Lack of Genomic Reassortment Following Infection of Infant Rats with Group A and Group B Rotaviruses

Abstract

Rotaviruses are members of the Reoviridae family of viruses and are recognized as an important cause of diarrheal disease in infants and young children [1]. Rotaviruses have been shown to display variation in neutralization specificities on the basis of epitopes mapped to outer capsid proteins [2]. Until recently it was thought that all rotaviruses shared common group-reactive antigenic determinants located on internal proteins. It is the widespread distribution of these determinants that has allowed for the diagnosis and study of rotavirus gastroenteritis by means of sensitive immunoassay systems [3]. Recently, however, a number of fastidious rotavirus strains have been identified that do not contain these common determinants. These agents have been called atypical rotaviruses or non-group A rotaviruses to distinguish them from the group A viruses that contain the recognized common antigen. The non-group A rotaviruses have been further divided into groups B, C, D, and E on the basis of the length and nucleotide content of RNA gene segments [4], nucleic acid hybridization [5], and antigenic reactivity [6]. Non-group A rotaviruses have been identified as etiologic