Explore the vast range of titles available.

Congregate homeless shelters are disproportionately affected by infectious disease outbreaks. We describe enterovirus epidemiology across 23 adult and family shelters in King County, Washington, USA, during October 2019-May 2021, by using repeated cross-sectional respiratory illness and environmental surveillance and viral genome sequencing. Among 3,281 participants >3 months of age, we identified coxsackievirus A21 (CVA21) in 39 adult residents (3.0% [95% CI 1.9%-4.8%] detection) across 7 shelters during October 2019-February 2020. We identified enterovirus D68 (EV-D68) in 5 adult residents in 2 shelters during October-November 2019. Of 812 environmental samples, 1 was EV-D68-positive and 5 were CVA21-positive. Other enteroviruses detected among residents, but not in environmental samples, included coxsackievirus A6/A4 in 3 children. No enteroviruses were detected during April 2020-May 2021. Phylogenetically clustered CVA21 and EV-D68 cases occurred in some shelters. Some shelters also hosted multiple CVA21 lineages.

Human enteroviruses (EVs) comprise more than 100 types of coxsackievirus, echovirus, poliovirus and numbered enteroviruses, which are mainly transmitted by the faecal-oral route leading to diverse diseases such as aseptic meningitis, encephalitis, and acute flaccid paralysis, among others. Since enteroviruses are excreted in faeces, wastewater-based epidemiology approaches are useful to describe EV diversity in a community. In Uruguay, knowledge about enteroviruses is extremely limited. This study assessed the diversity of enteroviruses through Illumina next-generation sequencing of VP1-amplicons obtained by RT-PCR directly applied to viral concentrates of 84 wastewater samples collected in Uruguay during 2011–2012 and 2017–2018. Fifty out of the 84 samples were positive for enteroviruses. There were detected 27 different types belonging to Enterovirus A species (CVA2-A6, A10, A16, EV-A71, A90), Enterovirus B species (CVA9, B1-B5, E1, E6, E11, E14, E21, E30) and Enterovirus C species (CVA1, A13, A19, A22, A24, EV-C99). Enterovirus A71 (EV-A71) and echovirus 30 (E30) strains were studied more in depth through phylogenetic analysis, together with some strains previously detected by us in Argentina. Results unveiled that EV-A71 sub-genogroup C2 circulates in both countries at least since 2011–2012, and that the C1-like emerging variant recently entered in Argentina. We also confirmed the circulation of echovirus 30 genotypes E and F in Argentina, and reported the detection of genotype E in Uruguay. To the best of our knowledge this is the first report of the EV-A71 C1-like emerging variant in South-America, and the first report of EV-A71 and E30 in Uruguay.

Human enteroviruses are associated with various clinical syndromes from minor febrile illness to severe, potentially fatal conditions like aseptic meningitis, paralysis, myocarditis, and neonatal enteroviral sepsis. Between June 2000 and August 2008 echovirus (E) type 2, 4, 6, 7, 9, 11, 13, 25, 30, coxsackievirus (CV) -A16, -A19, -B5, and enterovirus 71 (EV71) were reported in Hungary. In this study, 29 previously enterovirus positive samples from 28 patients diagnosed with hand, foot and mouth disease, meningitis and encephalitis, were molecularly typed. The genetic relationships of identified serotypes CV-A16, EV71, and E30 were assessed by direct sequencing of genomic region encoding the capsid protein VP1. The sequences were compared to each other and sequences from other geographical regions possessed in Genbank. The phylogenetic analysis of CV-A16 revealed that the viruses were mostly of Far-Eastern or Asia-Pacific origin. Typing of EV71 showed that one virus from 2000 belonged to genotype C1 and five viruses observed in 2004 and 2005 were identified as genotype C4. The 11 echovirus 30 strains showed homology with those of neighbor European countries. The molecular examination of E30 revealed that three separate lineages circulated in 2000, 2001, and 2004-2006 in Hungary.

