011-07-01 |
| PublicationDateYYYYMMDD | 2011-07-01 |
| PublicationDate_xml | – month: 07 year: 2011 text: 2011-07-01 day: 01 |
| PublicationDecade | 2010 |
| PublicationPlace | Oxford |
| PublicationPlace_xml | – name: Oxford – name: England |
| PublicationTitle | Journal of antimicrobial chemotherapy |
| PublicationTitleAlternate | J Antimicrob Chemother |
| PublicationYear | 2011 |
| Publisher | Oxford University Press Oxford Publishing Limited (England) |
| Publisher_xml | – name: Oxford University Press – name: Oxford Publishing Limited (England) |
| References | (11_21588780) 2006; 57 Parkin (7_18103353) 2004; 9 Witvrouw (8_18103359) 2004; 9 Colson (10_18032997) 2004; 42 (13_30314687) 2008; 52 Damond (14_30572241) 2008; 22 Ohtaka (4_18547229) 2005; 88 de Mendoza (22_34340063) 2009; 11 (18_39882508) 2010; 15 (25_38265184) 2009; 48 (6_34905560) 2009; 53 Brower (12_30590652) 2008; 71 Poulsen (1_10274482) 1993; 6 Little (15_17185500) 2002; 347 de Mendoza (16_19449352) 2005; 41 (21_34948345) 2009; 37 Rodes (19_6537432) 2000; 38 Salgado (32_35331772) 2009; 46 Reeves (2_17069233) 2002; 83 Poveda (9_18161604) 2004; 20 (17_38264744) 2009; 48 (27_22989785) 2007; 51 (3_35411037) 1991; 180 Descamps (24_18302481) 2004; 74 Johnson (20_36474904) 2009; 17 (5_31749377) 2008; 62 Rod s (30_19737035) 2006; 20 Damond (23_18453096) 2004; 9 |
| References_xml | – volume: 38 start-page: 1370 issn: 0095-1137 issue: 4 year: 2000 ident: 19_6537432 publication-title: Journal of Clinical Microbiology doi: 10.1128/JCM.38.4.1370-1374.2000 – volume: 74 start-page: 197 issn: 0146-6615 issue: 2 year: 2004 ident: 24_18302481 publication-title: Journal of medical virology doi: 10.1002/jmv.20174 – volume: 42 start-page: 570 issn: 0095-1137 issue: 2 year: 2004 ident: 10_18032997 publication-title: Journal of Clinical Microbiology doi: 10.1128/JCM.42.2.570-577.2004 – volume: 71 start-page: 298 issn: 1747-0277 issue: 4 year: 2008 ident: 12_30590652 doi: 10.1111/j.1747-0285.2008.00647.x – volume: 9 start-page: 3 issn: 1359-6535 issue: 1 year: 2004 ident: 7_18103353 publication-title: Antiviral therapy doi: 10.1177/135965350400900112 – volume: 20 start-page: 347 issn: 0889-2229 issue: 3 year: 2004 ident: 9_18161604 publication-title: AIDS research and human retroviruses doi: 10.1089/088922204322996590 – volume: 83 start-page: 1253 issn: 0022-1317 issue: 6 year: 2002 ident: 2_17069233 publication-title: Journal of General Virology doi: 10.1099/0022-1317-83-6-1253 – volume: 15 start-page: 182 issn: 1359-6535 year: 2010 ident: 18_39882508 publication-title: Antiviral therapy – volume: 51 start-page: 604 issn: 0066-4804 issue: 2 year: 2007 ident: 27_22989785 publication-title: Antimicrobial Agents and Chemotherapy doi: 10.1128/AAC.00870-06 – volume: 347 start-page: 385 issn: 0028-4793 issue: 6 year: 2002 ident: 15_17185500 publication-title: New England Journal of Medicine doi: 10.1056/NEJMoa013552 – volume: 9 start-page: 635 issn: 1359-6535 issue: 4 year: 2004 ident: 23_18453096 publication-title: Antiviral therapy doi: 10.1177/135965350400900422 – volume: 180 start-page: 339 issn: 1096-0341 year: 1991 ident: 3_35411037 doi: 10.1016/0042-6822(91)90038-D – volume: 48 start-page: 1790 issn: 1058-4838 issue: 12 year: 2009 ident: 17_38264744 publication-title: Clinical Infectious Diseases doi: 10.1086/599107 – volume: 53 start-page: 3611 issn: 0066-4804 issue: 9 year: 2009 ident: 6_34905560 publication-title: Antimicrobial Agents and Chemotherapy doi: 10.1128/AAC.00154-09 – volume: 17 start-page: 138 issn: 2161-5845 issue: 5 year: 2009 ident: 20_36474904 – volume: 37 start-page: W634 issn: 0305-1048 issue: suppl_2 year: 2009 ident: 21_34948345 publication-title: Nucleic Acids Research doi: 10.1093/nar/gkp455 – volume: 52 start-page: 1545 issn: 0066-4804 issue: 4 year: 2008 ident: 13_30314687 publication-title: Antimicrobial Agents and Chemotherapy doi: 10.1128/AAC.01284-07 – volume: 88 start-page: 193 issn: 0079-6107 issue: 2 year: 2005 ident: 4_18547229 publication-title: Progress in biophysics and molecular biology doi: 10.1016/j.pbiomolbio.2004.07.005 – volume: 11 start-page: 39 issn: 1139-6121 issue: 1 year: 2009 ident: 22_34340063 publication-title: AIDS reviews – volume: 57 start-page: 709 issn: 0305-7453 issue: 4 year: 2006 ident: 11_21588780 publication-title: Journal of Antimicrobial Chemotherapy doi: 10.1093/jac/dkl034 – volume: 46 start-page: 173 issn: 1386-6532 issue: 2 year: 2009 ident: 32_35331772 publication-title: Journal of clinical virology : the official publication of the Pan American Society for Clinical Virology doi: 10.1016/j.jcv.2009.06.020 – volume: 22 start-page: 665 issn: 0269-9370 issue: 5 year: 2008 ident: 14_30572241 publication-title: AIDS (London, England) doi: 10.1097/QAD.0b013e3282f51203 – volume: 6 start-page: 941 issn: 0894-9255 issue: 8 year: 1993 ident: 1_10274482 publication-title: Journal of acquired immune deficiency syndromes – volume: 41 start-page: 1350 issn: 1058-4838 issue: 9 year: 2005 ident: 16_19449352 publication-title: Clinical Infectious Diseases doi: 10.1086/496982 – volume: 48 start-page: 476 issn: 1058-4838 issue: 4 year: 2009 ident: 25_38265184 publication-title: Clinical Infectious Diseases doi: 10.1086/596504 – volume: 9 start-page: 57 issn: 1359-6535 issue: 1 year: 2004 ident: 8_18103359 publication-title: Antiviral therapy doi: 10.1177/135965350400900115 – volume: 62 start-page: 914 issn: 0305-7453 issue: 5 year: 2008 ident: 5_31749377 publication-title: Journal of Antimicrobial Chemotherapy doi: 10.1093/jac/dkn335 – volume: 20 start-page: 127 issn: 0269-9370 issue: 1 year: 2006 ident: 30_19737035 publication-title: AIDS (London, England) doi: 10.1097/01.aids.0000196171.35056.6c |
| SSID | ssj0006568 |
| Score | 2.175337 |
| Snippet | Background
In contrast with HIV-1, information about drug resistance in HIV-2 is scarce and mainly derived from small series of patients failing antiretroviral... In contrast with HIV-1, information about drug resistance in HIV-2 is scarce and mainly derived from small series of patients failing antiretroviral therapy.... In contrast with HIV-1, information about drug resistance in HIV-2 is scarce and mainly derived from small series of patients failing antiretroviral... Background In contrast with HIV-1, information about drug resistance in HIV-2 is scarce and mainly derived from small series of patients failing antiretroviral... |
| SourceID | proquest pubmed pascalfrancis crossref oup |
| SourceType | Aggregation Database Index Database Enrichment Source Publisher |
