HIV-1 genotypes related to failure of nelfinavir as the first protease inhibitor treatment
Autor(a) principal: | |
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Data de Publicação: | 2005 |
Outros Autores: | , |
Tipo de documento: | Artigo |
Idioma: | eng |
Título da fonte: | Brazilian Journal of Infectious Diseases |
Texto Completo: | http://old.scielo.br/scielo.php?script=sci_arttext&pid=S1413-86702005000400009 |
Resumo: | Combined antiretroviral therapy results in sustained viral suppression and a decrease in mortality and morbidity due to HIV infection. Intrinsic strength, durability and absence of cross-resistance are key factors in the selection of antiretrovirals. Failure with nelfinavir has been associated with two protease gene mutations, D30N and L90M. The D30N mutation does not result in cross-resistance with other protease inhibitors, and it decreases viral fitness. In order to check for this mutation after failure with nelfinavir, the 246 HIV-1 genotyping test was performed on virus samples from 55 patients with failure of nelfinavir as the first protease inhibitor. Most (84%) of the viral strains were of subtype B. Nucleosides associated with mutations (NAM) were observed in 80% of the tests; no INS69, complex 151, K65R and L74V mutations, which give multi-resistance to nucleoside analogue reverse transcriptase inhibitors to tenofovir and DDI, respectively, were observed. In the tests for protease gene mutations, the D30N mutation was found in 57%, L90M in 18% and the wild-type virus in 25%. These data are similar to published reports, showing that alternative therapies used after failure with nelfinavir may be more successful, as the D30N mutation does not cause cross-resistance to other protease inhibitors. |
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Brazilian Journal of Infectious Diseases |
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HIV-1 genotypes related to failure of nelfinavir as the first protease inhibitor treatmentHIV-1protease inhibitorsnelfinavirCombined antiretroviral therapy results in sustained viral suppression and a decrease in mortality and morbidity due to HIV infection. Intrinsic strength, durability and absence of cross-resistance are key factors in the selection of antiretrovirals. Failure with nelfinavir has been associated with two protease gene mutations, D30N and L90M. The D30N mutation does not result in cross-resistance with other protease inhibitors, and it decreases viral fitness. In order to check for this mutation after failure with nelfinavir, the 246 HIV-1 genotyping test was performed on virus samples from 55 patients with failure of nelfinavir as the first protease inhibitor. Most (84%) of the viral strains were of subtype B. Nucleosides associated with mutations (NAM) were observed in 80% of the tests; no INS69, complex 151, K65R and L74V mutations, which give multi-resistance to nucleoside analogue reverse transcriptase inhibitors to tenofovir and DDI, respectively, were observed. In the tests for protease gene mutations, the D30N mutation was found in 57%, L90M in 18% and the wild-type virus in 25%. These data are similar to published reports, showing that alternative therapies used after failure with nelfinavir may be more successful, as the D30N mutation does not cause cross-resistance to other protease inhibitors.Brazilian Society of Infectious Diseases2005-08-01info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersiontext/htmlhttp://old.scielo.br/scielo.php?script=sci_arttext&pid=S1413-86702005000400009Brazilian Journal of Infectious Diseases v.9 n.4 2005reponame:Brazilian Journal of Infectious Diseasesinstname:Brazilian Society of Infectious Diseases (BSID)instacron:BSID10.1590/S1413-86702005000400009info:eu-repo/semantics/openAccessTupinambás,UnaíAleixo,AgdemirGreco,Dirceueng2005-11-01T00:00:00Zoai:scielo:S1413-86702005000400009Revistahttps://www.bjid.org.br/https://old.scielo.br/oai/scielo-oai.phpbjid@bjid.org.br||lgoldani@ufrgs.br1678-43911413-8670opendoar:2005-11-01T00:00Brazilian Journal of Infectious Diseases - Brazilian Society of Infectious Diseases (BSID)false |
