Spatiotemporal transmission of SARS-CoV-2 lineages during 2020-2021 in Pernambuco-Brazil.

SARS-CoV-2 virus emerged as a new threat to humans and spread around the world, leaving a large death toll. As of January 2023, Brazil is among the countries with the highest number of registered deaths. Nonpharmacological and pharmacological interventions have been heterogeneously implemented in the country, which, associated with large socioeconomic differences between the country regions, has led to distinct virus spread dynamics. Here, we investigate the spatiotemporal dispersion of SARS-CoV-2 lineages in the Pernambuco state (Northeast Brazil) throughout the distinct epidemiological scenarios that unfolded in the first 2 years of the pandemic. We generated a total of 1,389 new SARS-CoV-2 genomes from June 2020 to August 2021. This sampling captured the arrival, communitary transmission, and the circulation of the B1.1, B.1.1.28, and B.1.1.33 lineages; the emergence of the former variant of interest P.2; and the emergence and fast replacement of all previous variants by the more transmissible variant of concern P.1 (Gamma). Based on the incidence and lineage spread pattern, we observed an East-to-West to inner state pattern of transmission, which is in agreement with the transmission of more populous metropolitan areas to medium- and small-size country-side cities in the state. Such transmission patterns may be partially explained by the main routes of traffic across municipalities in the state. Our results highlight that the fine-grained intrastate analysis of lineages and incidence spread can provide actionable insights for planning future nonpharmacological intervention for air-borne transmissible human pathogens.IMPORTANCEDuring the COVID-19 pandemic, Brazil was one of the most affected countries, mainly due its continental-size, socioeconomic differences among regions, and heterogeneous implementation of intervention methods. In order to investigate SARS-CoV-2 dynamics in the state of Pernambuco, we conducted a spatiotemporal dispersion study, covering the period from June 2020 to August 2021, to comprehend the dynamics of viral transmission during the first 2 years of the pandemic. Throughout this study, we were able to track three significant epidemiological waves of transmission caused by B1.1, B.1.1.28, B.1.1.33, P.2, and P.1 lineages. These analyses provided valuable insights into the evolution of the epidemiological landscape, contributing to a deeper understanding of the dynamics of virus transmission during the early years of the pandemic in the state of Pernambuco.

Real-life evaluation of a rapid antigen test (DPP SARS-CoV-2 Antigen) for COVID-19 diagnosis of primary healthcare patients, in the context of the Omicron-dominant wave in Brazil.

OBJECTIVES: We aimed to investigate the real-life performance of the rapid antigen test in the context of a primary healthcare setting, including symptomatic and asymptomatic individuals that sought diagnosis during an Omicron infection wave. METHODS: We prospectively accessed the performance of the DPP SARS-CoV-2 Antigen test in the context of an Omicron-dominant real-life setting. We evaluated 347 unselected individuals (all-comers) from a public testing centre in Brazil, performing the rapid antigen test diagnosis at point-of-care with fresh samples. The combinatory result from two distinct real-time quantitative PCR (RT-qPCR) methods was employed as a reference and 13 samples with discordant PCR results were excluded. RESULTS: The assessment of the rapid test in 67 PCR-positive and 265 negative samples revealed an overall sensitivity of 80.5% (CI 95% = 69.1%-89.2%), specificity of 99.2% (CI 95% = 97.3%-99.1%) and positive/negative predictive values higher than 95%. However, we observed that the sensitivity was dependent on the viral load (sensitivity in Ct < 31 = 93.7%, CI = 82.8%-98.7%; Ct > 31 = 47.4%, CI = 24.4%-71.1%). The positive samples evaluated in the study were Omicron (BA.1/BA.1.1) by whole-genome sequencing (n = 40) and multiplex RT-qPCR (n = 17). CONCLUSIONS: Altogether, the data obtained from a real-life prospective cohort supports that the rapid antigen test sensitivity for Omicron remains high and underscores the reliability of the test for COVID-19 diagnosis in settings with high disease prevalence and limited PCR testing capability.

Evaluation of Polymorphisms in IL8 and IL16 Genes in Patients with Acute Coronary Syndrome

Abstract Background: Acute coronary syndrome (ACS) is a cardiovascular disease caused by obstruction of coronary arteries by atheromatous plaque. Susceptibility to this disease may be related to genetic variations, such as single nucleotide polymorphisms (SNPs). Objective: In this study, we evaluated the relationship between SNPs in IL8 (rs4073; -251 A/T) and IL16 (rs11556218; T/G) genes and SCA in a Brazilian population. Materials and Methods: A sample of 200 patients with ACS and 50 non-ACS patients hospitalized at the Real Hospital Português, Recife - PE, Brazil, and 220 blood donors (donors) was used. Genotyping was carried out by polymerase chain reaction, and DNA sequencing. Statistical analyzes were performed using the Williams G, Chi-square and Kruskal Wallis tests, using the BioEstat 5.0 program, and the data with a value of p < 0.05 were considered significant. Results: In the IL8 gene, the AT genotype was the most frequent (p > 0.05) in all three groups. In the IL16 gene, genotypic distributions were different between patients with ACS and the donor group (p = 0.002), with the most frequent G allele in the second group (p = 0.0052). The IL-16 cytokine was higher in donors than in patients with ACS (p = 0.04) and the G (TG + GG) allele had higher values of this cytokine (p = 0.01). Conclusions: The results demonstrate the important role of the rs11556218 SNP in IL16 gene in SCA, evidencing that the G allele may be associated with a decreased risk of the disease.

