Incomplete bunyavirus particles can cooperatively support virus infection and spread.

Bunyaviruses lack a specific mechanism to ensure the incorporation of a complete set of genome segments into each virion, explaining the generation of incomplete virus particles lacking one or more genome segments. Such incomplete virus particles, which may represent the majority of particles produced, are generally considered to interfere with virus infection and spread. Using the three-segmented arthropod-borne Rift Valley fever virus as a model bunyavirus, we here show that two distinct incomplete virus particle populations unable to spread autonomously are able to efficiently complement each other in both mammalian and insect cells following co-infection. We further show that complementing incomplete virus particles can co-infect mosquitoes, resulting in the reconstitution of infectious virus that is able to disseminate to the mosquito salivary glands. Computational models of infection dynamics predict that incomplete virus particles can positively impact virus spread over a wide range of conditions, with the strongest effect at intermediate multiplicities of infection. Our findings suggest that incomplete particles may play a significant role in within-host spread and between-host transmission, reminiscent of the infection cycle of multipartite viruses.

Succession in the caecal microbiota of developing broilers colonised by extended-spectrum ß-lactamase-producing Escherichia coli.

BACKGROUND: Broilers are among the most common and dense poultry production systems, where antimicrobials have been used extensively to promote animal health and performance. The continuous usage of antimicrobials has contributed to the appearance of resistant bacteria, such as extended-spectrum ß-lactamase-producing Escherichia coli (ESBL-Ec). Here, we studied the ESBL-Ec prevalence and successional dynamics of the caecal microbiota of developing broilers in a commercial flock during their production life cycle (0-35 days). Broilers were categorised as ESBL-Ec colonised (ESBL-Ec+) or ESBL-Ec non-colonised (ESBL-Ec-) by selective culturing. Using 16S rRNA gene sequencing, we i. compared the richness, evenness and composition of the caecal microbiota of both broilers' groups and ii. assessed the combined role of age and ESBL-Ec status on the broilers' caecal microbiota. RESULTS: From day two, we observed an increasing linear trend in the proportions of ESBL-Ec throughout the broilers' production life cycle, X2 (1, N = 12) = 28.4, p < 0.001. Over time, the caecal microbiota richness was consistently higher in ESBL-Ec- broilers, but significant differences between both broilers' groups were found exclusively on day three (Wilcoxon rank-sum test, p = 0.016). Bray-Curtis distance-based RDA (BC-dbRDA) showed no explanatory power of ESBL-Ec status, while age explained 14% of the compositional variation of the caecal microbiota, F (2, 66) = 6.47, p = 0.001. CONCLUSIONS: This study assessed the role of ESBL-Ec in the successional dynamics of the caecal microbiota in developing broilers and showed that the presence of ESBL-Ec is associated with mild but consistent reductions in alpha diversity and with transient bacterial compositional differences. We also reported the clonal spread of ESBL-Ec and pointed to the farm environment as a likely source for ESBLs.