Paola Cristina Resende

Bats are major natural reservoirs for coronaviruses, yet complete viral genomes from South America remain scarce, limiting evolutionary and taxonomic understanding. Here, we conducted metatranscriptomic sequencing of coronavirus-positive bat samples collected across two ecologically distinct Brazilian biomes: the Atlantic Forest and the semi-arid Caatinga. We recovered seven complete or near-complete genomes belonging to Alphacoronavirus and Betacoronavirus . Phylogenetic and comparative similarity analyses of conserved replicase domains (3CLpro, NiRAN, RdRp, ZBD, HEL1), following International Committee on Taxonomy of Viruses (ICTV) demarcation criteria, revealed significant viral diversity. Within Alphacoronavirus , two genomes from Atlantic Forest phyllostomid bats ( Artibeus lituratus and Carollia perspicillata ) formed a deeply divergent sister lineage to Amalacovirus , exhibiting a mean amino acid similarity of 76.7% with the reference genome. Within Betacoronavirus , one genome from a Caatinga phyllostomid bat ( Artibeus planirostris ) clustered within the recently described Ambecovirus clade, displaying 75.9% mean amino acid similarity with mormoopid-associated reference sequences. Based on these divergence levels and non-recombinant genomic architectures, we propose two novel candidate subgenera, Phyllacovirus and Phyllobecovirus , alongside potential novel viral species. Furthermore, our findings demonstrate strong host-associated structuring and biogeographical partitioning of viral lineages across Neotropical biomes. Overall, this study expands the genomic landscape of South American bat coronaviruses and underscores the importance of continuous genomic surveillance at human-wildlife interfaces.

Influenza A(H3N2) viruses show continuous antigenic and genetic evolution, requiring sustained molecular surveillance to understand their circulation and geographic spread. This study investigated the epidemiological, evolutionary, and phylogeographic dynamics of A(H3N2) viruses circulating in Brazil between 2011 and 2019. Epidemiological surveillance data from Northern and Northeastern Brazil were analyzed together with hemagglutinin (HA) gene sequences generated in this study and sequences retrieved from GISAID EpiFlu database. Phylogenetic and Bayesian phylogeographic analyses were performed to characterize genetic diversity and viral dispersal. Among 23,278 respiratory samples, 1,003 (4.31%) were positive for A(H3N2), with seasonal peaks occurring mainly between epidemiological weeks 13 and 16. Phylogenetic analyses revealed successive lineage replacement, with predominance of 3C.2a-derived clades after 2015. Phylogeographic reconstruction identified multiple international introductions into Brazil and extensive viral movement among Brazilian regions, with Southeastern Brazil acting as the main hub of national connectivity. Northern and Northeastern Brazil participated predominantly as recipient regions while also contributing to onward viral dissemination. These findings highlight the interconnected nature of A(H3N2) circulation in Brazil and reinforce the importance of integrating genomic and epidemiological surveillance to understand influenza dynamics.

Caused by the SARS-CoV-2 virus, the COVID-19 pandemic is still considered a complex challenge, with manifestations not only of respiratory issues, but also conditions related to chronic cerebrovascular damage. Endothelial biomarkers, neuropathological and neuroimaging findings indicate endothelial dysfunction, microthrombosis, and disruption of the blood–brain barrier (BBB) are central mechanisms for acute and chronic ischemic and hemorrhagic cerebral events. Understanding these mechanisms is vital to reducing their impact on population health, whether through treatment or prevention of adverse outcomes. The objective of this study is to perform a review of the scientific literature on the post-infection effects of SARS-CoV-2 affecting the cerebral endothelium and the BBB, correlating them with potential clinical outcomes. Material and Methods: Analysis of studies extracted from the PubMed database using the following terms: Long-COVID “AND” SARS-CoV-2 “AND” blood–brain barrier. Inclusion criteria: keywords, publications related to the topic, and primary studies published after peer review. Exclusion criteria: preprint studies, publication outside of the timeframe 2020–2025, study design not compatible with this research, and full text not available. Results: An initial 121 studies were identified, of which 105 were excluded due to not meeting all inclusion criteria and 6 studies were inaccessible due to not being in the English language and full-text access limitations. Fifteen articles were included in the analysis, for topics as expression of viral receptors in the endothelium, markers of their activation, cerebral microvascular injury and coagulopathies. To clarify the pathogenic cascade, the evidence was stratified by biological model where in vitro evidence demonstrates that the Spike protein induces direct endothelial toxicity and platelet aggregation, establishing the primary molecular insult. Animal models confirm the translation of this insult into structural degradation of the BBB and pericyte loss. Clinically, infection-phase findings, characterized by multifocal microthrombosis and permeability spikes, act as the determining event that predisposes to the persistent neuroinflammatory environment. Biomarkers of BBB disruption and neuronal damage were consistently reported, with persistence of BBB dysfunction modifying risk stratification and rehabilitation efforts. Reported cases of Long-COVID demonstrated normalization of BBB markers without correlation with long-term symptoms, suggesting that other mechanisms are involved in Long-COVID. Conclusion: Cerebral endotheliopathies and BBB dysfunction in patients with COVID-19 continue to impact the health of the population. The scientific literature indicates that SARS-CoV-2 induces cerebral endothelial injury, BBB disruption, and an increased risk of vascular events related to endotheliopathy, inflammation, and hypercoagulability. Understanding the impact of COVID-19 pathology on the population and developing prospective studies is essential to quantify the prevalence and mechanisms of brain injury. The identification of molecular targets and infection pathways are promising toward defining both preventive and therapeutic strategies to improve outcomes in the Long-COVID population.

