This initial binding changes the shape of the SU protein to one that facilitates interaction between SU and the chemokine receptor CXCR4.[9] This interaction causes the viral and cellular membranes to fuse, allowing the transfer of the viral RNA into the cytoplasm, where it is reverse transcribed and integrated into the cellular genome through nonhomologous recombination. Once integrated into the host cell's genome, the virus can lay dormant in the asymptomatic stage for extended periods of time without being detected by the immune system or can cause lysis of the cell.[2][11]