Study systems include
- Endogenous retroviruses
- Feline immunodeficiency virus (FIV)
Elleder, D., Kim, O., Padhi, A., et al. 2012. Polymorphic integrations of an endogenous gammaretrovirus in the mule deer genome. J Virol. 86:2787-96.
Elleder, D., Young, J.A., Baiga, T., Noel, J. 2009. Non-Nucleoside Reverse Transcriptase Inhibitors. International patent application, publication number WO/2009/061856.
Konig, R., Zhou, Y., Elleder, D., Diamond, T.L., et al. 2008. Global analysis of Host-Pathogen Interactions that Regulate Early-Stage HIV-1 Replication. Cell, 135:49-60.
Elleder, D., Stepanets, V., Melder, D.C., et al. 2005. The receptor for the subgroup C avian sarcoma and leukosis viruses, Tvc, is related to mammalian butyrophilins, members of the immunoglobulin superfamily. J. Virol., 79:10408-10419.
Elleder, D., Melder, D.C., Trejbalová, K., Svoboda, J. and Federspiel, M.J. 2004. Two different molecular defects in the Tva receptor gene explain the resistance of two tva-r lines of chickens to infection by subgroup A avian sarcoma and leukosis viruses. J. Virol., 78:13489-13500.
Elleder, D., Plachý, J., Hejnar, J., Geryk, J and Svoboda, J. 2004. Close linkage of genes encoding receptors for subgroups A and C of avian sarcoma/leucosis virus on chicken chromosome 28. Anim. Genet., 35:176-181.
We are characterizing a novel mammalian endogenous gammaretrovirus. This originated from a metagenomic study that employed 454 sequencing of tissue samples of wild mule deer (Odocoileus hemionus). In contrast to most currently known endogenous retroviruses (ERVs), this Cervid endogenous retrovirus (CrERV) is highly insertionally polymorphic in the natural deer population, which indicates a recent origin and the possibility of ongoing entry into the deer genome. The recently integrated proviruses serve as genetic markers for description of deer population structure and population history. We are studying the genetic and epigenetic characteristics of CrERV and the possibility of the existence of an exogenously replicating virus.
I am also involved in a project that uses a unique model of lentivirus pathogenesis in mammalian host, namely coinfection of cats with two feline immunodeficiency viruses (FIV). Infection with the non-pathogenic FIV derived from wild cougars can protect from otherwise progressive immune decline and ultimately death caused by a virulent FIV strain. We are trying to dissect the particular host and viral components that contribute to the protection. Specifically we are following the adaptive and innate immune responses elicited by the non-pathogenic FIV, the role played by the cat antiviral gene cytidine deaminase, and the role of the virus infectivity factor (Vif).