The dynamics of dengue virus (DENV) circulation depends on serotype, genotype and lineage replacement and turnover. In São José do Rio Preto, Brazil, we observed that the L6 lineage of DENV-1 (genotype V) remained the dominant circulating lineage even after the introduction of the L1 lineage. We investigated viral fitness and immunogenicity of the L1 and L6 lineages and which factors interfered with the dynamics of DENV epidemics. The results showed a more efficient replicative fitness of L1 over L6 in mosquitoes and in human and non-human primate cell lines. Infections by the L6 lineage were associated with reduced antigenicity, weak B and T cell stimulation and weak host immune system interactions, which were associated with higher viremia. Our data, therefore, demonstrate that reduced viral immunogenicity and consequent greater viremia determined the increased epidemiological fitness of DENV-1 L6 lineage in São José do Rio Preto. Since 2008 L6 is the endemic lineage that has circulated in SJRP. In 2010, the L1 lineage was first identified in the city. For a period, both lineages co-circulated, and then in 2013, L1 began to diminish until it was no longer detected in the population. Differences in replicative fitness are usually the main factor for clade replacement (CR) in DENV epidemics. However, despite the better viral fitness of the emerging lineage, the absence of CR could not be explained by these differences alone. Here, we combine epidemiological, phylogenetic, molecular and immunological analyses to provide a more precise understanding of the role of fitness in lineage dynamics with the persistence of L6 even after the introduction of L1 without CR. Differences in immune responses elicited by DENV-1 L1 and L6 lineages (genotype V), but not viral fitness in mosquito or human cells, explain the dynamics of circulating DENV in a city of Brazil.

Human bocavirus (HBoV) is commonly associated with acute respiratory tract illness and gastroenteritis. We report six complete genomic sequences of HBoV strains from patients with gastroenteritis in Belém do Pará and Tocantins in the North Region of Brazil. Phylogenetic analysis indicated that the six HBoV strains belong to genotypes 1, 2, and 3.

On 11 March 2020, the World Health Organization (WHO) declared a pandemic caused by SARS-CoV-2, raising global health concerns. Reports of persistent and new symptoms following the acute phase of infection highlighted the complexities of recovery and prompted the investigation of what is now termed long COVID. Officially recognized by the WHO in October 2021, long COVID presents various health implications, though the terminology—such as post-COVID syndrome and post-acute sequelae of COVID-19 (PASC)—remains inconsistent, complicating diagnostic standardization. Long COVID affects an estimated 10% to 30% of SARS-CoV-2-infected individuals, with common symptoms including fatigue, dyspnea, cognitive dysfunction, and joint pain, all of which significantly impair quality of life. Public perception is influenced by factors like education and health history, while misinformation and stigma hinder accurate diagnosis and treatment. The absence of biomarkers and overlap with other post-viral syndromes further complicate clinical recognition. Experts emphasize the need for refined diagnostic criteria and integrated strategies combining biomedical research, public policy, and educational initiatives to improve clinical management, address healthcare inequalities, and mitigate the impacts of long COVID. This review unveils the state of the art and knowledge gaps to encourage discussion, with the aim of achieving better clinical decision-making and public awareness related to long COVID.