| StartPage | 1484 |
| SubjectTerms | Adolescent Adult Aged Aged, 80 and over Anti-HIV Agents - pharmacology Antibiotics. Antiinfectious agents. Antiparasitic agents Antiretroviral drugs Biological and medical sciences Child Child, Preschool Drug resistance Drug Resistance, Viral Female HIV HIV Infections - virology HIV Protease - genetics HIV Reverse Transcriptase - genetics HIV-2 - drug effects HIV-2 - genetics HIV-2 - isolation & purification Human immunodeficiency virus Human immunodeficiency virus 1 Human immunodeficiency virus 2 Human viral diseases Humans Immunodeficiencies Immunodeficiencies. Immunoglobulinopathies Immunopathology Infectious diseases Integrases - genetics Male Medical sciences Middle Aged Mutation Mutation, Missense Pharmacology. Drug treatments Polymorphism Polymorphism, Genetic Sequence Analysis, DNA Spain Viral diseases Viral diseases of the lymphoid tissue and the blood. Aids Viral Proteins - genetics Young Adult |
| Title | Drug resistance mutations in patients infected with HIV-2 living in Spain |
| URI | https://www.ncbi.nlm.nih.gov/pubmed/21558334 https://www.proquest.com/docview/876288649 https://www.proquest.com/docview/880140288 https://www.proquest.com/docview/902366104 |
| Volume | 66 |
| hasFullText | 1 |
| inHoldings | 1 |
| isFullTextHit | |
| isPrint | |
| link | http://utb.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwnV1bb9MwFLZgSAgJIRi3MpgsgSahLVuaOE78iEanFrYxiRT1LbJjZwTWtOoFafv1HMd20omO20vUpidplPPZ_myf7xyE3hSRkgnJI0-RLvNIXiiPc6a8WIa-ihUTtFa5npzS_pB8GEWjdge_VpcsxH5-tVZX8j9ehXPgV62S_QfPNjeFE_AZ_AtH8DAc_8rH72fL812YL2sOqBvoeLlYiQ03GVNdvJULM-8PvnjB7kX5w4pZPk-5Tb79K0WFt16OyzpVk04j8lWNrV6rWYdPdZRwZaQyVdPDS6WjZeXkituYknErODvkQpdvMfKanpaqmLJHdttHzsrzpVnVXrlOtuussVuWsHIsP_JiYjIB7yvTuxLqgwNNeS7X_ZqiKxZm8Upf2jVZTt24DF-TtX2-yYf1jedwlN9nXUrasc3t559-yo6Gx8dZ2hult9GdIAYIagY9-NgM29ToJpvndrlsWXgA9z4wd77GXowi8v6Uz6E5FaYOys0TlZqwpA_RA-tG_M7A5hG6papNdPfExlJsop0zk7X8cg-nrQhvvod38Fmbz_zyMRpomOEWZriBGS4r7GCGHcywhhmuYYYNzLRZDbMnaHjUSw_7nq3A4eVAkxceLXgMjI9LFjHuUz_m3USJUMCUDNo-pzzmRMGkWMqcCRlIHorIDwqgkb6IKFPhU7RRTSr1HGFRRMxnuSpEwkkuoT8A6htwqgKiCrDuoLfuzWa5TU-vq6RcZCZMIszAC5nxQge9bmynJinLWqttcNDvDa75rjEF2pow4HQdtOWcmdlmP880fUgSSlgH4eZX6JP1Rhuv1GQJJjolExD35GYTpis3wNQFHuKZQUn770DxkzAkL_588Ra617a9l2hjMVuqV0CSF2K7BvdPtBXCjA |
| linkProvider | Flying Publisher |
| openUrl | ctx_ver=Z39.88-2004&ctx_enc=info%3Aofi%2Fenc%3AUTF-8&rfr_id=info%3Asid%2Fsummon.serialssolutions.com&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.genre=article&rft.atitle=Drug+resistance+mutations+in+patients+infected+with+HIV-2+living+in+Spain&rft.jtitle=Journal+of+antimicrobial+chemotherapy&rft.au=Trevino%2C+Ana&rft.au=de+Mendoza%2C+Carmen&rft.au=Caballero%2C+Estrella&rft.au=Rodriguez%2C+Carmen&rft.date=2011-07-01&rft.issn=0305-7453&rft.eissn=1460-2091&rft.volume=66&rft.issue=7&rft.spage=1484&rft.epage=1488&rft_id=info:doi/10.1093%2Fjac%2Fdkr164&rft.externalDBID=NO_FULL_TEXT |
| thumbnail_l | http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/lc.gif&issn=0305-7453&client=summon |
| thumbnail_m | http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/mc.gif&issn=0305-7453&client=summon |
| thumbnail_s | http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/sc.gif&issn=0305-7453&client=summon |