RESUMO
For the last 100 years, diagnosis of malaria has been based on examination of Giemsa-stained thick and thin blood films under the microscope. This is a time-consuming procedure which often fails to correctly diagnose the infecting species--especially when carried out by inexperienced technicians or when blood levels of parasite are low. Rapid Diagnostic Tests (RDTs) for antigen detection can distinguish between Plasmodium falciparum and Plasmodium vivax but cannot identify the species present in mixed infections. In the case reported here we used multiplex PCR to investigate suspected mixed infection in a pregnant woman from Nigeria. The results suggest that the method used is highly specific and can be very sensitive and that it has several advantages with respect to microscopy and RTDs.
Assuntos
Malária/diagnóstico , Malária/parasitologia , Plasmodium/fisiologia , Complicações Parasitárias na Gravidez/parasitologia , Adulto , Animais , DNA de Protozoário/análise , Feminino , Humanos , Nigéria , Plasmodium/genética , Reação em Cadeia da Polimerase , GravidezRESUMO
OBJECTIVES: A major barrier to successful viral suppression in HIV type 1 (HIV-1)-infected individuals is the emergence of virus resistant to antiretroviral drugs. We explored the evolution of genotypic drug resistance prevalence in treatment-failing patients from 1999 to 2005 in a clinical cohort. PATIENTS AND METHODS: Prevalence of major International AIDS Society-USA HIV-1 drug resistance mutations was measured over calendar years in a population with treatment failure and undergoing resistance testing. Predictors of the presence of resistance mutations were analysed by logistic regression. RESULTS: Significant reductions of the prevalence of resistance to all three drug classes examined were observed. This was accompanied by a reduction in the proportion of treatment-failing patients. Independent predictors of drug resistance were the earlier calendar year, prior use of suboptimal nucleoside analogue therapy, male sex and higher CD4 levels at testing. CONCLUSIONS: In a single clinical cohort, we observed a decrease in the prevalence of resistance to all three examined antiretroviral drug classes over time. If this finding is confirmed in multicentre cohorts it may translate into reduced transmission of drug-resistant virus from treated patients.
Assuntos
Fármacos Anti-HIV/uso terapêutico , Farmacorresistência Viral/genética , Infecções por HIV/tratamento farmacológico , HIV-1/genética , Mutação , RNA Viral , Adulto , Terapia Antirretroviral de Alta Atividade , Contagem de Linfócito CD4 , Estudos de Coortes , Feminino , Genótipo , Infecções por HIV/epidemiologia , Infecções por HIV/imunologia , Infecções por HIV/virologia , Humanos , Modelos Logísticos , Masculino , Pessoa de Meia-Idade , Razão de Chances , Vigilância da População , Prevalência , Medição de Risco , Fatores de Risco , Fatores Sexuais , Fatores de Tempo , Falha de TratamentoRESUMO
The aim of this study was to establish the prevalence and predictors of genotypic resistance of HIV-1 to lopinavir and fosamprenavir from patients failing protease inhibitors (PI)-based regimens. We selected 643 HIV-1-infected patients with available treatment history who underwent genotypic resistance assays for virological failure from a clinical site and from the Stanford database. According to the genotypic resistance interpretation of the Stanford algorithm, proportions of viruses showing full susceptibility to fosamprenavir and lopinavir were 32% and 34%, respectively (p =ns). Proportions of viruses fully susceptible to lopinavir/r and fosamprenavir/r according to the Agence Nationale pour la Recherche sur le SIDA (ANRS) algorithm, were 81% and 81%, respectively. According to the Rega algorithm, proportions of viruses showing full susceptibility to fosamprenavir/r and lopinavir were 80% and 70%, respectively (p<0.001). According to the ANRS and Rega interpretations, the time on therapy predicted susceptibility to lopinavir/r, while susceptibility to fosamprenavir/r according to ANRS was predicted by the number of prior PI regimens experienced. According to the Stanford interpretation, prior indinavir exposure predicted resistance to lopinavir/r and fosamprenavir/r while prior nelfinavir use predicted susceptibility to both drugs. After failing PI-based regimens, the majority of viruses retained a predicted susceptibility to fosamprenavir/r and lopinavir/r. In patients failing PIs, the interpretation of genotypic resistance to fosamprenavir may change considerably according to the different algorithms and in respect to the effect of pharmacokinetic boosting with ritonavir.