FUNCTIONAL EXCHANGE OF AN ONCORETROVIRUS AND A LENTIVIRUS MATRIX PROTEIN

To map functional domains in the retroviral Gag protein we have constr ucted chimeric viruses where regions of the murine leukemia virus (MuL V) Gag protein have been replaced with analogous sequences from human immunodeficiency virus type 1 (HIV-1). Here we describe the chimeric v irus MuLV(MA(HIV)) which contains the HIV-1 matrix (MA) protein in pla ce of the MuLV MA. MuLV(MA(HIV)) is infectious but grows at a reduced rate compared with wild-type MuLV. We found that the partial defect in replication of the chimeric virus is at a late stage in the viral lif e cycle. The MuLV(MA(HIV)) Gag proteins are distributed aberrantly wit hin cells and are not associated with cellular membranes. Unlike MuLV, HIV-1 is able to integrate into growth-arrested cells. Incorporation of the HIV-1 IMA, which is known to play a role in infection of nondiv iding cells, does not enable MuLV(MA(HIV)) to be expressed in growth-a rrested cells. While it possesses no amino acid homology, we found tha t the HIV-1 MA can efficiently replace the MuLV matrix protein in infe ction.