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Neuropathogenic mechanisms of feline...

Buck, Wayne R.

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Neuropathogenic mechanisms of feline immunodeficiency virus infection.

Record Type:	Electronic resources : Monograph/item
Title/Author:	Neuropathogenic mechanisms of feline immunodeficiency virus infection./
Author:	Buck, Wayne R.
Description:	159 p.
Notes:	Source: Dissertation Abstracts International, Volume: 65-02, Section: B, page: 0550.
Contained By:	Dissertation Abstracts International65-02B.
Subject:	Biology, Microbiology. -
Online resource:	http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3122584
ISBN:	0496699326

Neuropathogenic mechanisms of feline immunodeficiency virus infection.
Buck, Wayne R.

Neuropathogenic mechanisms of feline immunodeficiency virus infection. - 159 p.

Source: Dissertation Abstracts International, Volume: 65-02, Section: B, page: 0550.

Thesis (Ph.D.)--The Ohio State University, 2004.

Human immunodeficiency virus (HIV) causes neurological disease in a majority of infected persons, resulting in minor cognitive and motor disorders which begin early in infection. The feline immunodeficiency virus (FIV) model of HIV infection recapitulates the progression of immune system destruction and clinical and subclinical neurological abnormalities. In this study, we examined virological, neuropathological, and neurochemical parameters of cats infected at 3 days and 2 months of age.

ISBN: 0496699326Subjects--Topical Terms:

1017734
Biology, Microbiology.

Neuropathogenic mechanisms of feline immunodeficiency virus infection.
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035 $a (UnM)AAI3122584
035 $a AAI3122584
040 $a UnM $c UnM
100 1 $a Buck, Wayne R. $3 1933785
245 1 0 $a Neuropathogenic mechanisms of feline immunodeficiency virus infection.
300 $a 159 p.
500 $a Source: Dissertation Abstracts International, Volume: 65-02, Section: B, page: 0550.
500 $a Advisers: Lawrence E. Mathes; Maria H.-Neff.
502 $a Thesis (Ph.D.)--The Ohio State University, 2004.
520 $a Human immunodeficiency virus (HIV) causes neurological disease in a majority of infected persons, resulting in minor cognitive and motor disorders which begin early in infection. The feline immunodeficiency virus (FIV) model of HIV infection recapitulates the progression of immune system destruction and clinical and subclinical neurological abnormalities. In this study, we examined virological, neuropathological, and neurochemical parameters of cats infected at 3 days and 2 months of age.
520 $a Cerebral subcortical white matter volume was reduced 23% (n = 6) compared to age-matched controls (n = 6) in cats infected as neonates and killed 3 months post inoculation (PI), but was normal in cats 6 months PI (n = 6 infected, n = 6 controls). Caudate nucleus volume was reduced 19% in cats infected as juveniles and killed 6 (n = 6) and 24 (n = 6) months PI compared to 6 month old controls (n = 6). Cerebral neocortical gray matter volume was decreased 14% (n = 6) in cats infected as juveniles and killed 24 months PI compared to 6 month old controls (n = 6).
520 $a Neurochemical analysis of the caudate nucleus of cats infected as neonates revealed increased dopamine content at 3 and 18 months PI (222 +/- 27 pmol/mg protein, n = 6; 1785 +/- 281 pmol/mg protein, n = 4; respectively) compared against uninfected age matched controls (46 +/- 10 pmol/mg protein, n = 8; 422 +/- 64 pmol/mg protein, n = 7; respectively). Tyrosine hydroxylase immunoreactivity was increased 6 and 18 months PI (215 +/- 19% of control, n = 5 infected, n = 6 controls; and 163 +/- 16% of control, n = 6 infected, n = 6 controls; respectively).
520 $a In summary, low brain viral and proviral loads did not correlate with electrodiagnostic abnormalities, suggesting host responses to infection perpetuate functional disturbances. Cerebral neocortical gray matter atrophy without neuronal loss might be due to cell shrinkage, dendritic simplification, or filial cell loss, all of which might be reversible. Neurochemical abnormalities implicate altered dopamine synthesis and turnover in the caudate nucleus during FIV infection. Reductions in GLT1 mRNA in the caudate nucleus and reductions in glutamine synthetase activity in the frontal cortex both suggest astrocytic injury occurs during FIV infection of the feline central nervous system. (Abstract shortened by UMI.)
590 $a School code: 0168.
650 4 $a Biology, Microbiology. $3 1017734
650 4 $a Biology, Neuroscience. $3 1017680
650 4 $a Biology, Veterinary Science. $3 1021733
650 4 $a Health Sciences, Immunology. $3 1017716
650 4 $a Health Sciences, Pathology. $3 1017854
690 $a 0410
690 $a 0317
690 $a 0778
690 $a 0982
690 $a 0571
710 2 0 $a The Ohio State University. $3 718944
773 0 $t Dissertation Abstracts International $g 65-02B.
790 1 0 $a Mathes, Lawrence E., $e advisor
790 1 0 $a H.-Neff, Maria, $e advisor
790 $a 0168
791 $a Ph.D.
792 $a 2004
856 4 0 $u http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3122584