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Santiso-Bellon, C.

Publications and source records attributed to Santiso-Bellon, C..

2 recordsLinked to original sources
bioRxiv2021

Wide Diversity of Recombinant Noroviruses Circulating in Spain, 2016 to 2020

Noroviruses are the leading cause of sporadic cases and outbreaks of viral gastroenteritis. For more than 20 years most norovirus infections have been caused by the pandemic genotype GII.4, yet recent studies have reported the emergence of recombinant strains in many countries. In the present study, 4,950 stool samples collected between January 2016 and April 2020 in Valencia (Spain) from patients with acute gastroenteritis were analyzed to investigate the etiological agent. Norovirus was the most frequently detected enteric virus with a positive rate of 9.5% (471/4,950). Among 224 norovirus strains characterized, 175 belonged to genogroup GII and 49 to genogroup GI. Using dual genotyping based on sequencing the ORF1/ORF2 junction region we detected 25 different capsid-polymerase type associations. The most common GII capsid genotype was GII.4 Sydney 2012, followed by GII.2, GII.3, GII.6 and GII.17. A high prevalence of recombinant strains (90.4%) was observed among GII infections between 2018 and 2020. GII.4 Sydney[P16] was the predominant genotype from 2019 to 2020. In addition, GII.P16 polymerase was found harboring within six different capsid genes. A new subcluster of GII.4 Sydney associated with the P31 polymerase was identified by phylogenetic analysis. GI.4 and GI.3 were the predominant genotypes in genogroup GI, in which recombinant strains were also found, such as GI.3[P10], GI.3[P13] and GI.5[P4]. Interestingly, the GI.3[P10] strain could represent a new capsid genotype. This study shows the extensive diversity of recombinant noroviruses circulating in Spain and highlights the role of recombination events in the spread of noroviruses.

microbiology↗
bioRxiv2021

Microbiota depletion promotes human rotavirus replication in an adult mouse model

The study of human rotavirus (RV) infectivity in vivo has been limited by the lack of small animal models able to efficiently replicate the principal human RV genotypes. In recent years, intestinal microbiota-virus-host interaction has emerged as a key factor in mediating enteric virus pathogenicity. With the aim of developing an adult mouse infection model for RV we performed faecal microbiota transplant (FMT) with healthy infants as donors in antibiotic-treated mice. Contrarily to control mice, in the FMT group, but also in antibiotic-treated mice without FMT, challenge with the human RV G1P[8] genotype, Wa strain (RVwa), resulted in viral shedding in the faeces for 6 days. RV titres in faeces were also significantly higher in antibiotic-treated animals with or without FMT. This excluded the hypothesis that donors microbiota promoted infection. Antibiotic treatment followed by self-FMT resulted in incomplete re-establishment of mouse microbiota which partially restored suppression of RVwa infection. Microbial composition analysis revealed profound changes in the intestinal microbiota of antibiotic-treated animals, whereas some bacterial groups, including members of Lactobacillus, Bilophila, Mucispirillum and Oscillospira, reappeared after self-FMT. In antibiotic-treated and FMT animals, differences were observed in gene expression of immune mediators such as IL10, TNF- and IFN{gamma} and the fucosyltransferase FUT2, responsible for H-type antigen synthesis in the small intestine. Collectively, our results suggest that antibiotic-induced microbiota depletion eradicates the microbial taxa that restrict human RV infectivity in mice. Viral permissiveness could involve changes in the innate immune system at the small intestine and alterations in the bacteria population that potentially interact with RV, creating a favourable environment for human RV replication in mice.

microbiology↗