Related enteric viruses have different requirements for host microbiota in mice

Abstract

24Accumulating evidence suggests that intestinal bacteria promote enteric virus infection 25 in mice. For example, previous work demonstrated that antibiotic treatment of mice prior 26 to oral infection with poliovirus reduced viral replication and pathogenesis. Here we 27 examined the effect of antibiotic treatment on infection with coxsackievirus B3 (CVB3), a 28 picornavirus closely related to poliovirus. We treated mice with a mixture of five 29 antibiotics to deplete host microbiota and examined CVB3 replication and pathogenesis 30 following oral inoculation. We found that, like poliovirus, CVB3 shedding and 31 pathogenesis were reduced in antibiotic-treated mice. While treatment with just two 32 antibiotics, vancomycin and ampicillin, was sufficient to reduce CVB3 replication and 33 pathogenesis, this treatment had no effect on poliovirus. Quantity and composition of 34 bacterial communities were altered by treatment with the five antibiotic cocktail and by 35 treatment with vancomycin and ampicillin. To determine whether more subtle changes 36 in bacterial populations impact viral replication, we examined viral infection in mice 37 treated with milder antibiotic regimens. Mice treated with one-tenth the concentration of 38 the normal antibiotic cocktail supported replication of poliovirus but not CVB3. 39Importantly, a single dose of one antibiotic, streptomycin, was sufficient to reduce CVB3 40 shedding and pathogenesis, while having no effect on poliovirus shedding and 41 pathogenesis. Overall, replication and pathogenesis of CVB3 is more sensitive to 42 antibiotic treatment than poliovirus, indicating that closely related viruses may differ in 43 their reliance on microbiota. 44 45 46 3 Importance 47 Recent data indicate that intestinal bacteria promote intestinal infection of several 48 enteric viruses. Here we show that coxsackievirus, an enteric virus in the picornavirus 49 family, also relies on microbiota for intestinal replication and pathogenesis. Relatively 50 minor depletion of the microbiota was sufficient to decrease coxsackievirus infection, 51 while poliovirus infection was unaffected. Surprisingly, a single dose of one antibiotic 52 was sufficient to reduce coxsackievirus infection. Therefore, these data indicate that 53 microbiota can influence enteric virus infection through distinct mechanisms, even for 54 closely related viruses.55 56 57 Enteric viruses are spread through the fecal-oral route and cause morbidity and 58 mortality in humans worldwide (1-4). These viruses initiate infection in the 59 gastrointestinal tract, which is home to a community of bacteria, fungi, and viruses, 60 termed the microbiota. Microbiota play important roles in human development, 61 metabolism, and immunity (5). We and others have shown that intestinal bacteria can 62 enhance viral replication and pathogenesis of enteric viruses, including poliovirus, 63 reovirus, rotavirus, mouse mammary tumor virus, and noroviruses (6-11). While the 64 mechanisms underlying bacterial promotion of enteric virus repl...

Links between fecal microbiota and the response to vaccination against influenza A virus in pigs

“…In humans and mice, it has been shown that the stability and survival of certain viruses in the gut are enhanced when the viral particles are attached to bacterial components. For instance, gut bacteria that express histo-blood group antigens stabilize norovirus in humans 20 , while bacterial N-acetylglucosamine and lipopolysaccharides (LPS) have a similar effect for poliovirus in mice 21 , 22 . Furthermore, the gut microbiota can have effects on remote parts of the body, and, for example, can act on the respiratory system to influence the disease severity of influenza or the vaccine response.…”