Authors' contributions MI collected patient data regarding the ER and ICU and was a major contributor in writing the manuscript. OP was responsible for buccal swab and bronchoalveolar lavage specimens and for RT-PCR processing. FR interpreted radiological findings and provided the radiological differential diagnosis. GS provided a major contribution in data analysis and interpretation. RT provided a major contribution in data analysis and interpretation. EDR collected data regarding ER and ICU, contributed to the analysis and interpretation, and was a major contributor in writing the manuscript. All authors read and approved the final manuscript. Agricultural intensification, priming for persistence and the emergence of Nipah virus: a lethal bat-borne zoonosis Emerging zoonoses threaten global health, yet the processes by which they emerge are complex and poorly understood. Nipah virus (NiV) is an important threat owing to its broad host and geographical range, high case fatality, potential for human-to-human transmission and lack of effective prevention or therapies. Here, we investigate the origin of the first identified outbreak of NiV encephalitis in Malaysia and Singapore. We analyse data on livestock production from the index site (a commercial pig farm in Malaysia) prior to and during the outbreak, on Malaysian agricultural production, and from surveys of NiV's wildlife reservoir (flying foxes). Our analyses suggest that repeated introduction of NiV from wildlife changed infection dynamics in pigs. Initial viral introduction produced an explosive epizootic that drove itself to extinction but primed the population for enzootic persistence upon reintroduction of the virus. The resultant within-farm persistence permitted regional spread and increased the number of human infections. This study refutes an earlier hypothesis that anomalous El Niño Southern Oscillation-related climatic conditions drove emergence and suggests that priming for persistence drove the emergence of a novel zoonotic pathogen. Thus, we provide empirical evidence for a causative mechanism previously proposed as a precursor to widespread infection with H5N1 avian influenza and other emerging pathogens. Preventing and controlling emerging zoonoses require identification of the processes that drive cross-species pathogen transmission [1] . Agricultural intensification has been proposed as a major underlying cause of pathogen emergence from wildlife and domestic animal populations into human populations [2, 3] ; however, the precise mechanisms by which this occurs have rarely been demonstrated. Specific agricultural practices may increase frequency of cross-species pathogen transmission, setting the stage for persistence of new pathogens to occur. Pathogen introduction into a partially immune population-such as a population where some individuals are vaccinated or were previously infected-can result in longer and potentially larger epidemics than introduction into a naive population [4] . We refer to this phenomenon as immunity-based, population-level 'priming' for persistence. The potential of such priming to drive zoonotic emergence has been demonstrated theoretically in the general case [4] , as a possible precursor to measles emergence [5] and as a mechanism that could facilitate widespread emergence of H5N1 avian influenza in poultry [6] . Here, we present evidence that this process is not only theoretically possible but is likely to have played a key role in the first known outbreak of Nipah virus (NiV) encephalitis, and therefore for the emergence of a lethal zoonosis.