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JCM Accepts, published online ahead of print on 27 September 2006
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J. Clin. Microbiol. doi:10.1128/JCM.00577-06
Copyright (c) 2006, American Society for Microbiology and/or the Listed Authors/Institutions. All Rights Reserved.

NEUROLOGIC DISEASE IN CAPTIVE LIONS (PANTHERA LEO) WITH LOW TITER LION LENTIVIRUS INFECTION

Greg Brennan, Michael D. Podell, Raymund Wack, Susan Kraft, Jennifer L. Troyer, Helle Bielefeldt-Ohmann, and Sue Vande Woude*

From the Departments of Microbiology, Immunology, and Pathology, (Brennan, Troyer, Bielefeldt-Ohmann, VandeWoude) and Environmental and Radiologic Health Sciences (Kraft), Colorado State University, Fort Collins, CO, 80523-1619, USA; From the Department of Veterinary Clinical Sciences, The Ohio State University, Columbus, OH, 43210, USA (Podell); From the Department of Medicine and Epidemiology, University of California, Davis CA 95616-8747, USA (Wack)

* To whom correspondence should be addressed. Email: suev{at}lamar.colostate.edu.


   Abstract

Lion lentivirus (LLV, also FIV-Ple) is present in free-ranging and captive lion (Panthera leo) populations with up to 100% seroprevalence; however, clinical signs are rarely reported. LLV displays up to 25% inter-clade 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 partial lentiviral genomic sequence and to quantify proviral burden in eight post-mortem tissues. Phylogenetic analysis demonstrated the virus was consistent with LLV diagnosed in other captive and free-ranging lions. Despite progressive neurologic signs, proviral load in tissues, including several regions of brain, was low, and gross and histopathologic changes in the brain were minimal. These findings suggest the symptoms in these animals resulted from non-specific encephalopathy, similar to HIV, FIV and SIV neuropathy, 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, and indicates areas for further research of lentiviral infections of seemingly adapted natural hosts, including mechanisms of host control and viral adaptation.




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