Background: While enteroviruses (EVs) are recognized causes of diverse illnesses, little is known about the epidemiology and molecular characteristics of uncommon enterovirus C (EV-C) types, including EV-C104, EV-C105, and EV-C109. Methods: We conducted genomic surveillance of EVs at the Johns Hopkins Health System between 2018 and 2024 (a total of 3715 samples), identifying EV-C104, EV-C105, and EV-C109 in respiratory samples. VP4-VP2 and whole-genome sequencing were used to assess genetic diversity and intra-host evolution. Results: Five EV-C105 infections were identified primarily in pediatric patients, presenting with a range of clinical features including fever, gastrointestinal symptoms, and cerebellitis. Prolonged EV-C104 and EV-C109 infections were identified in two immunocompromised adults. EV-C104 persisted for over five months and showed evidence of viral genomic changes (intra-host evolution). EV-C109 was detected over a four-month period. Phylogenetic analysis revealed a novel EV-C105 clade (C3) closely related to recent USA strains. EV-C104 genomes aligned with genotype B sequences from the USA and Europe, while EV-C109 sequences were similar to 2014–2015 strains from the Netherlands. Conclusions: These findings highlight the emergence, persistence, and genetic evolution of uncommon EV-C types in Maryland, especially among immunocompromised hosts, emphasizing the importance of continued genomic surveillance and clinical correlations.

Background Rash is a common childhood infection, mainly caused by viruses. Hand, foot, and mouth disease (HFMD), a common viral rash infection, has become one of the most common infectious diseases in Asian countries and caused outbreaks in children and adults worldwide. Following the introduction of enterovirus A71 (EVA71) vaccines, Coxsackievirus A6 (CVA6) has recently emerged. However, the disease is not commonly reported in Africa, where studies are scarce. Methods In the current study, we focused on the HFMD outbreak that occurred in Cape Verde in July 2023 during field investigations around a cluster of patients with rash and fever. Samples collected from patients were tested using Measles and Rubella-specific immunoglobulin M and quantitative reverse transcription PCR (qRT-PCR) of a panel of viruses causing rashes and subjected to genome sequencing followed by phylogenetic analysis. Results Eighteen out of the 22 samples were tested positive for CVA6 RNA by real-time RT-PCR, of which two tested also positive for EVA71 and Coxsackievirus A16 (CVA16). Subsequent sequencing revealed that all CVA6 sequences belonged to the D genotype, particularly the D3 sub-genotype recently described in China. Conclusion Our study uncovers the first-ever reported outbreak of CVA6 associated with atypical HFMD in children from Cape Verde and highlights thus the need to implement an active hospital-based HFMD surveillance in Africa.

Background Hand, foot, and mouth disease (HFMD) remains a significant childhood infection in the Asia-Pacific region; however, the emergence of Coxsackievirus A6 (CVA6) since 2008 has reshaped its epidemiology. Despite extensive national surveillance, the evolutionary tempo-spatial dynamics of CVA6 in southern China remain poorly characterized. This study aimed to delineate the temporal phylodynamics of the CVA6 VP1 region in Shenzhen and identify lineage-defining mutations that may inform early-warning systems and control strategies. Methods Epidemiological surveillance data (2022–2024) were integrated with VP1 sequences from 47 Shenzhen isolates and 465 global reference strains (1949–2024). Real-time RT-PCR was used to determine serotype composition. Bayesian relaxed-clock, SkyGrid, and discrete phylogeographic models were applied to reconstruct substitution rates, lineage turnover, and transmission routes. Amino acid variability was mapped onto the VP1 protein structure. Results Among 195,951 notifiable disease cases, 11,427 (5.8%) were identified as HFMD, with seasonal peaks consistently observed in June and a maximum of 3,185 cases recorded in June 2023. CVA6 was detected in 30.9% of tested specimens and predominated in 2023 (64.6%). Root-to-tip regression showed a strong temporal signal (R² = 0.86), and the mean VP1 substitution rate was 4.78 × 10⁻³ substitutions/site/year (95% highest posterior density [HPD]: 4.39–5.16 × 10⁻³), with the estimated time to the most recent common ancestor (tMRCA) around 1945. All Shenzhen isolates belonged to genotype D3 and formed three temporally structured clades interspersed with isolates from various Chinese provinces, suggesting frequent interprovincial transmission and limited geographic clustering. SkyGrid analysis indicated a rapid expansion in the effective population size beginning in 2008, which stabilized after 2010. A total of 31 VP1 amino acid substitutions were identified; twelve (e.g., positions 5, 8, 10, 14, 32, 98, 160, 174, 194, 261, 279, 305) were fixed compared to the prototype strain Gdula, while six variable sites (e.g., S97N, N241D) were located in surface-exposed or BC-loop regions. Pairwise nucleotide distances among local strains were ≤ 6.7%, compared to 19.5–22.0% divergence from Gdula. Conclusions Genotype D3 of Coxsackievirus A6 appears to be a significant contributor to seasonal HFMD peaks in Shenzhen, particularly in early summer. Its high evolutionary rate, rapid lineage turnover, and limited geographic structuring emphasize the importance of coordinated, cross-regional molecular surveillance. The study identifies 31 amino acid substitutions, including surface-exposed sites, which may indicate ongoing antigenic drift and potential immune escape. These findings underscore the need for high-resolution genomic surveillance, early-warning systems, and region-specific control measures for effective management of HFMD. Clinical trial registration Not applicable.

