Characterization of astroglial dysfunction following feline immunodeficiency viral infection /

Lentiviruses including HIV and FIV are able to efficiently

Bibliographic Details
Main Author: Zenger, Elizabeth, 1963-
Format: Thesis Book
Language:English
Published: [Place of publication not identified] : [publisher not identified] ; 1997.
Subjects:
Online Access:http://proxy.library.tamu.edu/login?url=http://proquest.umi.com/pqdweb?did=736580661&sid=1&Fmt=2&clientId=2945&RQT=309&VName=PQD

MARC

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035 |9 AHP4127AM 
037 |a 98-00830  |b UMI 
040 |a TXA  |c TXA  |d UtOrBLW 
049 |a TXAM  |a TXAR 
099 |a 1997  |a Dissertation  |a Z422 
100 1 |a Zenger, Elizabeth,  |d 1963- 
245 1 0 |a Characterization of astroglial dysfunction following feline immunodeficiency viral infection /  |c by Elizabeth Zenger. 
264 1 |a [Place of publication not identified] :  |b [publisher not identified] ;  |c 1997. 
300 |a xiii, 101 leaves :  |b illustrations ;  |c 28 cm. 
336 |a text  |b txt  |2 rdacontent 
337 |a unmediated  |b n  |2 rdamedia 
338 |a volume  |b nc  |2 rdacarrier 
504 |a Includes bibliographical references: pages 88-100. 
500 |a Vita. 
502 |b Ph. D.  |c Texas A&M University  |d 1997. 
500 |a "Major Subject: Veterinary Anatomy". 
530 |a Issued also on microfiche from University Microfilms Inc. 
520 |a Lentiviruses including HIV and FIV are able to efficiently  
520 |a enter the central nervous system (CNS) and cause primary  
520 |a neurological disease that is not attributable to  
520 |a opportunistic infections or systemic disease. Although a  
520 |a substantial degree of neuronal loss can occur in the cortex  
520 |a of HIV- or FIV-infected patients, most studies agree that  
520 |a neurons are not infected and indirect mechanisms of  
520 |a neurotoxicity are postulated. Target cells for FIV in the  
520 |a brain are similar to those observed in HIV infection, i.e.,  
520 |a both viruses infecting astrocytes and microglia. The  
520 |a importance of asttoglia in the maintenance of CNS functions  
520 |a suggests that virally induced changes in infected astroglia  
520 |a may be essential in the progression of lentivirus-associated  
520 |a neurologic disease. This dissertation describes a model  
520 |a system that was developed to study the effects of two  
520 |a divergent FIV strains on astroglia in vitro. Effects of  
520 |a astroglial infection by the nonneurovirulent Petaluma strain  
520 |a of FIV (FIV-Pet) and the highly neurovirulent Maryland Strain  
520 |a of FIV (FIV-MD) were compared. Astroglia were readily  
520 |a infected by FIV-Pet and this infection was productive with  
520 |a high titers of virus being produced by infected cells within  
520 |a several days of infection. In contrast, astroglial infection  
520 |a by FIV-MD could only be accomplished by lymphocyte  
520 |a facilitation and was nonproductive. Results of assays  
520 |a examining the cytotoxic potential of these viruses suggest  
520 |a that FIV-Pet infection of astroglia seems to be much more  
520 |a cytotoxic than FIV-MD. Further, FIV-Pet causes a much more  
520 |a profound decrease in astroglial glutamate uptake than does  
520 |a FIV-MD. The results of this study suggest that the  
520 |a differences in neurovirulence observed in vivo may relate to  
520 |a specific differences in the mechanism of astroghal infection,  
520 |a viral expression, tendency to cause cytotoxicity, and ability  
520 |a to cause alteration of astroglial function. Although these  
520 |a in vitro results may seem contradictory to that expected  
520 |a initially, these results may actually correlate well with the  
520 |a paradoxical nature of CNS lesions and clinical neurological  
520 |a symptomatology associated with these viral strains. 
650 4 |a Major veterinary anatomy. 
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