英语翻译TheinabilityofPr4\235tosuppressanIFNresponseininfectedcellsmayaccountforitsgrowthdefectinmacrophagecellcultures.Pr4\235exhibitsa100-to1,000-foldgrowthdefectinmacrophagecellculturesthatischaracterizedbyear

Question

英语翻译
The inability of Pr4\235 to suppress an IFN response in
infected cells may account for its growth defect in macrophage
cell cultures.Pr4\235 exhibits a 100- to 1,000-fold growth defect
in macrophage cell cultures that is characterized by early
apoptotic cell death (54) (Zsak,unpublished).IFN-α has been
shown to inhibit ASFV replication in monocytes and alveolar
macrophages (16).IFN-induced antiviral cellular responses,
together with the potential for increased PKR activity in
Pr4△35-infected cells,may in part be responsible for the
growth defect and the apoptotic response.Increased apoptosis
of Pr4△35-infected cells may involve PKR or the IFN-induced
CARD domain-containing helicase gene.Increased expression
of the PKR activator gene PACT and decreased expression of
the inhibitor of PKR (P58) suggest that Pr4\235 infection may
affect PKR activity.PKR has a proapoptotic effect mediating
dsRNA- and virus-induced programmed cell death and renders
cells extremely susceptible to virus-induced apoptosis
(20).The helicase gene induced in Pr4△35-infected cells resembles
cellular Mda-5,an early-response gene responding
primarily to IFN-β and tumor necrosis factor α.It functions as
a dsRNA-dependent ATPase that contains a caspase recruitment
motif (CARD) (27).Direct involvement of Mda-5 in the
prevention or induction of apoptosis has yet to be clearly
demonstrated; however,caspases are critical activators of apoptosis,
and Mda-5 expression inhibits colony formation in melanoma
cells (27).

Answer 1

The inability of Pr4\235 to suppress an IFN response in
infected cells may account for its growth defect in macrophage
cell cultures.Pr4\235 exhibits a 100- to 1,000-fold growth defect
in macrophage cell cultures that is characterized by early
apoptotic cell death (54) (Zsak,unpublished).IFN-α has been
shown to inhibit ASFV replication in monocytes and alveolar
macrophages (16).IFN-induced antiviral cellular responses,
together with the potential for increased PKR activity in
Pr4△35-infected cells,may in part be responsible for the
growth defect and the apoptotic response.Increased apoptosis
of Pr4△35-infected cells may involve PKR or the IFN-induced
CARD domain-containing helicase gene.Increased expression
of the PKR activator gene PACT and decreased expression of
the inhibitor of PKR (P58) suggest that Pr4\235 infection may
affect PKR activity.PKR has a proapoptotic effect mediating
dsRNA- and virus-induced programmed cell death and renders
cells extremely susceptible to virus-induced apoptosis
(20).The helicase gene induced in Pr4△35-infected cells resembles
cellular Mda-5,an early-response gene responding
primarily to IFN-β and tumor necrosis factor α.It functions as
a dsRNA-dependent ATPase that contains a caspase recruitment
motif (CARD) (27).Direct involvement of Mda-5 in the
prevention or induction of apoptosis has yet to be clearly
demonstrated; however,caspases are critical activators of apoptosis,
and Mda-5 expression inhibits colony formation in melanoma
cells (27).