Hand, foot, and mouth disease (HFMD), a common childhood infection caused by enterovirus, poses a serious public health concern in China. We collected and analyzed epidemiological data on 62,133 HFMD cases in Shenyang City, Liaoning Province, from 2013 to 2023. The average annual incidence was 76.12 per 100,000 person-years; 99.45% of cases were mild, while 0.55% were severe. Only one patient died. HFMD infections peaked annually in July. Children in kindergartens and scattered children accounted for 44.6% and 42.2% of cases, respectively. Real-time RT-PCR detection of enteroviruses in 5534 patient samples revealed 3780 positives, of which 25.1% were CVA16-positive. Positives were randomly sampled, yielding 240 VP1 sequences of CVA16. Phylogenetic tree results showed that all VP1 sequences belonged to the B1 sub-genogroup. However, the sub-genogroup prevalence varied over time: from 2013 to 2014 and 2019 to 2021, the predominant sub-genogroup was B1a, while it was B1b from 2015 to 2018. Further phylogenetic analyses showed substantial divergence between B1a branches in CVA16, suggesting possible turnover of the B1a sub-genogroup in CVA16 due to evolution. This study provides epidemiological data on HFMD in Shenyang, and provides a phylogenetic analysis of CVA16, offering a theoretical basis for preventing and controlling HFMD in Shenyang City.

Hand, foot, and mouth disease (HFMD) is a global public health concern, notably within the Asia-Pacific region. Recently, the primary pathogen causing HFMD outbreaks across numerous countries, including China, is coxsackievirus (CV) A6, one of the most prevalent enteroviruses in the world. It is a new variant that has undergone genetic recombination and evolution, which might not only induce modifications in the clinical manifestations of HFMD but also heighten its pathogenicity because of nucleotide mutation accumulation. The study assessed the epidemiological characteristics of HFMD in China and characterized the molecular epidemiology of the major pathogen (CV-A6) causing HFMD. We attempted to establish the association between disease progression and viral genetic evolution through a molecular epidemiological study. Surveillance data from the Chinese Center for Disease Control and Prevention from 2021 to 2023 were used to analyze the epidemiological seasons and peaks of HFMD in Henan, China, and capture the results of HFMD pathogen typing. We analyzed the evolutionary characteristics of all full-length CV-A6 sequences in the NCBI database and the isolated sequences in Henan. To characterize the molecular evolution of CV-A6, time-scaled tree and historical population dynamics regarding CV-A6 sequences were estimated. Additionally, we analyzed the isolated strains for mutated or missing amino acid sites compared to the prototype CV-A6 strain. The 2021-2023 epidemic seasons for HFMD in Henan usually lasted from June to August, with peaks around June and July. The monthly case reporting rate during the peak period ranged from 20.7% (4854/23,440) to 35% (12,135/34,706) of the total annual number of cases. Analysis of the pathogen composition of 2850 laboratory-confirmed cases identified 8 enterovirus serotypes, among which CV-A6 accounted for the highest proportion (652/2850, 22.88%). CV-A6 emerged as the major pathogen for HFMD in 2022 (203/732, 27.73%) and 2023 (262/708, 37.01%). We analyzed all CV-A6 full-length sequences in the NCBI database and the evolutionary features of viruses isolated in Henan. In China, the D3 subtype gradually appeared from 2011, and by 2019, all CV-A6 virus strains belonged to the D3 subtype. The VP1 sequences analyzed in Henan showed that its subtypes were consistent with the national subtypes. Furthermore, we analyzed the molecular evolutionary features of CV-A6 using Bayesian phylogeny and found that the most recent common ancestor of CV-A6 D3 dates back to 2006 in China, earlier than the 2011 HFMD outbreak. Moreover, the strains isolated in 2023 had mutations at several amino acid sites compared to the original strain. The CV-A6 virus may have been introduced and circulating covertly within China prior to the large-scale HFMD outbreak. Our laboratory testing data confirmed the fluctuation and periodic patterns of CV-A6 prevalence. Our study provides valuable insights into understanding the evolutionary dynamics of CV-A6.

