6 
human cgIIs, there is a good chance that it would not be 
subject to the host's regulatory mechanism. Thus there is 
a real risk of completely disrupting some normal metabolic 
pathv/ay, sirailar to instances of inborn metcxbolic diseases where 
the defect appears to be in a control gene (or enzyme, such as 
ATPase) , resulting in a serious pathologic state. 
(2) There is a ch£ince that a piece of "foreign" DNA, 
even a relatively small piece, could exert a control function 
in tlie host cell, also leading to the disruption of a metabolic 
patJiway . 
(3) There is the risk that any foreign protein, even if 
it has no enzymatic function, could, if expressed in or on the 
surface of mammalian cells in sufficient quantity, elicit 
an immune response from the host, leading to the destruction of 
tlie cells, as in known auto immune diseases following certain 
bacterial infections. 
(4) The genetic basis of virulence in viruses or bacteria 
is not understood. Why certain viruses infect some hosts readily, 
but only to a benign degree in closely related hosts is not 
known. There is not yet any evidence that SV 40 virus and polyoma 
virus produce any pathologic symptoms in humans, although they 
infect many animals and produce tumors in certain hosts. SV 40 
virus has been found occasionally in patients suffering a variety 
of serious diseases, inluding cancer, but no causal relationship 
has been established. Papova virus is a himan pathogen and is 
similar to SV 40 in niany ways. Just how subtle a genetic alteration 
Appendix K — 60 
