Analysis of VSV pseudotype virus infection mediated by rubella virus envelope proteins

Sakata, Masafumi; Tani, Hideki; Anraku, Masaki; Kataoka, Michiyo; Nagata, Noriyo; Seki, Fumio; Tahara, Maino; Otsuki, Noriyuki; Okamoto, Kiyoko; Takeda, Makoto; Mori, Yoshio

The above data demonstrated that immune cells are much less susceptible to RV than non-immune cell lines. However, previous studies demonstrated that lymphocytes become susceptible to RV after stimulation by mitogen [41] [42] [43] . U937 and THP-1 cells, derived from histiocytic lymphoma and monocytic lymphoma, respectively, were stimulated with PMA, and then infected with VSV FLuc -RV/ CE2E1 or VSV FLuc -G. Unstimulated control cells were also infected with VSV FLuc -RV/CE2E1 or VSV FLuc -G. The positive effect on VSV FLuc -RV/CE2E1 entry by PMA stimulation was evident in THP-1 cells. The infectivity of VSV FLuc -G was unchanged by PMA stimulation, but the infectivity of VSV FLuc -RV/CE2E1 was increased by ~30-fold (Fig. 5 ). Similar effect was also observed in U937 cells. The infectivity of VSV FLuc -G and VSV FLuc -RV/ CE2E1 were increased by ~10-fold and ~200-fold, respectively (Fig. 5) . Therefore, the increase in VSV FLuc -RV/ CE2E1 infection was possibly in part due to the positive effect by PMA for VSV replication. However, further increase in VSV FLuc -RV/CE2E1 suggested that the VSV FLuc -RV/CE2E1 entry by RV envelope proteins was promoted by PMA stimulation. These data suggested that immune cells become susceptible to RV infection after stimulation, although the levels are still much lower than those in non-immune cells.