Following the 2022 global mpox outbreak, Brazil has experienced sustained low-level transmission driven by MPXV clade IIb. Since 2024, clade Ib has emerged globally, with increasing evidence of community transmission. We report early evidence consistent with local transmission of MPXV clade Ib in Rio de Janeiro, Brazil. In a prospective cohort at INI-Fiocruz, 23 people were diagnosed with mpox between March and April 2026, including 14 clade Ib infections (13 analyzed). All participants were cisgender men (median age 33 years), predominantly reporting sex with men, without recent international travel. Phylogenetic analysis identified a well-supported cluster consistent with local transmission, nested within a European lineage, suggesting recent introduction into Rio de Janeiro in early 2026, with onward spread. From April 7, all new diagnoses were clade Ib. Clinical features overlapped with clade IIb, limiting syndromic differentiation. Complications were frequent, and five required hospitalizations, highlighting need for enhanced surveillance and prevention.

The spread of high pathogenic avian influenza virus (HPAIV) H5N1 clade 2.3.4.4b into Antarctica poses a major threat to polar wildlife. We report the detection of H5N1 in carcasses of eight species during the 2023-2024 and 2024-2025 austral summers in the South Shetland Islands: Antarctic shag, Antarctic tern, kelp gull, pintado petrel, Antarctic petrel, skuas, Antarctic fur seal, and southern elephant seal. Whole-genome sequencing, mutational profiling, and phylogenetic reconstruction revealed that the viruses detected in these hosts descended from distinct introduction events. One group of strains including complete and partial viral genomes from a gull, skuas, fur seals, an Antarctic tern, and a southern elephant seal clustered with H5N1 strains previously detected in marine mammals in South America and formed a polyphyletic lineage consistent with at least two independent introductions into Antarctica. A second group of strains including complete and partial viral genomes from petrels, shags, and skuas clustered with H5N1 strains previously detected in seabirds and marine mammals in South Georgia and with a previously reported HPAIV detection from Torgersen Island, Antarctic Peninsula. These findings reveal extensive epidemiological connectivity between South America and Antarctica, with South Georgia serving as a “stepping stone” for virus spread in the region.

Understanding the circulation of influenza A viruses and other respiratory pathogens in Antarctic wildlife is essential for anticipating outbreaks and evaluating potential impacts on vulnerable populations. During the austral summer of December 2024 and January 2025, we conducted viral surveillance in six bird species breeding at Lions Rump, King George Island, South Shetland Islands, Antarctica. A total of 199 individuals were sampled, including Pygoscelis papua (gentoo penguin; n = 81), Pygoscelis adeliae (Adélie penguin; n = 79), Pygoscelis antarcticus (chinstrap penguin; n = 34), Stercorarius antarcticus (brown skua; n = 2), Chionis albus (snowy sheathbill; n = 2), and Eudyptes chrysolophus (macaroni penguin; n = 1). All cloacal and oropharyngeal swabs tested negative for influenza A viruses and coronaviruses by RT-PCR. Blood samples from 177 birds were screened by enzyme-linked immunosorbent assay, which detected influenza A virus antibodies in 20 individuals (11.3%). Hemagglutination inhibition assays identified subtypes H6 and H11 in two penguins and H1, H5, H6, and H9 in one skua. These findings reveal no evidence of active viral infection during the sampling period but provide serological evidence of past exposure in seabird populations at Lions Rump. Continued surveillance is essential to characterize viral dynamics in Antarctic ecosystems and to support early detection and preparedness for potential incursions of emerging high-pathogenicity influenza A viruses.

