Arch Virol (1998) 143: 1233–1244
Serotypic characterization of outer capsid spike protein VP4
of vervet monkey rotavirus SA11 strain
Y. Hoshino, R. W. Jones, and A. Z. Kapikian
Epidemiology Section, Laboratory of Infectious Diseases, National Institute of Allergy
and Infectious Diseases, National Institutes of Health, Bethesda, Maryland, U.S.A.
Accepted January 8, 1998
Summary. The vervet monkey rotavirus SA11, a prototype strain of group A
rotaviruses, has been shown to possess VP7 serotype 3 speciﬁcity but its
neutralization speciﬁcity with regard to the other outer capsid protein VP4 has
not been elucidated. We thus determined its VP4 speciﬁcity by two-way cross-
neutralization with guinea pig antiserum prepared with a single gene substitution
reassortant that had only the VP4-encoding gene from the simian rotavirus SA11
strain and remaining ten genes from human rotavirus DS-1 strain (G serotype 2).
The SA11 VP4 was related antigenically in a one-way fashion to rhesus
monkey rotavirus MMU18006 VP4 (a P5B strain) and marginally to human
and canine rotavirus VP4s with P serotype 5A speciﬁcity. In addition, the SA11
VP4 was shown to be distinct antigenically from those of other known P serotypes
(1–4, and 6–11) as well as those of uncharacterized equine, lapine, and avian
rotavirus strains. The SA11 VP4 is thus proposed for classiﬁcation as a P5B
Simian agent (SA) 11 was isolated in 1958 in vervet monkey kidney cell cultures
from a rectal swab obtained from a healthy vervet monkey at the Poliomyelitis
Research Foundation in Johannesburg, Republic of South Africa . Later the
SA11 virus was classiﬁed into the genus Rotavirus in the Reoviridae family .
Because it readily grew to a high titer in cell cultures, the SA11 virus quickly
became a major reference prototype strain in studies of group A rotaviruses. Thus,
the SA11 virus has played a key role in understanding of the molecular biology of
rotavirus with regard to the structure and function of rotavirus gene(s) and gene
product(s), as well as rotavirusmorphogenesis, genetics, and pathogenesis [1, 19].