HIV-1 genotypes related to failure of nelfinavir as the first protease inhibitor treatment

Detalhes bibliográficos
Autor(a) principal: Tupinambás,Unaí
Data de Publicação: 2005
Outros Autores: Aleixo,Agdemir, Greco,Dirceu
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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spelling 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
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