The history of recent epidemics or pandemics makes clear that delays in generating and releasing genomic data can directly limit our ability to detect, understand, and respond to emerging threats. Influenza-like illness (ILI) sentinel surveillance remains central to respiratory virus monitoring. Between September 2024 and July 2025, during episodic increases in ILI cases, in Rio de Janeiro, Brazil, an enhanced genomic surveillance strategy was implemented through collaboration between the Municipal Health Secretariat and the Laboratory of Respiratory Viruses and Measles (LVRE/IOC/Fiocruz). The strategy was triggered by epidemiological alerts from primary healthcare units performing routine SARS-CoV-2 antigen-detection rapid tests (Ag-RDTs). Increases in positivity prompted second-line RT-PCR and genomic sequencing. More than 200 nasopharyngeal samples were collected across 2-3 epidemiological weeks during each surge. SARS-CoV-2 RT-PCR–confirmed positives and samples with Ct<30 were sequenced using Illumina technology for lineage determination. Two enhanced surveillance operations were conducted within the study period. The first enabled the initial detection of the Variant Under Monitoring (VUM) XEC in Brazil. The second identified the emergence and local circulation of VUM XFG shortly after its WHO designation, as well as the first detection of VUM NB.1.8.1. In both events, local genomic signals preceded regional increases of these variants. Targeted genomic surveillance activated by syndromic and antigen-based alerts enabled the timely detection of emerging SARS-CoV-2 variants. This adaptive strategy highlights the importance of integrating genomic and epidemiological surveillance to ensure early identification and response in the post-pandemic period.

Background: Following the disruptions caused by the COVID-19 pandemic, influenza virus circulation in Brazil has been gradually re-establishing its pre-pandemic seasonality. Sustained genomic and antigenic monitoring by the National Influenza Centres (NICs) plays a pivotal role in characterizing viral evolution, informing vaccine strain selection, and ensuring robust preparedness for potential pandemic scenarios. Methods: The positivity of samples collected under Brazil's Ministry of Health (MoH) National Respiratory Viruses Surveillance Network, sourced from both, Influenza-Like Illness (ILI) sentinel sites and severe acute respiratory infection (SARI) universal surveillance were determined from epidemiological week (EW) 35/2024 to EW 35/2025 using seven-target respiratory virus panel followed by an in-house subtyping protocol. Whole-genome characterization was performed by M-RT-PCR protocol sequencing. Antigenic properties were evaluated by hemagglutination inhibition (HI) assays using ferret antisera provided by the WHO. Antiviral resistance mutations were assessed through NA and PA gene analyses and a phenotypic assay for oseltamivir phosphate (OST) susceptibility. Results: Among 106,740 ILI samples, 12.8% were positive for influenza A or B. Influenza A(H1N1)pdm09 predominated, followed by influenza B/Victoria lineage and A(H3N2) at lower levels. Co-circulation of multiple subclades was observed: A(H1N1)pdm09 (5a.2a.1 D.3.1, D.5), A(H3N2) (J.2.3 replacing J.2 within 2a.3a.1), and B/Victoria (C.5.1, C.5.7). All isolates were antigenically similar to vaccine reference strains. Antiviral resistance analysis identified eight H275Y NA mutations in A(H1N1)pdm09, associated with high reduced inhibition (HRI) to OST along with some NA and PA substitution, indicating potentially HRI or RI to peramivir or baloxavir (BXM), respectively. No B/Yamagata viruses were detected. One zoonotic A(H3N2)v case was reported in Paraná. Conclusions: Influenza activity in Brazil during 2024–2025 reflected global circulation trends, dominated by A(H1N1)pdm09 and B/Victoria lineages with minimal antigenic drift. Continued integrated genomic and antigenic surveillance remains critical to guide vaccine strain selection and detect emerging variants with zoonotic potential or antiviral resistance profile.

Background: Respiratory syncytial virus, a major cause of respiratory infections and hospitalizations in young children, especially bronchiolitis, is an important burden to the health system in Brazil. This study evaluated the trends, seasonality, and economic impact of hospitalizations associated with respiratory syncytial virus in Brazilian children. Methods: This study analyzed hospitalizations for acute bronchitis and bronchiolitis (International Code of Diseases-10 J20-J21) in Brazilian children <5 years of age from January 2014 and March 2025 using data from the Brazil’s Unified Health System. Annual trends were assessed with linear regression, while time series decomposition evaluated seasonality. Direct medical costs were adjusted for inflation and converted to international dollars (Int$). Pearson’s correlation coefficient was employed to analyze associations between length of stay and hospitalization cost. Results: A total of 727,808 hospitalizations were recorded, with 86.8% occurring in children under 5 years old. Hospitalizations increased by 307.8%, with marked declines in 2020 during the coronavirus disease-2019 pandemic and consistent seasonal peaks between March-June. Direct medical costs totaled Int$ 166.8 million, with 55.5% of expenditures after 2020. The mean cost per hospitalization increased by Int$ 21.48 between 2014-2024 (Int$ 118.16-139.64). Length of stay correlated moderately with cost (r = 0.55), particularly strongly in southeastern and southern Brazil. Conclusions: Our findings revealed distinct seasonal and regional patterns in hospitalizations and a post-pandemic increase in costs. The association between prolonged hospitalization and higher expenditures underscores the need for targeted, region-specific preventive strategies and timely clinical interventions, to reduce the growing economic burden on the system.