Rotavirus group A outer capsid glycoprotein VP7 (G1) (VP7 G1)

Rotavirus VP7 G1 refers to the **outer capsid glycoprotein VP7 from group A rotaviruses of G1 serotype**, a calcium-binding viral structural protein forming the outermost layer of the triple‑shelled rotavirus particle.[1][4][5] VP7 is a trimeric glycoprotein arranged in a T=13 icosahedral lattice that caps the underlying VP6 layer and locks the spike protein VP4 in place; removal of Ca²⁺ leads to VP7 trimer dissociation, uncoating, and conformational changes in VP4 required for membrane penetration during cell entry.[1][5] VP7 interacts with cellular receptors after initial attachment by VP4 and has been implicated in post-attachment interactions, including proposed binding to integrins once uncoated.[1][4] It is one of the two principal outer capsid antigens (with VP4) that induce **neutralizing antibodies**, and VP7-specific antibodies correlate with protection from rotavirus infection; structural studies show that neutralizing monoclonal antibodies bind conformational epitopes on the trimer (regions 7‑1 and 7‑2) and can neutralize infection by stabilizing the trimer and preventing uncoating.[1][2] The G1 designation reflects the VP7-defined G serotype/genotype, and VP7 G1 sequences cluster into defined phylogenetic lineages; specific amino acid signatures in exposed regions (including residues 87–101 and 208–211) determine G1 serotype and define neutralizing epitopes used for genotyping and vaccine design.[1][3] Licensed human rotavirus vaccines incorporate G1 VP7 as a major antigenic component, and comparison of circulating G1 VP7 sequences with vaccine strains shows lineage-specific amino acid and glycosylation differences in neutralization epitopes that may modulate antigenicity and vaccine match.[3][4]

Other names

Rotavirus VP7 G1Outer capsid glycoprotein VP7 (rotavirus G1)Rotavirus A VP7 G1Rotavirus group A glycoprotein VP7 (G1 serotype)Rotavirus VP7 outer capsid protein (G1)

Induction of VP7-specific neutralizing antibodies that block viral entry and uncoating by stabilizing the VP7 trimer and/or sterically hindering receptor interactions[1][2][3] Vaccine-induced polyclonal B‑cell activation and production of epitope‑specific antibodies against VP7 neutralizing epitopes (regions 7‑1 and 7‑2), correlating with protection from infection[1][2][3] Inhibition of Ca²⁺-dependent VP7 dissociation, thereby preventing conformational changes in VP4 required for membrane penetration and productive infection[1][2]