Neurologic disease in captive lions (Panthera leo) with low-titer lion lentivirus infection

Brennan, Greg., Podell, Michael D., Wack, Raymund, Kraft, Susan, Troyer, Jennifer L., Bielefeldt-Ohmann, Helle and VandeWoude, Sue (2006) Neurologic disease in captive lions (Panthera leo) with low-titer lion lentivirus infection. Journal of Clinical Microbiology, 44 12: 4345-4352. doi:10.1128/JCM.00577-06

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Author Brennan, Greg.
Podell, Michael D.
Wack, Raymund
Kraft, Susan
Troyer, Jennifer L.
Bielefeldt-Ohmann, Helle
VandeWoude, Sue
Title Neurologic disease in captive lions (Panthera leo) with low-titer lion lentivirus infection
Formatted title
Neurologic disease in captive lions (Panthera leo) with low-titer lion lentivirus infection
Journal name Journal of Clinical Microbiology   Check publisher's open access policy
ISSN 0095-1137
1098-660X
Publication date 2006-09-27
Year available 2006
Sub-type Article (original research)
DOI 10.1128/JCM.00577-06
Open Access Status File (Publisher version)
Volume 44
Issue 12
Start page 4345
End page 4352
Total pages 8
Place of publication Washington, DC, United States
Publisher American Society for Microbiology
Language eng
Abstract 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.
Keyword Lentiviruses
Feline Immunodeficiency Virus
Panthera leo
Lymph
Locomotor Performance
Neuropathogens
Abnormalities
Electrodiagnostic Evaluation
Radiologic Imaging
Phylogenetic Analyses
Human immunodeficiency virus--HIV
Q-Index Code C1
Institutional Status Non-UQ

Document type: Journal Article
Sub-type: Article (original research)
Collections: Excellence in Research Australia (ERA) - Collection
School of Veterinary Science Publications
 
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