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recombinant virus called a mink focus 
forming virus which results from 
recombination between MoMLV and 
endogenous murine leukemia virus 
sequences. These murine endogenous viral 
sequences are not present in humans. Also 
adult mice are not known to develop 
lymphomas after MoMLV, only newborn mice 
are susceptible, suggesting some step in 
T-cell development might be important in 
cellular transformation. Lastly, the 
tropism (ie specificity of MoMLV for the 
T-cell) and the strain dependence of 
MoMLV may not be shared with any human 
cell . 
Nevertheless, it is theoretically 
possible for a retrovirus to insert into 
a proto-oncogene or tumor suppressor gene 
leading to cellular transformation. The 
complex virus-oncogene tropism in the 
murine system, the presence of two copies 
of each tumor suppressor gene in most 
cells, and the multi-step process of 
malignant transformation suggest that the 
likelihood of RMGT leading to malignancy 
in primates will be low. 
Recombination with human endogenous 
retroviral sequences 
A theoretical concern is recombination of 
the retroviral vector with human 
endogenous retroviral sequences leading 
to the production of a replication- 
competent human retrovirus. The 
probability of this occurring appears 
small. No replication-competent human 
endogenous retrovirus has ever been 
isolated and all known sequences have 
deletions and frame-shift mutations in 
the viral genes. The sequences defective 
in human endogenous retroviruses (namely 
gag, pol, and env) , are the sequences 
deleted from the LNL-6 vector, so LNL-6 
is unable to provide the needed sequences 
to restore function to human endogenous 
retroviral sequences. Also, there is no 
homology known between the LNL-6 vector 
and the human retroviral sequences, so 
that homologous recombination is not 
expected. In addition, variation in the 
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Recombinant DNA Research, Volume 15 
