RVLA infection results in a net secretory state for water and in impaired sodium absorption. Relatively little is known about immune mechanisms in RVLA infection, but it is likely that there are similarities to immunity to mouse rotavirus infection. In addition to acquired immunity, intestinal mucins may inhibit rotavirus replication and may be dependent on specific mucin-virus interactions. Natural infection of rats with RVLA would probably confound studies involving the intestinal system. MTV is considered a member of the Herpesviridae, which are dsDNA viruses.
Transmission appears to be via direct contact and possibly via transmammary passage.
Natural infections are subclinical. Pathologic changes are limited to transient lymphoid necrosis of the thymus, lymph nodes, and spleen of neonatal mice, followed by a diffuse granulomatous response with giant cells, which eventually resolves. The virus also infects and persists in salivary glands. Natural infection of laboratory mice might therefore temporarily interfere with immune competence. Reovirus type 3.