PRISCILLA RAMOS COSTA

(Fonte: Lattes)
Índice h a partir de 2011
12
Projetos de Pesquisa
Unidades Organizacionais
LIM/60 - Laboratório de Imunologia Clínica e Alergia, Hospital das Clínicas, Faculdade de Medicina

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  • article 15 Citação(ões) na Scopus
    A generalizable method for estimating duration of HIV infections using clinical testing history and HIV test results
    (2019) PILCHER, Christopher D.; PORCO, Travis C.; FACENTE, Shelley N.; GREBE, Eduard; DELANEY, Kevin P.; MASCIOTRA, Silvina; KASSANJEE, Reshma; BUSCH, Michael P.; MURPHY, Gary; OWEN, S. Michele; WELTE, Alex; MATTEN, David; BRAND, Hilmarie; CHIBAWARA, Trust; MCKINNEY, Elaine; HALL, Jake; BUSCH, Michael; KEATING, Sheila; LEBEDEVA, Mila; HAMPTON, Dylan; PILCHER, Christopher; FACENTE, Shelley; MARSON, Kara; LAEYENDECKER, Oliver; QUINN, Thomas; BURNS, David; LITTLE, Susan; SANDS, Anita; HALLETT, Tim; OWEN, Sherry Michele; PAREKH, Bharat; SEXTON, Connie; PRICE, Matthew; KAMALI, Anatoli; LOEB, Lisa; MARTIN, Jeffrey; DEEKS, Steven G.; HOH, Rebecca; BARTOLOMEI, Zelinda; CERQUEIRA, Natalia; SANTOS, Breno; ZABTOSKI, Kellin; LIRA, Rita de Cassia Alves; SPERHACKE, Rosa Dea; MOTTA, Leonardo R.; PAGANELLA, Machline; KALLAS, Esper; TOMIYAMA, Helena; TOMIYAMA, Claudia; COSTA, Priscilla; NUNES, Maria A.; REIS, Gisele; SAUER, Mariana M.; NAKAGAWA, Zelinda; FERRARI, Lilian; AMARAL, Ana P.; MILANI, Karine; KARIM, Salim S. Abdool; KARIM, Quarraisha Abdool; NDUNGU, Thumbi; MAJOLA, Nelisile; SAMSUNDER, Natasha; NANICHE, Denise; MANDOMANDO, Inicio; V, Eusebio Macete; SANCHEZ, Jorge; LAMA, Javier; DUERR, Ann; CAPOBIANCHI, Maria R.; SULIGOI, Barbara; STRAMER, Susan; WILLIAMSON, Phillip; VERMEULEN, Marion; SABINO, Ester
    Objective: To determine the precision of new and established methods for estimating duration of HIV infection. Design: A retrospective analysis of HIV testing results from serial samples in commercially available panels, taking advantage of extensive testing previously conducted on 53 seroconverters. Methods: We initially investigated four methods for estimating infection timing: method 1, 'Fiebig stages' based on test results from a single specimen; method 2, an updated '4th gen' method similar to Fiebig stages but using antigen/antibody tests in place of the p24 antigen test; method 3, modeling of 'viral ramp-up' dynamics using quantitative HIV-1 viral load data from antibody-negative specimens; and method 4, using detailed clinical testing history to define a plausible interval and best estimate of infection time. We then investigated a 'two-step method' using data from both methods 3 and 4, allowing for test results to have come from specimens collected on different days. Results: Fiebig and '4th gen' staging method estimates of time since detectable viremia had similar and modest correlation with observed data. Correlation of estimates from both new methods (3 and 4), and from a combination of these two ('two-step method') was markedly improved and variability significantly reduced when compared with Fiebig estimates on the same specimens. Conclusion: The new 'two-step' method more accurately estimates timing of infection and is intended to be generalizable to more situations in clinical medicine, research, and surveillance than previous methods. An online tool is now available that enables researchers/clinicians to input data related to method 4, and generate estimated dates of detectable infection.
