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Journal of Virology, October 2006, p. 10281-10284, Vol. 80, No. 20
0022-538X/06/$08.00+0 doi:10.1128/JVI.00361-06
Copyright © 2006, American Society for Microbiology. All Rights Reserved.
HIV Drug Resistance Program,1 Data Management Services, National Cancer Institute at Frederick, Frederick, Maryland 21702-12012
Received 21 February 2006/ Accepted 31 July 2006
When the endogenous polypurine tract (PPT) of the Rous sarcoma virus (RSV)-derived vector RSVP(A)Z was replaced with alternate retroviral PPTs, the fraction of unintegrated viral DNA with the normal consensus ends significantly decreased and the retention of part of the PPT significantly increased. If the terminus of the U3 long terminal repeat (LTR) is aberrant, RSV integrase can correctly process and integrate the normal U5 LTR into the host genome. However, the canonical CA is not involved in joining the aberrant U3 LTR to the host DNA, generating either large duplications or deletions of the host sequences instead of the normal 5- or 6-bp duplication.
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