Dr. Antonio Condino-Neto

@article{pmid34022333,

title = {A simplified alternative diagnostic algorithm for SARS-CoV-2 suspected symptomatic patients and confirmed close contacts (asymptomatic): A consensus of Latin American experts},

author = {Fabian F Fay and Carlos Arturo Alvarez-Moreno and Pablo E Bonvehi and Carolina Cucho Espinoza and Marco Luis Herrera Hidalgo and Marcel Marcano-Lozada and Carlos M Perez and Alvaro Pulchinelli and Klever Vinicio Sáenz-Flor and Antonio Condino-Neto},

doi = {10.1016/j.ijid.2021.05.011},

issn = {1878-3511},

year  = {2022},

date = {2022-04-01},

urldate = {2022-04-01},

journal = {Int J Infect Dis},

volume = {117},

pages = {130--136},

abstract = {INTRODUCTION: Latin America accounts for one-quarter of global COVID-19 cases and one-third of deaths. Inequalities in the region lead to barriers to the best use of diagnostic tests during the pandemic. There is a need for simplified guidelines that consider the region's limited health resources, international guidelines, medical literature, and local expertise.nnMETHODS: Using a modified Delphi method, 9 experts from Latin American countries developed a simplified algorithm for COVID-19 diagnosis on the basis of their answers to 24 questions related to diagnostic settings, and discussion of the literature and their experiences.nnRESULTS: The algorithm considers 3 timeframes (≤7 days, 8-13 days, and ≥14 days) and presents diagnostic options for each. SARS-CoV-2 real- time reverse transcription-polymerase chain reaction is the test of choice from day 1 to 14 after symptom onset or close contact, although antigen testing may be used in specific circumstances, from day 5 to 7. Antibody assays may be used for confirmation, usually after day 14; however, if clinical suspicion is very high, but other tests are negative, these assays may be used as an adjunct to decision-making from day 8 to 13.nnCONCLUSION: The proposed algorithm aims to support COVID-19 diagnosis decision-making in Latin America.},

keywords = {COVID-19},

pubstate = {published},

tppubtype = {article}

}

@article{pmid34982304,

title = {CD40 Ligand Deficiency in Latin America: Clinical, Immunological, and Genetic Characteristics},

author = {Tábata Takahashi França and Lucila Akune Barreiros and Ranieri Coelho Salgado and Sarah Maria da Silva Napoleão and Lillian Nunes Gomes and Janáira Fernandes Severo Ferreira and Carolina Prando and Cristina Worm Weber and Regina Sumiko Watanabe Di Gesu and Cecilia Montenegro and Carolina Sanchez Aranda and Gisele Kuntze and Aidé Tamara Staines-Boone and Edna Venegas-Montoya and Juan Carlos Aldave Becerra and Liliana Bezrodnik and Daniela Di Giovanni and Ileana Moreira and Gisela Analia Seminario and Andrea Cecilia Gómez Raccio and Mayra de Barros Dorna and Nelson Augusto Rosário-Filho and Herberto Jose Chong-Neto and Elisa de Carvalho and Milena Baptistella Grotta and Julio Cesar Orellana and Miguel Garcia Dominguez and Oscar Porras and Laura Sasia and Karina Salvucci and Emilio Garip and Luiz Fernando Bacarini Leite and Wilma Carvalho Neves Forte and Fernanda Pinto-Mariz and Ekaterini Goudouris and María Enriqueta Nuñez Nuñez and Magdalena Schelotto and Laura Berrón Ruiz and Diana Inés Liberatore and Hans D Ochs and Otavio Cabral-Marques and Antonio Condino-Neto},

doi = {10.1007/s10875-021-01182-5},

issn = {1573-2592},

year  = {2022},

date = {2022-04-01},

urldate = {2022-04-01},

journal = {J Clin Immunol},

volume = {42},

number = {3},

pages = {514--526},

abstract = {CD40 ligand (CD40L) deficiency is a rare inborn error of immunity presenting with heterogeneous clinical manifestations. While a detailed characterization of patients affected by CD40L deficiency is essential to an accurate diagnosis and management, information about this disorder in Latin American patients is limited. We retrospectively analyzed data from 50 patients collected by the Latin American Society for Immunodeficiencies registry or provided by affiliated physicians to characterize the clinical, laboratory, and molecular features of Latin American patients with CD40L deficiency. The median age at disease onset and diagnosis was 7 months and 17 months, respectively, with a median diagnosis delay of 1 year. Forty-seven patients were genetically characterized revealing 6 novel mutations in the CD40LG gene. Pneumonia was the most common first symptom reported (66%). Initial immunoglobulin levels were variable among patients. Pneumonia (86%), upper respiratory tract infections (70%), neutropenia (70%), and gastrointestinal manifestations (60%) were the most prevalent clinical symptoms throughout life. Thirty-five infectious agents were reported, five of which were not previously described in CD40L deficient patients, representing the largest number of pathogens reported to date in a cohort of CD40L deficient patients. The characterization of the largest cohort of Latin American patients with CD40L deficiency adds novel insights to the recognition of this disorder, helping to fulfill unmet needs and gaps in the diagnosis and management of patients with CD40L deficiency.},

