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Host-Virus Evolution in the Canine Model

Jarosz-DiPietro, Abigail S
http://rave.ohiolink.edu/etdc/view?acc_num=bgsu167940078324862

Abstract Details

2023, Doctor of Philosophy (Ph.D.), Bowling Green State University, Biological Sciences.
All vertebrate genomes are littered with the remnants of once-infectious retroviruses that permanently integrated their genomes into the host germline, subsequently passing the insertion to offspring as an endogenous retrovirus (ERV). To date there have been no confirmed infectious exogenous retroviruses (XRVs) in the domestic dog. Despite this there have been numerous reports of gammaretrovirus-like particles and enzyme activities in canine leukemias and lymphomas. We hypothesize that members of this recently active ERV lineage is responsible for such observations. Our findings have identified members from the CfERV-Fc1(a) are transcriptionally active in canine tissues. Remarkably, the majority of CfERV-Fc1(a) env genes, responsible for host receptor recognition and binding, have complete reading frames and contain all the necessary motifs to maintain viral function. We demonstrate some of these polymorphic insertions have retained their fusogenic ability, using canine ASCT2 as a receptor, which was likely involved in ancestral, and putatively ongoing spread. Hosts have also evolved genes with antiretroviral functions to defend against incoming virus, one such family referred to as Tripartite motif (TRIM). Specifically, a TRIM5 orthologue induces premature disassembly of the retroviruses and is capable of inhibiting HIV-1 infection by this mechanism in monkeys. Also, part of this cluster is TRIM22, which appears to have evolved discordantly from TRIM5 in mammals. TRIM22 has been shown to inhibit HIV infection through repressing retroviral transcription as well as interfering with viral assembly. Intriguingly, the TRIM5 gene in canine has been disrupted, while several TRIM orthologues, including TRIM22 and others, have been preserved in the canine but their role(s) in antiviral restriction remain to be explored. We hypothesize canine TRIM proteins have evolved to play a role in the yet-described retroviral purging mechanism in canines. To begin to explore if TRIM22 and other closely related TRIMs, known as the “antiviral TRIMs”, are involved in an antiviral response in canines, we performed analysis of TRIM gene expression in response to IFNs. Our research shows despite the interruption in the canine TRIM5 gene, the remaining members of the antiviral TRIMs contain intact open reading frames and expression is in fact up-regulated by type I IFN.
Julia Halo, Ph.D. (Committee Chair)
Timothy Pogacar, Ph.D. (Other)
Amanda Pendleton, Ph.D. (Committee Member)
Raymond Larsen, Ph.D. (Committee Member)
Daniel Pavuk, Ph.D. (Committee Member)
Vipaporn Phuntumart, Ph.D. (Committee Member)
132 p.
Cellular Biology; Molecular Biology
Endogenous Retroviruses; Canines; Paleovirology

Recommended Citations

Citations

  • Jarosz-DiPietro, A. S. (2023). Host-Virus Evolution in the Canine Model [Doctoral dissertation, Bowling Green State University]. OhioLINK Electronic Theses and Dissertations Center. http://rave.ohiolink.edu/etdc/view?acc_num=bgsu167940078324862

    APA Style (7th edition)

  • Jarosz-DiPietro, Abigail. Host-Virus Evolution in the Canine Model. 2023. Bowling Green State University, Doctoral dissertation. OhioLINK Electronic Theses and Dissertations Center, http://rave.ohiolink.edu/etdc/view?acc_num=bgsu167940078324862.

    MLA Style (8th edition)

  • Jarosz-DiPietro, Abigail. "Host-Virus Evolution in the Canine Model." Doctoral dissertation, Bowling Green State University, 2023. http://rave.ohiolink.edu/etdc/view?acc_num=bgsu167940078324862

    Chicago Manual of Style (17th edition)

bgsu167940078324862
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This open access ETD is published by Bowling Green State University and OhioLINK.