Acute coronary syndrome: Relationship between genetic variants and TIMI risk.

Acute Coronary Syndrome (ACS) is a multifactorial disease, including the genetic factor, caused by coronary artery obstruction by atheroma. Some genetic variants have been described as risk factors for this disease. Its early diagnosis and stratification of risk of death by Thrombolysis in Myocardial Infarction (TIMI) are important. Therefore, we evaluated variants in the IL6R (c950-1722C>T), TNFa (c.-488G>A), LEPR (c.2673+1118C>T) and IL1b (c.-598T>C) genes in relation to TIMI risk, cytokine serum levels, and risk factors for ACS. We selected 200 patients with ACS, 50 without ACS from the Real Hospital Português, Recife - PE, and 295 blood donors at the Fundação de Hematologia e Hemoterapia de Pernambuco (Hemope). Variants were determined by DNA sequencing or enzymatic cleavage. Cytokine levels were measured by ELISA. The most frequent risk factors found in the patients were dyslipidemia and hypertension, this latter associated with high TIMI risk (p = 0.003). Genotype frequencies of IL6R and TNFa differed between patients with ACS and the blood donors (p = 0.0002 and p = 0.01, respectively), and TNF-α levels differed between genotypes. The TT genotype of the IL6R gene is as a possible protective factor for ACS because it was significantly more present in blood donors (32.2%) than in patients with ACS (18.0%), and was more frequent in low TIMI risk (22.9%) than in the intermediate (20.2%) or high (4.9%). In patients with ACS, the TT genotype in IL6R was related to a lower concentration of c-reactive protein (p = 0.03) and troponin (p = 0.02), showing a less inflammatory reaction and tissue damage. The differences in the frequencies of variants in genes of medical interest among the groups show the importance of studies in specific populations groups to establish the relationship between genes and diseases.

Avaliação do Polimorfismo -174 G/C do gene IL-6 na Síndrome Coronariana Aguda no Nordeste do Brasil / Evaluation of IL-6 (-174 G/C) Polymorphism in Acute Coronary Syndrome in the Northeast of Brazil

Fundamento: A síndrome coronariana aguda (SCA) é a principal causa de morbidade e mortalidade no mundo. É uma doença multifatorial causada por obstrução das artérias coronárias por placa ateromatosa que leva à isquemia cardíaca. Diversos estudos sugerem que alguns polimorfismos genéticos alteram os níveis de citocinas e influenciam o desenvolvimento de SCA. Objetivo: Neste estudo, avaliamos o polimorfismo - 174 G/C do gene IL-6 , níveis séricos de citocina e sua relação com SCA e escore de risco de thrombolysis in myocardial infarction (TIMI). Materiais e métodos: Foram selecionados 200 pacientes com SCA [risco de TIMI ­ Baixo (70), Intermediário (89), Alto (41)] na população brasileira. A genotipagem foi feita pela reação em cadeia da polimerase (PCR), seguida de sequenciamento de DNA. Resultados: Não houve diferenças significativas na distribuição dos genótipos (p = 0,53) e dos alelos (p = 0,32) entre grupos de pacientes com SCA e sem SCA no polimorfismo alélico do IL-6 , nem entre os três escores de risco TIMI (p > 0,05). Além disso, o polimorfismo do IL-6 não afetou os níveis de citocina, os quais não estavam relacionados ao escore de TIMI. Conclusões: Com esses resultados, sugerimos que o polimorfismo ­ 174 G/C do gene IL-6, até agora, não está relacionado à SCA e não alterou os níveis de citocina na população estudada. Novos estudos em populações diferentes devem ser feitos para verificar esses resultados. É importante enfatizar que, como a SCA é uma doença multifatorial, outros fatores de risco e outras citocinas pró-inflamatórias devem ser avaliadas para o conhecimento dessa patologia

Background: Acute coronary syndrome (ACS) is a leading cause of morbidity and mortality worldwide. It is a multifactorial disease caused by obstruction of the coronary arteries by atheromatous plaques and leads to heart ischemia. Several studies suggest that some genetic polymorphisms change the cytokines levels and influence ACS development. Objective: In this study, we evaluated the IL-6 polymorphism -174 G/C, serum levels of cytokine and its relationship with ACS and the thrombolysis in myocardial infarction (TIMI) risk score. Materials and Methods: A sample of 200 patients with ACS [TIMI risk ­ Low (70); Intermediate (89); High (41)] in Brazilian population was used. Genotyping was carried out by polymerase chain reaction, followed by DNA sequencing. Results: There was no significant differences in genotype (p = 0.53) and allele (p = 0.32) distributions between ACS patient and without ACS patients groups on IL-6 allelic polymorphism and between the three different TIMI risk score (p > 0.05). Moreover IL-6 polymorphism did not affect the cytokine levels and these levels were not related to the TIMI score. Conclusions: With these results, we suggest that the IL-6 (-174 G/C) polymorphism, until now, is not related to ACS and did not change the levels of the cytokine in studied population. Further studies with different populations should be done to verify those results. It is important to emphasize that, since ACS is a multifactorial disease, other risk factors and other pro-inflammatory cytokines should be assessed to better understand this pathology