keywords = {imunidade},

pubstate = {published},

tppubtype = {article}

}

@article{pmid35063670b,

title = {Health-related quality of life in primary immunodeficiencies: Impact of delayed diagnosis and treatment burden},

author = {John T Anderson and Juthaporn Cowan and Antonio Condino-Neto and Donald Levy and Subhransu Prusty},

doi = {10.1016/j.clim.2022.108931},

issn = {1521-7035},

year  = {2022},

date = {2022-03-01},

journal = {Clin Immunol},

volume = {236},

pages = {108931},

abstract = {Accurate and timely diagnosis of primary immunodeficiencies (PID) is an ongoing effort. Individuals with PID can be severely impacted by their disease and many experience chronic complications, treatment burden, and reduced quality of life (QoL). This review focuses on the impact of delayed diagnosis and treatment burden on patient QoL and outcomes. Adults tend to experience longer delays in diagnosis than pediatric populations. The median diagnostic delay has reduced over recent decades, but remains high for some antibody deficiency variants, such as common variable immunodeficiency. The largest burden impacting QoL tends to be poorly controlled disease and persistent chronic conditions rather than treatment burden. Hospitalization, physician/emergency room visits, and bronchiectasis were the most expensive PID complications prior to diagnosis and cost analyses estimate cost reductions once appropriate treatment is initiated. A combination of poor awareness, lack of infrastructure, and resources supporting national registries play a major role in delayed diagnosis.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{pmid35269470b,

title = {Severe COVID-19 Shares a Common Neutrophil Activation Signature with Other Acute Inflammatory States},

author = {Lena F Schimke and Alexandre H C Marques and Gabriela Crispim Baiocchi and Caroline Aliane de Souza Prado and Dennyson Leandro M Fonseca and Paula Paccielli Freire and Desirée Rodrigues Plaça and Igor Salerno Filgueiras and Ranieri Coelho Salgado and Gabriel Jansen-Marques and Antonio Edson Rocha Oliveira and Jean Pierre Schatzmann Peron and Gustavo Cabral-Miranda and José Alexandre Marzagão Barbuto and Niels Olsen Saraiva Camara and Vera Lúcia Garcia Calich and Hans D Ochs and Antonio Condino-Neto and Katherine A Overmyer and Joshua J Coon and Joseph Balnis and Ariel Jaitovich and Jonas Schulte-Schrepping and Thomas Ulas and Joachim L Schultze and Helder I Nakaya and Igor Jurisica and Otávio Cabral-Marques},

doi = {10.3390/cells11050847},

issn = {2073-4409},

year  = {2022},

date = {2022-03-01},

journal = {Cells},

volume = {11},

number = {5},

abstract = {Severe COVID-19 patients present a clinical and laboratory overlap with other hyperinflammatory conditions such as hemophagocytic lymphohistiocytosis (HLH). However, the underlying mechanisms of these conditions remain to be explored. Here, we investigated the transcriptome of 1596 individuals, including patients with COVID-19 in comparison to healthy controls, other acute inflammatory states (HLH, multisystem inflammatory syndrome in children [MIS-C], Kawasaki disease [KD]), and different respiratory infections (seasonal coronavirus, influenza, bacterial pneumonia). We observed that COVID-19 and HLH share immunological pathways (cytokine/chemokine signaling and neutrophil-mediated immune responses), including gene signatures that stratify COVID-19 patients admitted to the intensive care unit (ICU) and COVID-19_nonICU patients. Of note, among the common differentially expressed genes (DEG), there is a cluster of neutrophil-associated genes that reflects a generalized hyperinflammatory state since it is also dysregulated in patients with KD and bacterial pneumonia. These genes are dysregulated at the protein level across several COVID-19 studies and form an interconnected network with differentially expressed plasma proteins that point to neutrophil hyperactivation in COVID-19 patients admitted to the intensive care unit. scRNAseq analysis indicated that these genes are specifically upregulated across different leukocyte populations, including lymphocyte subsets and immature neutrophils. Artificial intelligence modeling confirmed the strong association of these genes with COVID-19 severity. Thus, our work indicates putative therapeutic pathways for intervention.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{pmid35063670,

title = {Health-related quality of life in primary immunodeficiencies: Impact of delayed diagnosis and treatment burden},

author = {John T Anderson and Juthaporn Cowan and Antonio Condino-Neto and Donald Levy and Subhransu Prusty},

doi = {10.1016/j.clim.2022.108931},

issn = {1521-7035},

year  = {2022},

date = {2022-03-01},

urldate = {2022-03-01},

journal = {Clin Immunol},

volume = {236},

pages = {108931},

abstract = {Accurate and timely diagnosis of primary immunodeficiencies (PID) is an ongoing effort. Individuals with PID can be severely impacted by their disease and many experience chronic complications, treatment burden, and reduced quality of life (QoL). This review focuses on the impact of delayed diagnosis and treatment burden on patient QoL and outcomes. Adults tend to experience longer delays in diagnosis than pediatric populations. The median diagnostic delay has reduced over recent decades, but remains high for some antibody deficiency variants, such as common variable immunodeficiency. The largest burden impacting QoL tends to be poorly controlled disease and persistent chronic conditions rather than treatment burden. Hospitalization, physician/emergency room visits, and bronchiectasis were the most expensive PID complications prior to diagnosis and cost analyses estimate cost reductions once appropriate treatment is initiated. A combination of poor awareness, lack of infrastructure, and resources supporting national registries play a major role in delayed diagnosis.},

