Publications by authors named "Ricardo Jorge Camacho"
Background: Portugal has one of the most severe HIV-1 epidemics in Western Europe. Two subtypes circulate in parallel since the beginning of the epidemic. Comparing their transmission patterns and its association with transmitted drug resistance (TDR) is important to pinpoint transmission hotspots and to develop evidence-based treatment guidelines.
View Article and Find Full Text PDFArticle Synopsis
- CCR5-coreceptor antagonists are important for treating HIV-2, but it's crucial to determine whether the virus can only use the CCR5 coreceptor to avoid treatment failure.
- A new online tool, geno2pheno[coreceptor-hiv2], was created to predict HIV-2 coreceptor usage based on the V3 loop of the virus's glycoprotein, achieving high accuracy in distinguishing coreceptor types.
- This tool not only matched existing methods in predictive performance but also identified new markers for CXCR4 usage, enhancing the understanding of HIV-2 coreceptor dynamics.
Background: Epidemic HIV-2 (groups A and B) emerged in humans circa 1930-40. Its closest ancestors are SIVsmm infecting sooty mangabeys from southwestern Côte d'Ivoire. The earliest large-scale serological surveys of HIV-2 in West Africa (1985-91) show a patchy spread.
View Article and Find Full Text PDFTo characterize the HIV-2 integrase gene polymorphisms and the pathways to resistance of HIV-2 patients failing a raltegravir-containing regimen, we studied 63 integrase strand transfer inhibitors (INSTI)-naïve patients, and 10 heavily pretreated patients exhibiting virological failure while receiving a salvage raltegravir-containing regimen. All patients were infected by HIV-2 group A. 61.
View Article and Find Full Text PDFQuantitation of HIV-1 RNA levels in plasma has significant prognostic value since high viral load concentrations in plasma are associated with a faster disease progression. Viral load testing became one the most important tools for monitoring HIV patients. New real time methodologies to quantify HIV viral load had arisen in the last decade.
View Article and Find Full Text PDFObjectives: Despite a decreasing mortality and morbidity in treated HIV-1 patients, highly active antiretroviral treatment (HAART) can still fail due to the development of drug resistance. Especially, multidrug-resistant viruses pose a threat to efficient therapy. We studied the changing prevalence of multidrug resistance (MDR) over time in a cohort of HIV-1-infected patients in Portugal.
View Article and Find Full Text PDFObjectives: To investigate mutations selected in viruses from HIV-2-infected patients failing a highly active antiretroviral treatment (HAART) regimen including atazanavir/ritonavir.
Methods: Twenty-eight HIV-2-infected patients previously exposed to atazanavir/ritonavir and failing therapy were studied. The protease (PR) gene was amplified and sequenced, and mutations emerging under atazanavir/ritonavir selective pressure were reported.
Objectives: The purpose of this study was the qualitative and quantitative assessment of the in vitro effect of HIV-1 protease (PR) mutation 82M on replication capacity and susceptibility to the eight clinically available PR inhibitors (PIs).
Methods: The 82M substitution was introduced by site-directed mutagenesis in wild-type subtype B and G strains, as well as reverted back to wild-type in a therapy-failing strain. The recombinant viruses were evaluated for their replication capacity and susceptibility to PIs.
HIV-2 is responsible for a limited epidemic in West Africa. Around 20% of all infected patients will progress to AIDS, and will need antiretroviral therapy. Unfortunately, antiretrovirals were developed to suppress HIV-1 replication; not all of them are active against HIV-2, e.
View Article and Find Full Text PDFEurope is currently observing a significant rise in non-B subtypes. Consequently, the effect of genetic variability on therapy response or genotypic resistance interpretation algorithms is an emerging concern. The purpose of this study is to investigate the amino acid substitutions selected under drug pressure in the protease of human immunodeficiency virus type 1 (HIV-1) subtypes B and G, and determine if there are any significant differences.
View Article and Find Full Text PDFPurpose Of Review: This review summarizes our knowledge of HIV-1 subtype-related differences associated with antiretroviral drug resistance and its interpretation, and with clinical, immunological and virological therapy outcomes. It also addresses the problem that subtypes are only a crude classification of the genetic diversity relevant to these topics.
Recent Findings: Subtype-related variability is responsible for differences in drug resistance.
Article Synopsis
- The study aims to analyze and compare how different HIV-1 subtypes (C, F, G, and CRF02_AG) respond to protease inhibitors to better understand variations in susceptibility and related genetic factors.
- Using samples from drug-naive patients, researchers employed both phenotyping and genotyping techniques to identify specific polymorphisms linked to drug susceptibility, revealing unique susceptibility patterns across the subtypes.
- Results indicated that certain polymorphisms, like 70R and 37D/S/T, significantly influenced drug response, suggesting that understanding these genetic variations can enhance the accuracy of genotyping algorithms across different HIV subtypes.
Objective: To investigate whether and how mutations at position 89 of HIV-1 protease were associated with protease inhibitor (PI) failure, and what is the impact of the HIV-1 subtype.
Methods: In a database containing pol nucleotide sequences and treatment history, the correlation between PI experience and mutations at codon 89 was determined separately for subtype B and several non-B subtypes. A Bayesian network model was used to map the resistance pathways in which M89I/V is involved for subtype G.