variability relative to what would have been transmitted via conventional breeding. On the other hand, cloning makes it possible to save and utilize genetic variability that would not otherwise be available, for example, the genetic resources from a steer proven to be high performing. The tradeoff between the competing processes is hard to quantify in the absence of simulation modeling with validation from field observations. Whatever the mechanism causing it, loss of genetic diversity could limit the potential for future genetic improvement of breeds by selective breeding or biotechnologic approaches. Further, disease could spread through susceptible populations more rapidly than through more genetically diverse populations.

This latter concern is well documented and several studies illustrate the susceptibility of species with low genetic diversity to infectious disease. Diversity of animal populations, particularly at major histocompatibility (MHC) loci, is a major factor preventing spread of disease, particularly viral disease (Xu et al., 1993; Schook et al., 1996; Kaufman and Lamont, 1996; Lewin et al., 1999). Different MHC types recognize different viral or bacterial epitopes encoded by pathogens for presentation to the immune system. In genetically diverse populations, pathogens can evade the immune response only if they adapt to each individual MHC type following transmission from one individual to another. The requirement for this evolutionary process provides a population of animals with significant protection against the spread of infection. Pathogens can more easily evade host immune response in genetically uniform populations (Yuhki and O’Brien, 1990). The consequences of the failure of immunorecognition is illustrated by the deadly epidemics of diseases—such as measles—spread by initial contact between Europeans and isolated New World populations that lacked adequate MHC diversity. Not only could enhanced susceptibility create significant risk for the spread of “new” infectious diseases in “monocultures” of cloned or highly inbred animal populations; it also could create new reservoirs for spread of zoonotic infections—like new strains of influenza—to humans. The seriousness of these concerns, particularly relative to current practice (see Chapter 1) obviously must vary considerably from one type of animal to another, and might be alleviated with further technologic advances.

CONCLUSIONS

The technology for modifying the germline of domestic animals is being advanced at a very rapid pace. Indeed, some major advances were reported during the brief period in which this report was being prepared. Although many of the detailed issues discussed in this chapter will no doubt soon become outdated to be replaced by new ones not yet considered, some general issues will remain. In particular, there will (probably) always be concerns regarding



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