Twelve marmosets (Saguinus mystax) were inoculated intravenously (iv) with hepatitis A virus (HAV). One died early (day 12); seven were sacrificed at the time of elevation in level of alanine aminotransferase (serum glutamic-pyruvic transaminase), and four without elevation were not sacrificed but seroconverted. In the seven marmosets sacrificed during the acute stage of illness, hepatitis A antigen (HA Ag) was detected in the liver by immunofluorescence in all cases, by immune electron microscopy in four, and by enzyme-linked immunosorbent assay (ELISA) in three. The HA Ag appeared by immunofluorescence as very fine granules in the cytoplasm of hepatocytes and Kupffer cells. The HA Ag could not be detected by immunofluorescence in biopsy specimens taken from the duodenum, jejunum, ileum, or transverse colon in any of eight marmosets in which necropsy was performed during the acute or preacute stage of illness. These findings suggest that the gut is not involved during the acute phase of HAV infection following iv inoculation into marmosets. The ELISA results showed that only three of 12 marmoset livers obtained during the acute phase of HAV infection could be used as an antigen source in serologic testing for antibody to HA Ag. Thus, marmoset livers were no better as a source of HA Ag than acute-phase stools from patients with type A hepatitis.

Moustached marmosets (Saguinus mystax) were infected intranasally with either of two low-passaged, wildlike strains of measles virus, strain Edmonston or strain JM. The infection resulted in 25 and 100% mortality, respectively, 12 to 14 days after infection. Clinical signs, gross pathological findings, and histology lacked the characteristic features of measles in other primates. A deficient immune response and widespread gastroenterocolitis appeared to be the main causes for the fatal outcome. Fluorescent-antibody staining detected large amounts of measles antigen in lymphatic tissues, the gastrointestinal and respiratory tracts, the salivary glands, pancreas, liver, kidney, and other visceral tissues. Live attenuated or inactivated measles vaccine proved equally effective in preventing fatal measles in marmosets. Challenge with live virus of animals which were primed 1 year previously with inactivated alum-absorbed vaccine resulted in a precipitous response, with a 100- to 1,000-fold increase in antibody titers. This vigorous booster response suggests the existence of a primary deficiency in lymphocyte cooperation in marmosets, which upon adequate priming is followed by extensive clonal expansion and antibody synthesis. Marmosets appear to be the most susceptible primate species to measles infection. They are capable of distinguishing differences in virulence of virus strains with a level of sensitivity not available in other animals.

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Marnosets infected intracerebrally with the wild Edmonston strain of measles virus developed encephalitis, demonstrated histologically and by the fluorescentantibody technique. The infection remained clinically silent over a 14-day observation period. Animals infected intracerebrally with the JM strain of wild measles virus had only mild encephalitic changes but died of the visceral form of measles infection. Marmosets inoculated with measles vaccine had no encephalitis and remained clinically well. Marmosets appear to be a sensitive indicator of the viscerotropic and neurotropic properties of measles virus.