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Published on: February 19, 2013
Microbiota Depletion Promotes Human Rotavirus Replication in an Adult Mouse Model
Roberto Gozalbo-Rovira1, Cristina Santiso-Bellón1, Javier Buesa1,2
1Department of Microbiology, School of Medicine, University of Valencia, Av. Blasco Ibáñez 17, 46010 Valencia, Spain.
Abstract:
Intestinal microbiota-virus-host interaction has emerged as a key factor in mediating enteric virus pathogenicity. With the aim of analyzing whether human gut bacteria improve the inefficient replication of human rotavirus in mice, we performed fecal microbiota transplant (FMT) with healthy infants as donors in antibiotic-treated mice. We showed that a simple antibiotic treatment, irrespective of FMT, resulted in viral shedding for 6 days after challenge with the human rotavirus G1P[8] genotype Wa strain (RVwa). Rotavirus titers in feces were also significantly higher in antibiotic-treated animals with or without FMT but they were decreased in animals subject to self-FMT, where a partial re-establishment of specific bacterial taxons was evidenced. 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, recovered after self-FMT. In antibiotic-treated and FMT animals where the virus replicated more efficiently, differences were observed in gene expression of immune mediators, such as IL1β and CXCL15, as well as in 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 rotavirus infectivity in mice.
Insights
Antibiotic treatment disrupts the gut microbiota, increasing human rotavirus (RVwa) replication in mice. Specific bacteria normally restrict rotavirus infectivity, and their depletion by antibiotics enhances viral shedding and titers.
Area of Science:
- Microbiology
- Virology
- Immunology
- Gastroenterology
Background:
- Intestinal microbiota-virus-host interactions critically influence enteric virus pathogenicity.
- Human rotavirus (RVwa) replication is inefficient in mice, necessitating investigation into factors modulating its infectivity.
Purpose of the Study:
- To determine if human gut bacteria, introduced via fecal microbiota transplant (FMT), enhance the replication of human rotavirus (RVwa) in mice.
- To investigate the impact of antibiotic-induced microbiota depletion and FMT on RVwa infection dynamics and host gene expression.
Main Methods:
- Antibiotic treatment and fecal microbiota transplant (FMT) from healthy infants into mice.
- Challenge with human rotavirus G1P[8] genotype Wa strain (RVwa).
- Quantification of viral shedding and fecal rotavirus titers.
- Analysis of microbial composition and host gene expression (IL1β, CXCL15, FUT2).
Main Results:
- Antibiotic treatment alone, irrespective of FMT, led to prolonged viral shedding (6 days) and increased rotavirus titers in mice.
- Self-FMT partially restored specific bacterial taxa, correlating with decreased rotavirus titers.
- Antibiotic-treated and FMT groups showed increased viral replication, altered immune mediator gene expression (IL1β, CXCL15), and changes in FUT2 expression.
Conclusions:
- Antibiotic-induced depletion of the gut microbiota eliminates bacterial taxa that naturally restrict human rotavirus infectivity in mice.
- Restoration of specific gut bacteria, as seen in self-FMT, can reduce rotavirus replication.
- Modulation of host immune responses and fucosyltransferase FUT2 expression are associated with enhanced rotavirus replication in a depleted microbiota environment.