keywords = {imunidade},

pubstate = {published},

tppubtype = {article}

}

@article{pmid35269470,

title = {Severe COVID-19 Shares a Common Neutrophil Activation Signature with Other Acute Inflammatory States},

author = {Lena F Schimke and Alexandre H C Marques and Gabriela Crispim Baiocchi and Caroline Aliane de Souza Prado and Dennyson Leandro M Fonseca and Paula Paccielli Freire and Desirée Rodrigues Plaça and Igor Salerno Filgueiras and Ranieri Coelho Salgado and Gabriel Jansen-Marques and Antonio Edson Rocha Oliveira and Jean Pierre Schatzmann Peron and Gustavo Cabral-Miranda and José Alexandre Marzagão Barbuto and Niels Olsen Saraiva Camara and Vera Lúcia Garcia Calich and Hans D Ochs and Antonio Condino-Neto and Katherine A Overmyer and Joshua J Coon and Joseph Balnis and Ariel Jaitovich and Jonas Schulte-Schrepping and Thomas Ulas and Joachim L Schultze and Helder I Nakaya and Igor Jurisica and Otávio Cabral-Marques},

doi = {10.3390/cells11050847},

issn = {2073-4409},

year  = {2022},

date = {2022-03-01},

urldate = {2022-03-01},

journal = {Cells},

volume = {11},

number = {5},

abstract = {Severe COVID-19 patients present a clinical and laboratory overlap with other hyperinflammatory conditions such as hemophagocytic lymphohistiocytosis (HLH). However, the underlying mechanisms of these conditions remain to be explored. Here, we investigated the transcriptome of 1596 individuals, including patients with COVID-19 in comparison to healthy controls, other acute inflammatory states (HLH, multisystem inflammatory syndrome in children [MIS-C], Kawasaki disease [KD]), and different respiratory infections (seasonal coronavirus, influenza, bacterial pneumonia). We observed that COVID-19 and HLH share immunological pathways (cytokine/chemokine signaling and neutrophil-mediated immune responses), including gene signatures that stratify COVID-19 patients admitted to the intensive care unit (ICU) and COVID-19_nonICU patients. Of note, among the common differentially expressed genes (DEG), there is a cluster of neutrophil-associated genes that reflects a generalized hyperinflammatory state since it is also dysregulated in patients with KD and bacterial pneumonia. These genes are dysregulated at the protein level across several COVID-19 studies and form an interconnected network with differentially expressed plasma proteins that point to neutrophil hyperactivation in COVID-19 patients admitted to the intensive care unit. scRNAseq analysis indicated that these genes are specifically upregulated across different leukocyte populations, including lymphocyte subsets and immature neutrophils. Artificial intelligence modeling confirmed the strong association of these genes with COVID-19 severity. Thus, our work indicates putative therapeutic pathways for intervention.},

keywords = {COVID-19},

pubstate = {published},

tppubtype = {article}

}

@article{pmid35205902,

title = {The Dermatophyte  Induces Neutrophil Extracellular Traps Release by Human Neutrophils},

author = {Ana Paula Carvalho Reis and Giovanna Azevedo Celestrino and Mariana Villas Bôas Igoa and Thais Martins Jesus and Tábata Takahashi França and Daniel Valério Silva Moreira and Paula Ordonhez Rigato and Paula Keiko Sato and Antonio Condino-Neto and Irene L Noronha and Luciane Alarcão Dias-Melicio and Pritesh Jaychand Lalwani and Gil Benard and Maria Gloria Teixeira Sousa},

doi = {10.3390/jof8020147},

issn = {2309-608X},

year  = {2022},

date = {2022-01-01},

journal = {J Fungi (Basel)},

volume = {8},

number = {2},

abstract = {Neutrophils are the first leukocytes recruited to the site of infection and are thought to be responsible for fungal elimination from the skin such as dermatophytes. Neutrophils are able to secrete reactive oxygen species (ROS) and neutrophil extracellular traps (NETs) that can kill different fungi, including , spp., , and . However, NET production in response to , the main etiologic agent of dermatophytosis, has yet to be studied. We demonstrated that human neutrophils produce NETs against different morphotypes of  in a dose-dependent manner and NET formation is dependent on ROS production. In addition, ROS production by human neutrophils in response to  is dependent on NADPH oxidase, but not on fungal viability. NETs mediated killing of  Collectively, these results demonstrate that  was able to trigger the production of NETs, suggesting that these extracellular structures may represent an important innate immune effector mechanism controlling physiological response to  infection.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}