  • article 14 Citação(ões) na Scopus
    Performance comparison of the Maxim and Sedia Limiting Antigen Avidity assays for HIV incidence surveillance
    (2019) SEMPA, Joseph B.; WELTE, Alex; BUSCH, Michael P.; HALL, Jake; HAMPTON, Dylan; FACENTE, Shelley N.; KEATING, Sheila M.; MARSON, Kara; PARKIN, Neil; PILCHER, Christopher D.; MURPHY, Gary; GREBE, Eduard; SEMP, Joseph; MATTEN, David; BRAND, Hilmarie; CHIBAWARA, Trust; MCKINNEY, Elaine; FACENTE, Shelley; KEATING, Sheila; LEBEDEVA, Mila; KASSANJEE, Reshma; LAEYENDECKER, Oliver; QUINN, Thomas; BURNS, David; LITTLE, Susan; SANDS, Anita; HALLETT, Tim; OWEN, Sherry Michele; PAREKH, Bharat; SEXTON, Connie; PRICE, Matthew; KAMALI, Anatoli; LOEB, Lisa; MARTIN, Jeffrey; DEEKS, Steven G.; HOH, Rebecca; BARTOLOMEI, Zelinda; CERQUEIRA, Natalia; SANTOS, Breno; ZABTOSKI, Kellin; LIRA, Rita de Cassia Alves; SPERHACKE, Rosa Dea; MOTTA, Leonardo R.; PAGANELLA, Machline; KALLAS, Esper; TOMIYAMA, Helena; TOMIYAMA, Claudia; COSTA, Priscilla; NUNES, Maria A.; REIS, Gisele; SAUER, Mariana M.; NAKAGAWA, Zelinda; FERRARI, Lilian; AMARAL, Ana P.; MILANI, Karine; KARIM, Salim S. Abdool; KARIM, Quarraisha Abdool; NDUNGU, Thumbi; MAJOLA, Nelisile; SAMSUNDER, Natasha; NANICHE, Denise; MANDOMANDO, Inacio; V, Eusebio Macete; SANCHEZ, Jorge; LAMA, Javier; DUERR, Ann; CAPOBIANCHI, Maria R.; SULIGOI, Barbara; STRAMER, Susan; WILLIAMSON, Phillip; VERMEULEN, Marion; SABINO, Ester
    Background Two manufacturers, Maxim Biomedical and Sedia Biosciences Corporation, supply CDC-approved versions of the HIV-1 Limiting Antigen Avidity EIA (LAg) for detecting 'recent' HIV infection in cross-sectional incidence estimation. This study assesses and compares the performance of the two assays for incidence surveillance. Methods We ran both assays on a panel of 2,500 well-characterized HIV-1-infected specimens. We analysed concordance of assay results, assessed reproducibility using repeat testing and estimated mean durations of recent infection (MDRIs) and false-recent rates (FRRs) for a range of normalized optical density (ODn) thresholds, alone and in combination with viral load thresholds. We defined three hypothetical surveillance scenarios, similar to the Kenyan and South African epidemics, and a concentrated epidemic. These scenarios allowed us to evaluate the precision of incidence estimates obtained by means of various recent infection testing algorithms (RITAs) based on each of the two assays. Results The Maxim assay produced lower ODn values than the Sedia assay on average, largely as a result of higher calibrator readings (mean OD of 0.749 vs. 0.643), with correlation of normalized readings lower (R-2 = 0.908 vs. R-2 = 0.938). Reproducibility on blinded control specimens was slightly better for Maxim. The MDRI of a Maxim-based algorithm at the 'standard' threshold (ODn <= 1.5 & VL > 1,000) was 201 days (95% CI: 180,223) and for Sedia 171 (152,191). The difference Differences in MDRI were estimated at 32.7 (22.9,42.8) and 30.9 days (21.7,40.7) for the two algorithms, respectively. Commensurately, the Maxim algorithm had a higher FRR in treatment-naive subjects (1.7% vs. 1.1%). The two assays produced similar precision of incidence estimates in the three surveillance scenarios. Conclusions Differences between the assays can be primarily attributed to the calibrators supplied by the manufacturers. Performance for surveillance was extremely similar, although different thresholds were optimal (i.e. produced the lowest variance of incidence estimates) and at any given ODn threshold, different estimates of MDRI and FRR were obtained. The two assays cannot be treated as interchangeable: assay and algorithm-specific performance characteristic estimates must be used for survey planning and incidence estimation.
