Although host
protein synthesis is preferentially inhibited, there is a steady decline in the ability of Chinese hamster ovary (CHO) cells infected with
vesicular stomatitis virus (VSV) to synthesize both host and
viral proteins. We previously reported finding an
mRNA-
ribonucleoprotein particle (
mRNP) that contained all five VSV mRNAs and
viral N protein exclusively. This particle apparently regulates translation by sequestering a majority of the VSV
mRNA made late in
infection and thus rendering it unavailable for
protein synthesis. In the present investigation the
mRNP was also shown to inhibit in vitro
protein synthesis in rabbit reticulocyte and wheat germ lysates programmed with
mRNA isolated from VSV-infected cells. The synthesis of
eIF-2 X
GTP X Met-
tRNA (ternary) complex, the first step in initiation of
protein synthesis, was markedly inhibited by the
mRNP. The inhibition was partially reversed by addition of purified
eIF-2 to the inhibited lysate or ternary complex formation reaction. These results indicate a dual role of the
mRNP in regulating
protein synthesis during
infection. Nucleocapsid also inhibited in vitro
protein synthesis, although this inhibition was not reversed by
eIF-2. Nucleocapsid did not inhibit ternary complex formation in vitro. Consequently, nucleocapsid may also regulate in vivo
protein synthesis, but by a mechanism different from the
mRNP.