Exploring the interaction between rotavirus and Lactobacillus

Abstract

Background Enteric viruses enter the host via the fecal-oral route and in the intestine, viruses encounter a dynamic community of microbes. Select intestinal microbes have been shown to bind viruses and inhibit infection. Viral adhesion to bacteria has been characterized with astrovirus, norovirus, and poliovirus, but few studies have addressed the interaction between rotavirus and bacteria. Rotavirus is a leading cause of diarrheal diseases in children, with an estimated 258 million cases and 128,500 deaths per year. As a result, identifying mechanisms by which microbes influence rotavirus infection remains an important question. We hypothesized that certain intestinal microbes would bind to rotavirus and potentially participate in infection. Methods & Results To address this questions we fluorescently tagged commensal gut microbes Bacteroides ovatus ATCC 8384, Bacteroides thetaioatomicron ATCC 29148, Ruminococcus torques ATCC 2775, Akkermansia muciniphila ATCC BAA-835, Escherichia coli K12, Lactobacillus reuteri M27163, Lactobacillus rhamnosus GG, Lactobacillus acidophilus ATCC 4356, Bifidobacterium longum subsp. infantis ATCC 15697, Bifidobacterium bifidum ATCC 29521, Prevotella copri CB7 DSM 18205, Clostridium sporogenes DSM 795 ATC 3585, Fusobacterium nucleatum polymorphum ATCC 10953, Enterococcus faecalis Symbioflor DSM 16431, Streptococcus thermophilus ATTC 491, and Faecalibacterium prausnitzii A2-165. All microbes were adjusted to OD600nm =1 and incubated with 107 PFU BFP-tagged rotavirus for 1 hr. After washing, adhesion was examined by fluorescence. Interestingly, only L. acidophilus was found to bind rotavirus. Next, we sought to identify how Lactobacillus levels were modulated during rotavirus infection. 16S rRNA sequencing the ileum of neonatal mice demonstrated the gut microbiome was dominated by Lactobacillus (60%), followed by Staphylococcus (20%), Escherichia (15%), Enterobacter (3%), and Bacteroides (2%). Infection of neonatal pups with rotavirus significantly decreased ileal Lactobacillus (40%) and increased Enterobacter (10%), Bacteroides (7%), and Akkermansia (5%) after one day post-infection. Conclusions Based on this data we speculate that select Lactobacillus can bind rotavirus and prevent rotavirus access to the epithelium. Decreased levels of Lactobacilli during infection may inadvertently promote infection. This data also points to the potential for Lactobacillus administration in minimizing infection and may provide a new strategy for rotavirus treatment.