Both modeled the proteins after non-human primate TRIMCyps. 14.1). Zoonotic transmission of FFV into humans seems unlikely [28,31]. Restriction of feline CD134 expression to CD4+ T cells. Mel Campbell, ... Paul A. Luciw, in Encyclopedia of Virology (Second Edition), 1999. Copyright © 2021 Elsevier B.V. or its licensors or contributors. FIV targets CD4+ helper T cells via an initial high affinity interaction between Env and CD134 (OX40) [4••,5•] and a subsequent interaction with the chemokine receptor CXCR4 [6,7]. Seroprevalence of FeFV infection in … Each of these infections results in a typical retroviral infection – i.e., a DNA copy of the retroviral genome is incorporated into the host genome. Introduction Host restriction factors are the cellular proteins associ-ated with the function of the host innate immune systems against the infecting viruses (Lilly 1970). A caveat to be considered in such an approach is that fusing the biologically potent CypA domain to the TRIM5 N-terminal domains in a species that has not co-evolved potentially needed compensatory adaptations in other cellular systems could prove to have unpredictable deleterious effects. The reverse transcription step uniquely occurs late in virus replication, after capsid assembly in the cytoplasm and prior to budding into the endoplasmic reticulum or from the plasma membrane of infected cells. CD134 expression was evaluated by flow cytometry on feline peripheral blood mononuclear cells, setting analysis gates for either lymphocytes (L), monocytes (M) or neutrophils (N). Isolates of FeFV, representing two serotypes, have been identified in domestic cats from three continents (Table 1), and an isolate has also been obtained from a European wildcat. A weakness of the model relates to the limited variety of reagents available for identifying cells of the cat immune system. Retrovirolgists have known for some time that domestic cat cell lines were relatively easily transduced with pseudotyped gammaretroviral and lentiviral vectors. Brian J Willett, Margaret J Hosie, in Current Opinion in Virology, 2013. Effects of A3 on MMTV replication were most apparent in mouse strains that express high levels of this deaminase (Okeoma et al., 2009b), whereas the related TBLV, which has an altered LTR and induces T-cell lymphomas, replicates well in mouse strains that express either high or low levels of A3 (Bhadra et al., 2009; Meyers et al., 1989; Mustafa et al., 2003). FeLV has been studied to understand retroviral-induced immunodeficiency, particularly hematopoietic tumors such as acute lymphoblastic leukemia and lymphoma. Interestingly, the betaretroviruses lack a common mechanism to avoid APOBEC-mediated restriction. However, … The mechanism of virus transmission between hosts remains poorly understood, although human infections have been documented in veterinarians and zoo staff working with nonhuman primates. The Rem precursor is cleaved into an N-terminal signal peptide (Rem-SP) that serves a Rev-like function, whereas the function of the C-terminal 203 amino acid protein has not been determined (Byun et al., 2010, 2012). IFITM; feline foamy virus; late step 1. The abundance of different retroviruses in cats necessitates the presence of potent and broadly specific host restriction factors. CD134 expression was evaluated by flow cytometry on feline peripheral blood mononuclear cells, setting analysis gates for either lymphocytes (L), monocytes (M) or neutrophils (N). We use cookies to help provide and enhance our service and tailor content and ads. Recent studies further suggest that the spumavirus Bet protein functions in an analogous manner to the lentivirus Vif protein, by blocking the function of cellular cytidine deaminase (APOBEC) antiviral proteins edit/mutate viral mRNA. Resulting replication-defective FV vectors have been successfully used in both mice and dogs to repopulate all hematopoeitic cell lineages with the gene encoded by the vectors. Immunodeficiency disease of cats caused by the lentivirus FIV is considered by many to be one of the most relevant naturally occurring models of human acquired immune deficiency syndrome (AIDS) (Hartmann, 2012; Magden et al., 2011; Elder et al., 2010). Feline Herpesvirus. 1). Domestic cats are susceptible to three retroviruses: feline immunodeficiency virus (FIV), genus Lentivirus; feline leukemia virus (FeLV), genus Gammaretrovirus; and feline foamy virus (FFV), genus Spumavirus. Remarkably, in vitro studies using reverse transcriptase inhibitors have demonstrated that this virion DNA contributes significantly to virus infectivity. Genetically, domestic cats are indistinguishable from the African wildcat, Felis sylvestris lybica, and archaeological evidence confirms that the close relationship between cats and humans was evident nearly 10 000 years ago in the Middle East [2]. FeFV has been identified in healthy cats as well as in cats with neoplasms or nonneoplastic diseases. From: Vaccine, 2008. Verstraete , 1 and Dori L. Borjesson 2 Feline FV Bet has been shown to bind to feline A3 (Lochelt et al., 2005), and prototype FV Bet can prevent human A3G dimerization and function (Jaguva Vasudevan et al., 2013; Perkovic et al., 2009; Russell et al., 2005). CD134 was first described as a surface antigen that was expressed almost exclusively on CD4+ T cells [10], thus the extended tropism of FIV during the course of infection would seem counter-intuitive. Interestingly, Bet is expressed at high levels in infected cells, both in culture and in animals, consistent with inactivation of A3 by Bet binding or sequestration (Alke et al., 2001; Lukic et al., 2013). For example, primate lentiviruses encounter a strong post-entry block in lion cells (W. McEwan and B. Willett, personal communication). Infection with FeFV is persistent, and previous studies have indicated that seroprevalences of FeFV infection in domestic cats range between 7 and 100% ( 1 , 3 , 9 , 11 , 12 , 16 , 20 , 23 ). Like many MuLVs, the packaged A3 caused only low-level hypermutation of the proviruses that escaped A3 inhibition (MacMillan et al., 2013). In addition, A3s may be able to inhibit FV replication in both producer as well as target cells (Lochelt et al., 2005), which may be linked to the fact that spumaviruses can initiate reverse transcription in producer cells (Moebes et al., 1997). The integration of provirus into the host genome is also unique, both in the molecular mechanism and in the specificity of the site of integration. We hypothesized that the cytopathic effects were caused by infection with a retrovirus, feline foamy virus (FFV). This protein does not restrict HIV-1, SIVmac, or N-tropic murine leukemia virus (N-MLV) due to a stop codon in exon 8, 5′ to the V1 region of the B30.2 domain (McEwan et al., 2009). Nothing is known about the seasonal distribution of foamy viruses in any mammalian species. Resulting replication-defective FV vectors have been successfully used in both mice and dogs to repopulate all hematopoeitic cell lineages with the gene encoded by the vectors. Feline foamy virus (FeFV) is a typical spumavirus that resembles the primate foamy viruses and bovine foamy virus in its morphology and molecular structure (4, 19). The subfamily Spumaretrovirinae includes a single genus, Spumavirus (Fig. Helicobacter felis is a naturally occurring pathogen in cats that appears to be prevalent in some colonies, but its prevalence or significance as an agent of clinical diseases in the general cat population is not clear (Lee et al., 1988; Perkins et al., 1996). During the past two decades, the many unique features of the life cycle of spumaviruses have been examined and exploited by researchers interested in developing spumavirus-based gene therapy vector systems. The ensuing immunodeficiency manifests with chronic gingivitis and stomatitis, anorexia, cachexia, neurological signs and an increased incidence of malignancy. Two groups have recently made progress in this area, with “humanized” and “felinized” TRIMCyps respectively (Dietrich et al., 2010; Neagu et al., 2009). Furthermore, unlike MPMV, MMTV, and TBLV, complex retroviruses express a doubly spliced mRNA and the Rem precursor protein (Indik et al., 2005; Mertz et al., 2005). Note that other post-entry restrictions exist in some felids. 24 Host-specific viruses of this genus have been isolated from some mammalian species. FVs are rather stable. Helicobacter felis is a naturally occurring pathogen in cats that appears to be prevalent in some colonies, but its prevalence or significance as an agent of clinical diseases in the general cat population is not clear (Lee et al., 1988; Perkins et al., 1996). After infection with FeLV, a fraction of cats become persistently viremic and virus is excreted, particularly through saliva and nasal secretions. Unlike Vif, which acts as an adapter between APOBEC and an E3 ligase, Bet does not induce A3 degradation, but prevents packaging of particular A3s into foamy virus particles. We experimentally infected five cats with FFV to study viral kinetics and tropism, peripheral blood mononuclear cell (PBMC) phenotype, urinary parameters, and histopathology. Transcription at both the 5′ LTR and internal promoters are markedly activated by the presence of the Tas transcription factor. Of the 37 known species of felids, 21 species including the African lion (Panthera leo), the North American puma (Puma concolor) and the domestic cat have been shown to harbor antibodies reactive to FIV and many of these species harbor viral sequences consistent with species-specific strains (VandeWoude and Apetrei, 2006; Troyer et al., 2008). Nothing is known about the seasonal distribution of foamy viruses in any mammalian species. Feline Foamy Virus. While simian and feline FVs have been developed as vectors, most work has been concentrated on PFV. Es teilt die Gattung Felispumavirus nur mit Puma Katzenschaumvirus. 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