PSIP1 and viral infectious disease: The model accounts for the retention of the weakly favored target DNA consensus sequence at the sites of HIV-1 integration [82]–[85] in the absence of LEDGF/p75 [18], and also explains why a detectable shift in the distribution of HIV-1 integration sites occurred under partial LEDGF/p75 knockdown conditions that nonetheless were insufficiently weak to affect the overall level of virus infection [14].