is used to found a transgenic line. This can result in a profound genetic bottleneck unless genetic variability is restored to a production line by purposeful utilization of a mating strategy involving backcrossing of the transgenic line to a large number of distinct, presumably nontransgenic, mates. The effects of cloning are more difficult to anticipate because competing processes are at issue. On the one hand, cloning by its nature produces identical copies of a particular individual, reducing genetic 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, cloning could be employed to utilize the genetic resources from a steer that had proven to be a high performing individual. Cryopreserved cells could be utilized as donor material. Moreover, cloning is a tool that actually can be used to increase/maintain genetic variance in some situations quite independently of exploiting castrates (Seidel, Jr., 2001). The tradeoff between the competing processes of loss and gain of genetic variance would be case-specific, and it 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. Furthermore, disease could spread through susceptible populations more rapidly than through more genetically diverse populations.

A particularly serious concern that arises is 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 evade host immune response more easily in genetically uniform populations (Yuhki and O’Brien, 1990). The consequences of the failure of immunorecognition are 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 spread of “new” infectious diseases in “monocultures” of cloned or highly inbred animal populations, it also could create new reservoirs for the spread of zoonotic infections—like new strains of influenza—to humans.



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