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This introduction provides a telegraphic overview of the processes of zoonotic viral emergence, the intricacies of host–virus interactions, and the distinct role of biological transitions and modifying factors. The process of emergence is conceptualized as two transition stages which are common and required for all disease emergence, (1) human contact with the infectious agent and (2) cross-species transmission of the agent, and two transition stages which are not required for emergence and appear unavailable to many zoonotic pathogens, (3) sustained human-to-human transmission and (4) genetic adaptation to the human host. The latter two transitions are presumably prerequisites for the pandemic emergence of a pathogen. The themes introduced herein are amplified and explored in detail by the contributors to this volume. Each author explores the mechanisms and unique circumstances by which evolution, biology, history, and current context have contrived to drive the emergence of different zoonotic agents by a series of related events; although recognizable similarities exist among the events leading to emergence the details and circumstances are never repetitive.

The dynamics of any infectious disease are heavily dependent on the rate of transmission from infectious to susceptible hosts. In many disease models, this rate is captured in a single compound parameter, the probability of transmission β. However, closer examination reveals how β can be further decomposed into a number of biologically relevant variables, including contact rates among individuals and the probability that contact events actually result in disease transmission. We start by introducing some of the basic concepts underlying the different approaches to modeling disease transmission and by laying out why a more detailed understanding of the variables involved is usually desirable. We then describe how parameter estimates of these variables can be derived from empirical data, drawing primarily from the existing literature on human diseases. Finally, we discuss how these concepts and approaches may be applied to the study of pathogen transmission in wildlife diseases. In particular, we highlight recent technical innovations that could help to overcome some the logistical challenges commonly associated with empirical disease research in wild populations.

Despite the wealth of data describing the ecological factors that underpin viral emergence, little is known about the evolutionary processes that allow viruses to jump species barriers and establish productive infections in new hosts. Understanding the evolutionary basis to virus emergence is therefore a key research goal and many of the debates in this area can be considered within the rigorous theoretical framework established by evolutionary genetics. In particular, the respective roles played by natural selection and genetic drift in shaping genetic diversity are also of fundamental importance for understanding the nature of viral emergence. Herein, we discuss whether there are evolutionary rules to viral emergence, and especially whether certain types of virus, or those that infect a particular type of host species, are more likely to emerge than others. We stress the complex interplay between rates of viral evolution and the ability to recognize cell receptors from phylogenetically divergent host species. We also emphasize the current lack of convincing data as to whether viral emergence requires adaptation to the new host species during the early stages of infection, or whether it is largely a chance process involving the transmission of a viral strain with the necessary genetic characteristics.

Influenza viruses belong to the family . Genus Influenza A viruses are true zoonotic agents with many animal reservoirs, whereas genus Influenza B viruses are generally considered to be a virus of humans. The genome of influenza A viruses consists of eight unique segments of single-stranded RNA of negative polarity; they are typed according to their surface proteins, hemagglutinin (HA) and neuraminidase (NA).

An emerging pathogen has been defined as the causative agent of an infectious disease whose incidence is increasing following its appearance in a new host population or whose incidence is increasing in an existing population as a result of long-term changes in its underlying epidemiology (Woolhouse and Dye 2001). Although we appear to be in a period where novel diseases are appearing and old diseases are spreading at an unprecedented rate, disease emergence is not a new phenomenon. It is almost certain that disease emergence is a routine event in the evolutionary ecology of pathogens, and part of a ubiquitous response of pathogen populations to shifting arrays of host species. While our knowledge of emerging diseases is, for the most part, limited to the time span of the human lineage, this history provides us with a modern reflection of these deeper evolutionary processes, and it is clear from this record that at many times throughout human history, demographic and behavioural changes in society have provided opportunities for pathogens to emerge.

Infection and disease in reservoir and spillover hosts determine patterns of infectious agent availability and opportunities for infection, which then govern the process of transmission between susceptible species. In this chapter, using the zoonotic agents Hendra virus and Nipah virus as examples, the pathogenesis of infection in various species including the wildlife reservoirs and domestic spillover hosts is reviewed with an emphasis on the aspects of pathogenesis which contribute to the dissemination of infection. Through these discussions, the emergence of these zoonotic agents is explored.

Two related, novel, zoonotic paramyxoviruses have been described recently. Hendra virus was first reported in horses and thence humans in Australia in 1994; Nipah virus was first reported in pigs and thence humans in Malaysia in 1998. Human cases of Nipah virus infection, apparently unassociated with infection in livestock, have been reported in Bangladesh since 2001. Species of fruit bats (genus ) have been identified as natural hosts of both agents. Anthropogenic changes (habitat loss, hunting) that have impacted the population dynamics of species across much of their range are hypothesised to have facilitated emergence. Current strategies for the management of henipaviruses are directed at minimising contact with the natural hosts, monitoring identified intermediate hosts, improving biosecurity on farms, and better disease recognition and diagnosis. Investigation of the emergence and ecology of henipaviruses warrants a broad, cross-disciplinary ecosystem health approach that recognises the critical linkages between human activity, ecological change, and livestock and human health.

Rabies has a long history of occurrence throughout Africa, spanning hundreds of years. At least four distinct species persist throughout the continent, among carnivores, bats and other mammals. Rabies virus is the most cosmopolitan member, with primary reservoirs within dogs and mongoose, but other wildlife vectors are important in viral maintenance, such as jackals. Besides a prominent toll on humans and domestic animals, the disease has an underappreciated role in conservation biology, especially for such highly endangered fauna as African wild dogs and Ethiopian wolves. Both Duvenhage and Lagos bat viruses are adapted to bats, but their epidemiology, together with Mokola virus, is poorly understood. Significantly, less than ideal crossreactivity with modern biologicals used for veterinary and public health interventions is a major cause for concern among these emerging viral agents.

Complex interactions involving humans, domestic animals, and wildlife create environments favorable to the emergence of new diseases. Today, reservoirs of , the causative agent of tuberculosis in animals and a serious zoonosis, exist in wildlife. The presence of these wildlife reservoirs is the direct result of spillover from domestic livestock in combination with anthropogenic factors such as translocation of wildlife, supplemental feeding of wildlife and wildlife populations reaching densities beyond normal habitat carrying capacities. As many countries attempt to eradicate from domestic livestock, efforts are impeded by spillback from wildlife reservoirs. It will not be possible to eradicate from livestock until transmission between wildlife and domestic animals is halted. Such an endeavor will require a collaborative effort between agricultural, wildlife, environmental and political interests.

Hantaviral diseases have been recognized for hundreds of years but, until 1976, they had not been associated with an infectious agent. When Lee and colleagues isolated what is now known as Hantaan virus, the techniques they introduced allowed further investigations into the etiology of the classical hantavirus disease, hemorrhagic fever with renal syndrome (HFRS), now known to be caused by any of multiple hantaviruses. The discovery of hantavirus pulmonary syndrome (HPS) in the New World, and that it also can be caused by any of multiple hantaviruses (family , genus ), has opened an entire field of epidemiologic, virologic, molecular, behavioral, and ecologic studies of these viruses. There appears to be a single hantavirus-single rodent host association, such that understanding the idiosyncrasies of each rodent host species and the ecologic variables that affect them are recognized as critical if we are to reduce human risk for infection.