dc.title.none.fl_str_mv |
HIV-1 genotypes related to failure of nelfinavir as the first protease inhibitor treatment |
title |
HIV-1 genotypes related to failure of nelfinavir as the first protease inhibitor treatment |
spellingShingle |
HIV-1 genotypes related to failure of nelfinavir as the first protease inhibitor treatment Tupinambás,Unaí HIV-1 protease inhibitors nelfinavir |
title_short |
HIV-1 genotypes related to failure of nelfinavir as the first protease inhibitor treatment |
title_full |
HIV-1 genotypes related to failure of nelfinavir as the first protease inhibitor treatment |
title_fullStr |
HIV-1 genotypes related to failure of nelfinavir as the first protease inhibitor treatment |
title_full_unstemmed |
HIV-1 genotypes related to failure of nelfinavir as the first protease inhibitor treatment |
title_sort |
HIV-1 genotypes related to failure of nelfinavir as the first protease inhibitor treatment |
author |
Tupinambás,Unaí |
author_facet |
Tupinambás,Unaí Aleixo,Agdemir Greco,Dirceu |
author_role |
author |
author2 |
Aleixo,Agdemir Greco,Dirceu |
author2_role |
author author |
dc.contributor.author.fl_str_mv |
Tupinambás,Unaí Aleixo,Agdemir Greco,Dirceu |
dc.subject.por.fl_str_mv |
HIV-1 protease inhibitors nelfinavir |
topic |
HIV-1 protease inhibitors nelfinavir |
description |
Combined antiretroviral therapy results in sustained viral suppression and a decrease in mortality and morbidity due to HIV infection. Intrinsic strength, durability and absence of cross-resistance are key factors in the selection of antiretrovirals. Failure with nelfinavir has been associated with two protease gene mutations, D30N and L90M. The D30N mutation does not result in cross-resistance with other protease inhibitors, and it decreases viral fitness. In order to check for this mutation after failure with nelfinavir, the 246 HIV-1 genotyping test was performed on virus samples from 55 patients with failure of nelfinavir as the first protease inhibitor. Most (84%) of the viral strains were of subtype B. Nucleosides associated with mutations (NAM) were observed in 80% of the tests; no INS69, complex 151, K65R and L74V mutations, which give multi-resistance to nucleoside analogue reverse transcriptase inhibitors to tenofovir and DDI, respectively, were observed. In the tests for protease gene mutations, the D30N mutation was found in 57%, L90M in 18% and the wild-type virus in 25%. These data are similar to published reports, showing that alternative therapies used after failure with nelfinavir may be more successful, as the D30N mutation does not cause cross-resistance to other protease inhibitors. |
publishDate |
2005 |
dc.date.none.fl_str_mv |
2005-08-01 |
dc.type.driver.fl_str_mv |
info:eu-repo/semantics/article |
dc.type.status.fl_str_mv |
info:eu-repo/semantics/publishedVersion |
format |
article |
status_str |
publishedVersion |
dc.identifier.uri.fl_str_mv |
http://old.scielo.br/scielo.php?script=sci_arttext&pid=S1413-86702005000400009 |
url |
http://old.scielo.br/scielo.php?script=sci_arttext&pid=S1413-86702005000400009 |
dc.language.iso.fl_str_mv |
eng |
language |
eng |
dc.relation.none.fl_str_mv |
10.1590/S1413-86702005000400009 |
dc.rights.driver.fl_str_mv |
info:eu-repo/semantics/openAccess |
eu_rights_str_mv |
openAccess |
dc.format.none.fl_str_mv |
text/html |
dc.publisher.none.fl_str_mv |
Brazilian Society of Infectious Diseases |
publisher.none.fl_str_mv |
Brazilian Society of Infectious Diseases |
dc.source.none.fl_str_mv |
Brazilian Journal of Infectious Diseases v.9 n.4 2005 reponame:Brazilian Journal of Infectious Diseases instname:Brazilian Society of Infectious Diseases (BSID) instacron:BSID |
instname_str |
Brazilian Society of Infectious Diseases (BSID) |
instacron_str |
BSID |
institution |
BSID |
reponame_str |
Brazilian Journal of Infectious Diseases |
collection |
Brazilian Journal of Infectious Diseases |
repository.name.fl_str_mv |
Brazilian Journal of Infectious Diseases - Brazilian Society of Infectious Diseases (BSID) |
repository.mail.fl_str_mv |
bjid@bjid.org.br||lgoldani@ufrgs.br |
_version_ |
1754209239062020096 |