Penghui Yang

Between March and July 1997, a devastating outbreak of foot-and-mouth disease (FMD), serotype O, occurred in pigs in Taiwan. A total of 6,147 pig farms with more than 4 million pigs were infected, and 37.7 per cent of the pigs in Taiwan either died (0.18 million pigs) or were killed (3.85 million pigs). The epidemic reached its peak during the fifth week after it was first recognised. During the eighth and ninth weeks, a two-dose blanket vaccination programme was instituted which led to a large reduction in new outbreaks. Except for two cities, the whole of Taiwan was declared an FMD-infected zone. During the four months in which new farm outbreaks occurred, 21.7 per cent of the pigs on infected farms showed clinical signs, and there was an overall mortality of 3.95 per cent. During the early stages of the epidemic, the incubation period was as short as 24 hours and the case fatality rates for suckling piglets reached 100 per cent. The financial cost of the epidemic was estimated at US$ 378.6 million, including indemnities, vaccines, carcase disposal plus environmental protection, miscellaneous expenses, and loss of market value. Owing to the ban on exports of pork to Japan, it is estimated that the total economic cost to Taiwan's pig industry will be about US$ 1.6 billion.

SARS-CoV-2 is the cause of the current global pandemic of COVID-19; this virus infects multiple organs, such as the lungs and gastrointestinal tract. The microbiome in these organs, including the bacteriome and virome, responds to infection and might also influence disease progression and treatment outcome. In a cohort of 13 COVID-19 patients in Beijing, China, we observed that the gut virome and bacteriome in the COVID-19 patients were notably different from those of five healthy controls. We identified a bacterial dysbiosis signature by observing reduced diversity and viral shifts in patients, and among the patients, the bacterial/viral compositions were different between patients of different severities, although these differences are not entirely distinguishable from the effect of antibiotics. Severe cases of COVID-19 exhibited a greater abundance of opportunistic pathogens but were depleted for butyrate-producing groups of bacteria compared with mild to moderate cases. We replicated our findings in a mouse COVID-19 model, confirmed virome differences and bacteriome dysbiosis due to SARS-CoV-2 infection, and observed that immune/infection-related genes were differentially expressed in gut epithelial cells during infection, possibly explaining the virome and bacteriome dynamics. Our results suggest that the components of the microbiome, including the bacteriome and virome, are affected by SARS-CoV-2 infections, while their compositional signatures could reflect or even contribute to disease severity and recovery processes.