A previous study demonstrates that most of severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) Brazilian strains fell in three local clades that were introduced from Europe around late February 2020. Here we investigated in more detail the origin of the major and most widely disseminated SARS-CoV-2 Brazilian lineage B.1.1.33. We recovered 190 whole viral genomes collected from 13 Brazilian states from February 29 to April 31, 2020 and combined them with other B.1.1 genomes collected globally. Our genomic survey confirms that lineage B.1.1.33 is responsible for a variable fraction of the community viral transmissions in Brazilian states, ranging from 2% of all SARS-CoV-2 genomes from Pernambuco to 80% of those from Rio de Janeiro. We detected a moderate prevalence (5–18%) of lineage B.1.1.33 in some South American countries and a very low prevalence (<1%) in North America, Europe, and Oceania. Our study reveals that lineage B.1.1.33 evolved from an ancestral clade, here designated B.1.1.33-like, that carries one of the two B.1.1.33 synapomorphic mutations. The B.1.1.33-like lineage may have been introduced from Europe or arose in Brazil in early February 2020 and a few weeks later gave origin to the lineage B.1.1.33. These SARS-CoV-2 lineages probably circulated during February 2020 and reached all Brazilian regions and multiple countries around the world by mid-March, before the implementation of air travel restrictions in Brazil. Our phylodynamic analysis also indicates that public health interventions were partially effective to control the expansion of lineage B.1.1.33 in Rio de Janeiro because its median effective reproductive number (Re) was drastically reduced by about 66% during March 2020, but failed to bring it to below one. Continuous genomic surveillance of lineage B.1.1.33 might provide valuable information about epidemic dynamics and the effectiveness of public health interventions in some Brazilian states.

BackgroundThe virulence and pathogenicity of different influenza strains are responsible for a more or less severe disease. Recent studies have attempted to understand how host genetic factors may influence the clinical presentation of the disease. In the present study, the His131Arg (rs1801274) polymorphism was investigated in individuals from a Brazilian admixed population with a diagnosis of influenza A(H1N1)pdm09 infection.MethodsIn the present study, the influence of the His131Arg (rs1801274) polymorphism, a variant of the FCGR2A gene, was investigated in 436 patients with a diagnosis of influenza A(H1N1)pdm09, evaluated at health services in the northern and northeastern regions of Brazil between June 2009 and August 2010. Patients were divided into a group of non-hospitalized patients (n = 192) and a group of hospitalized patients (n = 244; 100 of them died).ResultsNo significant difference in the allele or genotype frequencies of the rs1801274 polymorphism was observed between groups (p = 0.952 and p = 0.388). Multinomial logistic regression showed no effect of the rs1801274 polymorphism on severity or death of patients from the Brazilian admixed population (p = 0.368 and p = 0.469).ConclusionsThe rs1801274 polymorphism is not associated with severe disease in patients infected with influenza A(H1N1)pdm09.

The influenza A virus (IAV) is of a major public health concern as it causes annual epidemics and has the potential to cause pandemics. At present, the neuraminidase inhibitors (NAIs) are the most widely used anti-influenza drugs, but, more recently, the drug baloxavir marboxil (BXM), a polymerase inhibitor, has also been licensed in some countries. Mutations in the viral genes that encode the antiviral targets can lead to treatment resistance. Worldwide, a low prevalence of antiviral resistant strains has been reported. Despite that, this situation can change rapidly, and resistant strain surveillance is a priority. Thus, the aim of this was to evaluate Brazilian IAVs antiviral resistance from 2017 to 2019 through the identification of viral mutations associated with reduced inhibition of the drugs and by testing the susceptibility of IAV isolates to oseltamivir (OST), the most widely used NAI drug in the country. Initially, we analyzed 282 influenza A(H1N1)pdm09 and 455 A(H3N2) genetic sequences available on GISAID. The amino acid substitution (AAS) NA:S247N was detected in one A(H1N1)pdm09 strain. We also identified NA:I222V (n = 6) and NA:N329K (n = 1) in A(H3N2) strains. In addition, we performed a molecular screening for NA:H275Y in 437 A(H1N1)pdm09 samples, by pyrosequencing, which revealed a single virus harboring this mutation. Furthermore, the determination of OST IC50 values for 222 A(H1N1)pdm09 and 83 A(H3N2) isolates revealed that all isolates presented a normal susceptibility profile to the drug. Interestingly, we detected one A(H3N2) virus presenting with PA:E119D AAS. Moreover, the majority of the IAV sequences had the M2:S31N adamantanes resistant marker. In conclusion, we show a low prevalence of Brazilian IAV strains with NAI resistance markers, in accordance with what is reported worldwide, indicating that NAIs still remain an option for the treatment of influenza infections in Brazil. However, surveillance of influenza resistance should be strengthened in the country for improving the representativeness of investigated viruses and the robustness of the analysis.

Detecção e caracterização de adenovírus humano proveniente de casos de paralisia flácida aguda, na Região Norte do Brasil Detección y caracterización de adenovirus humano proveniente de casos de parálisis fláccida aguda, en la Región Norte de Brasil Detection and characterization of human adenoviruses from cases of acute flaccid paralysis in

Introdução: A recente pandemia de gripe de 2009 e 2010 causada pelo vírus Influenza A (H1N1) pandêmico (pdm) mostrou um perfil de gravidade diferente da gripe sazonal, pois um percentual considerável de casos graves e fatais ocorreu em indivíduos adultos jovens, sem comorbidade. A virulência do vírus H1N1 pdm resulta de interações proteicas complexas e depende essencialmente de alguns genes virais. Objetivos: O objetivo deste estudo foi caracterizar os genes codificadores da hemaglutinina subtipo 1 (H1) e polimerase básica 2 (PB2) do vírus H1N1 pdm mediante a obtenção de cepas provenientes de pacientes com gripe procedente da mesorregião metropolitana de Belém, Estado do Pará, Brasil. Materiais e Métodos: O tamanho amostral foi constituído de 87 amostras aleatórias de pessoas de ambos os sexos, com idade de 0 a 96 anos, com síndrome respiratória aguda grave, sem nenhuma comorbidade relatada, no período de maio de 2009 a agosto de 2010. As amostras foram isoladas em cultura de célula MDCK e analisadas por técnicas de biologia molecular que compreenderam três etapas principais: a) extração do RNA viral (RNAv), a partir do sobrenadante celular; b) amplificação do RNAv pela técnica de reação em cadeia mediada pela polimerase precedida de transcrição reversa (RT-PCR); c) sequenciamento completo dos genes codificadores da H1 e PB2. O presente estudo foi apreciado pelo Comitê de Ética em Pesquisa do Instituto Evandro Chagas, nº 0027/2008, aprovado em 24 de novembro de 2011. Resultados: Das 87 cepas amplificadas pelo RT-PCR, em 82 tornou-se possível a obtenção e análise de sequências para o gene H1, enquanto que de 81 amostras virais foram obtidas sequências para o gene PB2. A análise comparativa das sequências adquiridas com a sequência da cepa vacinal (A/California/07/2009(H1N1)) revelou substituições aminoacídicas na H1 (P83S; D97N; S203T; D222G; Q293H e I321V) e na PB2 (K340N; K526R e M631L), no entanto sem associação à hospitalização. Na substituição da H1, a D97N isolada ou associada à S203T, foi detectada com mais frequência na primeira onda. Em relação ao nível da PB2, a substituição K526R também foi