  • article 45 Citação(ões) na Scopus
    Predictors of mortality in patients with yellow fever: an observational cohort study
    (2019) KALLAS, Esper G.; ZANELLA, Luiz Gonzaga F. A. B. D'Elia; V, Carlos Henrique Moreira; BUCCHERI, Renata; DINIZ, Gabriela B. F.; CASTINEIRAS, Anna Carla P.; COSTA, Priscilla R.; DIAS, Juliana Z. C.; MARMORATO, Mariana P.; SONG, Alice T. W.; MAESTRI, Alvino; BORGES, Igor C.; JOELSONS, Daniel; CERQUEIRA, Natalia B.; SOUZA, Nathalia C. Santiago e; CLARO, Ingra Morales; SABINO, Ester C.; LEVI, Jose Eduardo; I, Vivian Avelino-Silva; HO, Yeh-Li
    Background Yellow fever virus infection results in death in around 30% of symptomatic individuals. The aim of this study was to identify predictors of death measured at hospital admission in a cohort of patients admitted to hospital during the 2018 outbreak of yellow fever in the outskirts of Sao Paulo city, Brazil. Methods In this observational cohort study, we enrolled patients with yellow fever virus from two hospitals in Sao Paolo-the Hospital das Clinicas, University of Sao Paulo and the Infectious Diseases Institute ""Emilio Ribas"". Patients older than 18 years admitted to hospital with fever or myalgia, headache, arthralgia, oedema, rash, or conjunctivitis were consecutively screened for inclusion in the present study. Consenting patients were included if they had travelled to geographical areas in which yellow fever virus cases had been previously confirmed. Yellow fever infection was confirmed by real-time PCR in blood collected at admission or tissues at autopsy. We sequenced the complete genomes of yellow fever virus from infected individuals and evaluated demographic, clinical, and laboratory findings at admission and investigated whether any of these measurements correlated with patient outcome (death). Findings Between Jan 11, 2018, and May 10, 2018, 118 patients with suspected yellow fever were admitted to Hospital das Clinicas, and 113 patients with suspected yellow fever were admitted to Infectious Diseases Institute ""Emilio Ribas"". 95 patients with suspected yellow fever were included in the study, and 136 patients were excluded. Three (3%) of 95 patients with suspected yellow fever who were included in the study were excluded because they received a different diagnosis, and 16 patients with undetectable yellow fever virus RNA were excluded. Therefore, 76 patients with confirmed yellow fever virus infection, based on detectable yellow fever virus RNA in blood (74 patients) or yellow fever virus confirmed only at the autopsy report (two patients), were included in our analysis. 27 (36%) of 76 patients died during the 60 day period after hospital admission. We generated 14 complete yellow fever virus genomes from the first 15 viral load-detectable samples. The genomes belonged to a single monophyletic clade of the South America I genotype, sub-genotype E. Older age, male sex, higher leukocyte and neutrophil counts, higher alanine aminotransferase, aspartate transaminase (AST), bilirubin, and creatinine, prolonged prothrombin time, and higher yellow fever virus RNA plasma viral load were associated with higher mortality. In a multivariate regression model, older age, elevated neutrophil count, increased AST, and higher viral load remained independently associated with death. All 11 (100%) patients with neutrophil counts of 4000 cells per mL or greater and viral loads of 5.1 log(10) copies/mL or greater died (95% CI 72-100), compared with only three (11%) of 27 (95% CI 2-29) among patients with neutrophil counts of less than 4000 cells per mL and viral loads of less than 5.1 log(10) copies/mL. Interpretation We identified clinical and laboratory predictors of mortality at hospital admission that could aid in the care of patients with yellow fever virus. Identification of these prognostic markers in patients could help clinicians prioritise admission to the intensive care unit, as patients often deteriorate rapidly. Moreover, resource allocation could be improved to prioritise key laboratory examinations that might be more useful in determining whether a patient could have a better outcome. Our findings support the important role of the virus in disease pathogenesis, suggesting that an effective antiviral could alter the clinical course for patients with the most severe forms of yellow fever.
  • conferenceObject
    SYNDECAN-1 AS A BIOMARKER OF SEVERITY IN ACUTE YELLOW FEVER
    (2019) SOUSA, Francielle Tramontini Gomes de; MANULI, Erika R.; ZANELLA, Luiz G.; HO, Yeh-Li; NETTO, Lucas Chaves; MARMORATO, Mariana P.; DIAS, Juliana Z.; THOMAZELLA, Mateus V.; CORREIA, Carolina A.; SILVEIRA, Cassia G.; COSTA, Priscilla R.; PEREIRA, Geovana M.; FERREIRA, Midia S.; ROMANO, Camila M.; KALLAS, Esper G.; HARRIS, Eva; SABINO, Ester C.
