Baboons in a captive breeding colony were monitored twice a year, and new additions were screened on arrival for shedding of Herpesvirus papio 2 (HVP2) and serologic reactivity to the agent. For 128 individual animals tested over a period of 1.5 years, shedding of infective virus was detected in 13 of 342 swab specimens (3.8%), each of these incidents representing shedding by a different animal. Among long-term colony animals, infective virus was recovered on only two occasions (5 of 236 swab specimens from five individuals). In all but one instance, animals shedding virus were infants, not adults, and all animals were shedding virus in the oral cavity. One of these five instances was an isolated case, but four (three infants and one adult) were clustered within a single breeding group. Molecular analyses of the HVP2 isolates from this cluster indicated that they likely arose from a single common source, probably the mother of one of the infants. None of 31 wildcaught baboons added to the colony during this period were found to be shedding infective virus, despite 93.5% of them being seropositive for HVP2. In contrast, 6 of 18 adult baboons (all seropositive) transferred into the colony from another breeding colony were found to be shedding HVP2 either orally (3 of 6) or genitally (3 of 6). In addition, 2 of 8 juvenile baboons in this shipment were found to be shedding virus in the oropharynx. Overall, 10 of 13 instances of HVP2 isolation were from the oropharynx rather than the genital tract, and 6 of 13 baboons shedding virus were infants or juveniles rather than adults. These results suggest that, although venereal transmission of HVP2 occurs among adult animals, oral infection of young, sexually immature baboons is not uncommon.
|Original language||English (US)|
|Number of pages||6|
|Journal||Laboratory Animal Science|
|State||Published - 1998|
ASJC Scopus subject areas
- Biochemistry, Genetics and Molecular Biology(all)
- Animal Science and Zoology