Browsing by Author "Wayne A. Tompkins, Committee Member"

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    Canine Babesiosis: Epidemiological, Molecular and Therapeutic Investigations
    (2004-04-21) Birkenheuer, Adam Joseph; Edward B. Breitschwerdt, Committee Chair; Michael G. Levy, Committee Member; Mary B. Tompkins, Committee Member; Wayne A. Tompkins, Committee Member
    Canine babesiosis is an emerging infectious disease in the United States (US). An epidemic of Babesia gibsoni infections in the US was identified. An association between dog breed and B. gibsoni infections was detected. Babesia gibsoni-infected dogs were more likely to be American pit bull terriers and B. canis vogeli infected dogs were more likely to be greyhounds. An association between a recent dog bite and B. gibsoni infection was detected, implicating direct dog-to-dog transmission as a route of infection in the US. Several genes from canine Babesia spp. were characterized, including 18S ribosomal RNA (rRNA), internal transcribed spacer regions (ITS), cytochrome B (cytB), and rhoptry-associated protein-1 (RAP-1). These genetic data were used to develop a sensitive and specific diagnostic semi-nested polymerase chain reaction (PCR) test for canine babesiosis. Using this assay, a novel large Babesia organism was identified in a blood sample obtained from a clinical patient. Molecular and phylogenetic characterization of this large Babesia spp. determined that it was most closely related to B. bigemina. Lastly, an atovaquone and azithromycin drug combination was shown to be the first treatment to clear canine B. gibsoni infections.
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    Role of the Cytoplasmic Tail of Equine Infectious Anemia Virus Transmembrane Glycoprotein in Acute Disease Induction
    (2004-12-26) Jia, Bin; Barbara Sherry, Committee Member; Scott M. Laster, Committee Member; Wayne A. Tompkins, Committee Member; Frederick J. Fuller, Committee Chair
    Equine infectious anemia virus (EIAV) is a macrophage-tropic lentivirus of horses. EIAV is unique among lentiviruses in that a further cleavage event occurs within the N-terminus of the cytoplasmic tail (CT) of transmembrane (TM) glycoprotein and yields a C-terminal non-glycosylated p20 protein. The p20 comprises more than two-third of the CT domain and contains both of the amphipathic α-helices. To test the role of the EIAV CT domain in acute disease induction, we constructed a p20-truncated clone (p19/wenv17Δ20) on the background of a highly virulent EIAV infectious clone p19/wenv17 by introducing three termination codons into the N-terminal coding region of p20. The derived virus replicated at a delayed and lower level compared with that of parental virus in equine macrophages in vitro. In vivo, the p19/wenv17Δ20 virus showed attenuation and did not induce acute disease like the parental (p19/wenv17) virus. The viral load in ponies infected by p19/wenv17Δ20 virus was about 10-1000 fold lower than that of ponies infected by parental (p19/wenv17) virus. In vitro studies on the properties of the p20-truncated virus showed that truncation of the p20 did not impair the envelope glycoprotein incorporation into virions. There was also no severe defect in virus replication. The delayed and lower level replication of p20-truncated virus compared with parental virus was most probably due to small delays in several steps in the virus life cycle. In addition, p20 expressed in trans could not compensate for the absence of p20 in the p20-truncated virus.