  • article 11 Citação(ões) na Scopus
    Frequency of subtype B and F1 dual infection in HIV-1 positive, Brazilian men who have sex with men
    (2012) OLIVEIRA, Ana Carolina Soares de; FARIAS, Rodrigo Pessoa de; COSTA, Antonio Charlys da; SAUER, Mariana Melillo; BASSICHETTO, Katia Cristina; OLIVEIRA, Solange Maria Santos; COSTA, Priscilla Ramos; TOMIYAMA, Claudia; TOMIYAMA, Helena Tomoko Iwashita; SABINO, Ester Cerdeira; KALLAS, Esper Georges; SANABANI, Sabri Saeed
    Background: Because various HIV vaccination studies are in progress, it is important to understand how often inter- and intra-subtype co/superinfection occurs in different HIV-infected high-risk groups. This knowledge would aid in the development of future prevention programs. In this cross-sectional study, we report the frequency of subtype B and F1 co-infection in a clinical group of 41 recently HIV-1 infected men who have sex with men (MSM) in Sao Paulo, Brazil. Methodology: Proviral HIV-1 DNA was isolated from subject's peripheral blood polymorphonuclear leukocytes that were obtained at the time of enrollment. Each subject was known to be infected with a subtype B virus as determined in a previous study. A small fragment of the integrase gene (nucleotide 4255-4478 of HXB2) was amplified by nested polymerase chain reaction (PCR) using subclade F1 specific primers. The PCR results were further confirmed by phylogenetic analysis. Viral load (VL) data were extrapolated from the medical records of each patient. Results: For the 41 samples from MSM who were recently infected with subtype B virus, it was possible to detect subclade F1 proviral DNA in five patients, which represents a co-infection rate of 12.2%. In subjects with dual infection, the median VL was 5.3 x 10(4) copies/ML, whereas in MSM that were infected with only subtype B virus the median VL was 3.8 x 10(4) copies/ML (p > 0.8). Conclusions: This study indicated that subtype B and F1 co-infection occurs frequently within the HIV-positive MSM population as suggested by large number of BF1 recombinant viruses reported in Brazil. This finding will help us track the epidemic and provide support for the development of immunization strategies against the HIV.
  • conferenceObject
    Frequency of subtype B and F1 dual infection in HIV-1 positive, Brazilian men who have sex with men
    (2012) SANABANI, Sabri Saeed; OLIVEIRA, Ana Carolina Soares de; COSTA, Antonio Charlys da; MELILLO, Mariana; SOLANGE, Sauer Katia Cristina Bassichetto; OLIVEIRA, Maria Santos; COSTA, Priscilla Ramos; TOMIYAMA, Claudia; TOMIYAMA, Helena Tomoko Iwashita; CERDEIRA, Ester; ESPER, Sabino; KAL, Georges
  • article 12 Citação(ões) na Scopus
    Immune effects ofLactobacillus caseiShirota in treated HIV-infected patients with poor CD4+T-cell recovery
    (2020) TENORE, Simone de Barros; AVELINO-SILVA, Vivian Iida; COSTA, Priscilla Ramos; FRANCO, Lucas M.; SABINO, Ester Cerdeira; KALIL, Jorge; CERQUEIRA, Natalia Barros; NAKAGAWA, Zelinda; KALLAS, Esper Georges
    Background: HIV infection leads to depletion of intestinal CD4+ T cells, mucosal barrier dysfunction, increased gut permeability and microbial translocation even among patients on suppressive ART. Previous studies suggest probiotics may help restore intestinal function. Methods: In this double-blind, placebo-controlled pilot study, we enrolled HIV-infected patients on suppressive ART with poor CD4+ recovery to address the effect of daily oral use ofLactobacillus caseiShirota (LcS) on CD4+ T-cell count and CD4+/CD8+ ratio at 6 and 12 weeks after treatment initiation; immune activation and intestinal microbiome composition were addressed as secondary outcomes. Results: From January 2015 to July 2016, 48 patients were randomized (1 : 1) to active intervention or placebo. Groups had comparable demographic and clinical characteristics; only CD4+ T-cell nadir was statistically different between groups. All participants were virologically suppressed under ART. At week 6, the increment in CD4+ T-cell count was 17 cells/mu l [interquartile range (IQR) -33 to 74] in the active intervention arm and 4 cells/mu l (IQR -43 to 51) in the placebo arm (P = 0.291); at week 12, the change in CD4+ T-cell count was 8 cells//mu l (IQR -30 to 70) in the active arm and 10 cells//mu l (IQR -50 to 33) among participants allocated to placebo (P = 0.495). Median change in CD4+/CD8+ ratio at week 6 compared with baseline was 0 (IQR -0.04 to 0.05) in the active intervention arm and -0.01 in the placebo arm (IQR -0.06 to 0.03;P = 0.671). At week 12, the change in CD4+/CD8+ ratio was higher in the active product group compared with placebo (respectively 0.07 and 0.01), but this difference failed to reach statistical significance (P = 0.171). We found no significant effects of LcS on immune activation markers, CD4+ and CD8+ subpopulations, sCD14 levels or NK cells at week 12. Finally, we found no statistically significant differences between groups in the change of enteric microbiome at week 12. Conclusion: In this pilot study, we found no statistically significant effect of LcS probiotic on CD4+ T-cell counts, CD4+/CD8+ ratio, immune activation or intestinal microbiome among HIV-infected patients on suppressive ART with poor CD4+ recovery.