Yt. Ting et al., SIMIAN SARCOMA-ASSOCIATED VIRUS FAILS TO INFECT CHINESE-HAMSTER CELLSDESPITE THE PRESENCE OF FUNCTIONAL GIBBON APE LEUKEMIA-VIRUS RECEPTORS, Journal of virology (Print), 72(12), 1998, pp. 9453-9458
We have sequenced the envelope genes from each of the five members of
the gibbon ape leukemia virus (GALV) family of type C retroviruses. Fo
ur of the GALVs, including GALV strain SEATO (GALV-S), were originally
isolated from gibbon apes, whereas the fifth member of this family, s
imian sarcoma-associated virus (SSAV), was isolated from a woolly monk
ey and shares 78% amino acid identity with GALV-S, To determine whethe
r these viruses have identical host ranges, we evaluated the susceptib
ility of several tell lines to either GALV-S or SSAV infection. GALV-S
and SSAV have the same host range with the exception of Chinese hamst
er lung E36 cells, which are susceptible to GALV-S but not SSAV. We us
ed retroviral vectors that differ only in their envelope composition (
e.g., they contain either SSAV or GALV-S envelope protein) to show tha
t the envelope of SSAV restricts entry into E36 cells. Although unable
to infect E36 cells, SSAV infects GALV-resistant murine cells express
ing the E36-derived viral receptor, HaPit2. These results suggest that
the receptors present on E36 cells function for SSAV. We have constru
cted several vectors containing GALV-S/SSAV chimeric envelope proteins
to map the region of the SSAV envelope that blocks infection of E36 c
ells. Vectors bearing chimeric envelopes comprised of the N-terminal r
egion of the GALV-S SU protein and the C-terminal region of SSAV infec
t E36 cells, whereas vectors containing the N-terminal portion of the
SSAV SU protein and C-terminal portion of GALV-S fail to infect E36 ce
lls. This finding indicates that the region of the SSAV envelope prote
in responsible for restricting SSAV infection of E36 cells lies within
its amino-terminal region.