Chronic wasting disease agents in nonhuman primates.
Bottom Line: Assessment of its zoonotic potential is critical.To evaluate primate susceptibility, we tested monkeys from 2 genera.We found that 100% of intracerebrally inoculated and 92% of orally inoculated squirrel monkeys were susceptible, but cynomolgus macaques were not, suggesting possible low risk for humans.
Chronic wasting disease is a prion disease of cervids. Assessment of its zoonotic potential is critical. To evaluate primate susceptibility, we tested monkeys from 2 genera. We found that 100% of intracerebrally inoculated and 92% of orally inoculated squirrel monkeys were susceptible, but cynomolgus macaques were not, suggesting possible low risk for humans.
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Mentions: Two SM-CWD brain samples were inoculated into squirrel monkeys and cynomolgus macaques to verify that SM-CWD was infectious, test for further adaptation, and to see if SM-CWD was infectious to a broader range of nonhuman primates. Two squirrel monkeys inoculated intracerebrally with SM-CWD brain homogenates (SMP2-CWD) were euthanized at 23–24 mpi (Table 1). These incubation periods decreased by >11 months compared with that of the donor squirrel monkey. Neurologic signs in the 2 SMP2-CWD were more pronounced than observed during the first passage; however, weight loss was reduced. Neuropathologic examination and Western blot for PrPres confirmed TSE in both squirrel monkeys. In contrast to SM-CWD infections, the SMP2-CWD-infected brains had spongiform lesions and PrPres deposition in the occipital lobe (Figure 2, panels A, B). Biochemical comparison of glycoform patterns among CWD, SM-CWD, and SMP2-CWD were made by using 3 different anti-PrP antibodies (L42, 6H4, and 3F4) (Technical Appendix). In all cases, SM2-CWD had a greater proportion of unglycosylated PrPres and a lower proportion of double glycosylated PrPres than did SM-CWD (Figure 2, panel C). The decreased time of manifestation of disease, differences in glycoform patterns, and distribution of PrPres in brain tissue suggested that the CWD agent was still adapting within the squirrel monkey. However, similar to CWD, SM-CWD had not caused prion disease in cynomolgus macaques by 72 mpi (Table 2).