capsid surface is uneven, has plateaus and canyons. aa residue lining canyon more conserved than others
bind to host cell receptors called CD155
what is CD155
member of ig superfamily. found on epithelial tissues and nervous tissues
attachment to CD155 causes endocytosis. conformational change in VP1. hydrophobic N terminus of VP1 which is internal in virion becomes exposed on capsid surface. can insert in endosomal membrane forming pore
can exit capsid. released into cytoplasm. called uncoating
VPg is removed from genome, +ive strand RNA is translated as one polyprotein
part of it folds up and becomes active protease that cuts polyprotein in 2 places. pieces further cut up by another viral protease
viral RNA has no cap, 5’ UTR forms series of stem loops which fn as internal ribosome entry site. allows binding of 40S r subunit. process uses C terminal fragment of a host eIF called eIF4G
eIF4G is required for 40S r subunit to bind to 5’ cap of host mRNA. viral protease cleaves eIF4G into 2 pieces and host mRNA cannot be translated
inhibition of mRNA host translation and is required for viral mRNA translation
endomembrane system b/c it is naked therefore does not have spike proteins
viral protein inhibits fusion of transport vesicle from the RER to the golgi apparatus
surface of membrane vesicles
used as mRNA and new genome
surface of membrane vesicle. +ive strand RNA used as template to make -ive RNA
VPg is a 22 aa residue protein. RDRP adds 2 uracil to VPG
primer is transferred to 3’ end of +ive strand RNA H2 bonds to poly-a-tail. RDRP uses 3’ OH of primer to synthesize -ive RNA. binding of primer to polyatail ensures synthesis occurs correct site. 2 strands separate
RI used as template. RDRP uses same primer
polyatail is virally encoded. dsRNA is separated
-ive RI. + is genome, also VPG removed to make mRNA
VP0,3,1 form capsid enclosing genome. VP0 cleaved to produce VP4 AND VP2. VP4 interacts w/other capsid components providing stability to virion
lysis