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Journal of Clinical Microbiology, December 2006, p. 4345-4352, Vol. 44, No. 12
0095-1137/06/$08.00+0     doi:10.1128/JCM.00577-06
Copyright © 2006, American Society for Microbiology. All Rights Reserved.

Neurologic Disease in Captive Lions (Panthera leo) with Low-Titer Lion Lentivirus Infection

Greg Brennan,^1, Michael D. Podell,² Raymund Wack,^3, Susan Kraft,⁴ Jennifer L. Troyer,^1, Helle Bielefeldt-Ohmann,¹ and Sue VandeWoude^1*

Departments of Microbiology, Immunology, and Pathology,¹ Environmental and Radiologic Health Sciences, Colorado State University, Fort Collins Colorado 80523,⁴ Department of Veterinary Clinical Sciences, The Ohio State University, Columbus, Ohio 43210,² Department of Medicine and Epidemiology, University of California, Davis, California 95616-8747³

Received 17 March 2006/ Returned for modification 23 July 2006/ Accepted 17 September 2006

Lion lentivirus (LLV; also known as feline immunodeficiency virus of lion, Panthera leo [FIVPle]) is present in free-ranging and captive lion populations at a seroprevalence of up to 100%; however, clinical signs are rarely reported. LLV displays up to 25% interclade sequence diversity, suggesting that it has been in the lion population for some time and may be significantly host adapted. Three captive lions diagnosed with LLV infection displayed lymphocyte subset alterations and progressive behavioral, locomotor, and neuroanatomic abnormalities. No evidence of infection with other potential neuropathogens was found. Antemortem electrodiagnostics and radiologic imaging indicated a diagnosis consistent with lentiviral neuropathy. PCR was used to determine a partial lentiviral genomic sequence and to quantify the proviral burden in eight postmortem tissue specimens. Phylogenetic analysis demonstrated that the virus was consistent with the LLV detected in other captive and free-ranging lions. Despite progressive neurologic signs, the proviral load in tissues, including several regions of the brain, was low; furthermore, gross and histopathologic changes in the brain were minimal. These findings suggest that the symptoms in these animals resulted from nonspecific encephalopathy, similar to human immunodeficiency virus, FIV, and simian immunodeficiency virus (SIV) neuropathies, rather than a direct effect of active viral replication. The association of neuropathy and lymphocyte subset alterations with chronic LLV infection suggests that long-term LLV infection can have detrimental effects for the host, including death. This is similar to reports of aged sootey mangabeys dying from diseases typically associated with end-stage SIV infection and indicates areas for further research of lentiviral infections of seemingly adapted natural hosts, including mechanisms of host control and viral adaptation.

Published ahead of print on 27 September 2006.

Present address: Department of Microbiology, University of Washington, Seattle, WA 98195.

Present address: Sacramento Zoo, 3900 Land Park Dr., Sacramento, CA 95822.

Present address: Laboratory of Genomic Diversity, SAIC-Frederick, Inc., NCI-Frederick, Frederick, MD 21702.

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