Enterovirus D68 was implicated in a widespread outbreak of severe respiratory illness across the USA in 2014 and has also been reported sporadically in patients with acute flaccid myelitis. We aimed to investigate the association between enterovirus D68 infection and acute flaccid myelitis during the 2014 enterovirus D68 respiratory outbreak in the USA. Patients with acute flaccid myelitis who presented to two hospitals in Colorado and California, USA, between Nov 24, 2013, and Oct 11, 2014, were included in the study. Additional cases identified from Jan 1, 2012, to Oct 4, 2014, via statewide surveillance were provided by the California Department of Public Health. We investigated the cause of these cases by metagenomic next-generation sequencing, viral genome recovery, and enterovirus D68 phylogenetic analysis. We compared patients with acute flaccid myelitis who were positive for enterovirus D68 with those with acute flaccid myelitis but negative for enterovirus D68 using the two-tailed Fisher's exact test, two-sample unpaired t test, and Mann-Whitney U test. 48 patients were included: 25 with acute flaccid myelitis, two with enterovirus-associated encephalitis, five with enterovirus-D68-associated upper respiratory illness, and 16 with aseptic meningitis or encephalitis who tested positive for enterovirus. Enterovirus D68 was detected in respiratory secretions from seven (64%) of 11 patients comprising two temporally and geographically linked acute flaccid myelitis clusters at the height of the 2014 outbreak, and from 12 (48%) of 25 patients with acute flaccid myelitis overall. Phylogenetic analysis revealed that all enterovirus D68 sequences associated with acute flaccid myelitis grouped into a clade B1 strain that emerged in 2010. Of six coding polymorphisms in the clade B1 enterovirus D68 polyprotein, five were present in neuropathogenic poliovirus or enterovirus D70, or both. One child with acute flaccid myelitis and a sibling with only upper respiratory illness were both infected by identical enterovirus D68 strains. Enterovirus D68 viraemia was identified in a child experiencing acute neurological progression of his paralytic illness. Deep metagenomic sequencing of cerebrospinal fluid from 14 patients with acute flaccid myelitis did not reveal evidence of an alternative infectious cause to enterovirus D68. These findings strengthen the putative association between enterovirus D68 and acute flaccid myelitis and the contention that acute flaccid myelitis is a rare yet severe clinical manifestation of enterovirus D68 infection in susceptible hosts. National Institutes of Health, University of California, Abbott Laboratories, and the Centers for Disease Control and Prevention.

Hand, foot and mouth disease (HFMD) is usually caused by coxsackievirus A16 or enterovirus 71 (EV71). Between 2011 and 2013, HFMD cases were reported from different Cuban provinces. A total of 42 clinical specimens were obtained from 23 patients. Detection, identification and phylogenetic analysis of enterovirus-associated HFMD were carried out by virus isolation, specific enterovirus PCR and partial VP1 sequences. HEV was detected in 11 HFMD cases. Emerging genetic variants of coxsackievirus A6 and EV71 were identified as the causative agents of the Cuban HFMD cases.