As the reverse transcriptase activity of the HIV-1 RT heterodimer catalyzes the extension of the minus-strand DNA, the RNaseH activity catalyzes the degradation of the complementary viral genomic RNA sequences. Telesnitsky and Goff (1993) observed that two defective forms of reverse transcriptase can complement to restore retroviral infectivity. The RNase H active site is positioned within the HIV-1 RT heterodimer so as to attack the RNA strand of the RNA:DNA duplex at a point 18 bases behind the site of reverse transcription (Furfine and Reardon 1991; Ghosh et al. 1995; Gopalakrishnan et al. 1992; Wohrl and Moelling 1990). The rate of RNase H cleavage is substantially lower than the rate of DNA synthesis and the level of its activity in vivo is unclear, however (Kati et al. 1992). The product of these combined DNA synthesis and RNA degradation events is a DNA strand still duplexed with extended viral genomic RNA fragments.