SIV in primates. I've got tons of stuff relating to neurological dysfunction, no reason why all other boxes would not be ticked:
SIV model of neuroaids
http://www.scripps.edu/mind/fox/research.html
J Neurovirol. 2008 Aug;14(4):301-8.
Behavioral and neurophysiological hallmarks of simian immunodeficiency virus infection in macaque monkeys.
Cheney PD, Riazi M, Marcario JM.Department of Molecular and Integrative Physiology, University of Kansas Medical Center, Kansas City, Kansas 66160-7185, USA.
pcheney@kumc.edu
Macaque monkeys infected with various neurovirulent forms of simian immunodeficiency virus (SIV) represent highly effective models, not only of systemic acquired immunodeficiency virus (AIDS), but also neuroAIDS. Behavioral studies with this model have clearly established that SIV-infected monkeys show both cognitive and motor impairments resembling those that have been reported in human immunodeficiency virus (HIV)-infected humans. This paper combines data from a number of behavioral studies in SIV-infected macaque monkeys to obtain an overall estimate of the frequency of impairments in various motor and cognitive domains. The results were then compared to similar data from studies of HIV-infected humans. Whereas cognitive functions are most commonly impaired in HIV-infected humans, m
otor function is the domain most commonly impaired in SIV-infected monkeys. Electrophysiological studies in SIV-infected macaques have revealed deficits in motor-, somatosensory-, visual-, and auditory-evoked potentials that also resemble abnormalities in human HIV infection. Abnormalities in motor-evoked potentials were among the most common evoked potential deficits observed. Although differences in behavioral profiles of human HIV disease and SIV disease in monkeys exist, the results, nevertheless, provide strong validation for the use of macaque models for translational studies of the virology, immunology, pathophysiology, and treatment of neuroAIDS.PMID: 18780231
....Significant correlations were found between impaired performance on the bimanual motor test and axonal damage (accumulation of beta-amyloid precursor protein in the corpus callosum) as well as increased microglial activation and macrophage infiltration (levels of CD68 and Ham56 immunostaining). These results suggest that axonal damage is related to the behavioral impairment induced by infection with SIV.
The axonal damage may result from neuroimmune responses, including microglial and macrophage activation. Therefore, axonal damage may be a morphologic manifestation of neuronal dysfunction that underlies development of behavioral impairment in HIV/SIV CNS infection. PMID: 12907390
This model provides outstanding opportunities to delineate the pathogenesis of infection, to study the regulation of virus gene expression, and to identify host immune responses throughout the acute, clinically silent and late stages of infection. Using this model, the authors have demonstrated that the virus enters the brain within days after inoculation, that CCL2 (monocyte chemoattractant protein [MCP]-1) plays a major role in recruiting monocytes/macrophages to the brain, and that type I interferons are critical in suppressing early virus replication and inducing viral latency. This model provides a rigorous platform for the testing of potential antiretroviral, immune reconstituting, and/or neuroprotective agents and already has been used to confirm the neuroprotective properties of
minocycline, which now is being tested in clinical trials of HIV-infected individuals. PMID: 18780232
Gerwyn you'll love this one:
... STUDY DESIGN/METHODS: Cognitive and motor function was assessed in rhesus macaque monkeys infected with simian immunodeficiency virus (SIV). In situ hybridization, immunohistochemistry, and quantitative image analysis were employed to assess the relations among productive infection, NO synthase (iNOS), and dendritic injury. RESULTS: Productive infection of cells of the macrophage lineage in CNS is associated with inflammation, increased expression of iNOS, and dendritic injury. The tests of cognitive and motor function employed were abnormal in both animals that had evidence of productive infection and those that did not. CONCLUSIONS: Increased NO accompanying productive infection and encephalitis may be one cause of neuronal injury in lentivirus infections of the CNS. Extension of tests of cognitive and motor function to late-stage AIDS in rhesus monkeys is needed to assess the potential role of NO-induced dendritic damage in lentiviral encephalopathy/AIDS dementia complex. PMID: 10413365
