Ducks: a new experimental host system for studying persistent infection with avian leukaemia retroviruses

Nehyba, Jiřı́; Svoboda, Jan; Karakoz, I; Geryk, Josef; Hejnar, Jiřı́

doi:10.1099/0022-1317-71-9-1937

Cited by 14 publications

(9 citation statements)

References 37 publications

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“…The receptor-mediated interference between exogenous and endogenous retroviruses is a phenomenon also observed in the chicken RAV-0 (5, 6) and in murine ecotropic (45) and xenotropic (46) retroviruses. The Tvb S3 allele, which confers resistance to the E subgroup of ASLV (6,47), and the XPR1 alleles, which confer resistance to murine xenotropic retroviruses (28), are believed to be products of the selection pressure imposed by such endogenous retroviruses. Nonspecific restriction mechanisms should also be taken into account in the case of cross-species retrovirus infection.…”

Section: Discussionmentioning

confidence: 99%

Nonconserved Tryptophan 38 of the Cell Surface Receptor for Subgroup J Avian Leukosis Virus Discriminates Sensitive from Resistant Avian Species

Kučerová

Plachý

Reinišová

et al. 2013

J Virol

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Subgroup J avian leukosis virus (ALV-J) is unique among the avian sarcoma and leukosis viruses in using the multimembranespanning cell surface protein Na ؉ /H ؉ exchanger type 1 (NHE1) as a receptor. The precise localization of amino acids critical for NHE1 receptor activity is key in understanding the virus-receptor interaction and potential interference with virus entry. Because no resistant chicken lines have been described until now, we compared the NHE1 amino acid sequences from permissive and resistant galliform species. In all resistant species, the deletion or substitution of W38 within the first extracellular loop was observed either alone or in the presence of other incidental amino acid changes. Using the ectopic expression of wild-type or mutated chicken NHE1 in resistant cells and infection with a reporter recombinant retrovirus of subgroup J specificity, we studied the effect of individual mutations on the NHE1 receptor capacity. We suggest that the absence of W38 abrogates binding of the subgroup J envelope glycoprotein to ALV-J-resistant cells. Altogether, we describe the functional importance of W38 for virus entry and conclude that natural polymorphisms in NHE1 can be a source of host resistance to ALV-J.T he first step in retrovirus infection is attachment of the virus envelope glycoproteins to the specific cell surface receptor. Consequently, the susceptibility of each cell strictly depends on the expression and display of proper receptor molecules. This attachment, as well as the following phases of virus entry, requires a perfect match of receptors and envelope glycoproteins (1). Structural alterations within variable and hypervariable envelope glycoprotein regions easily abrogate the infectivity or even change the receptor usage and broaden the host range. This is best exemplified by avian sarcoma and leukosis viruses (ASLVs), a closely related group of retroviruses which evolved into five subgroups, A to E, that utilize three different receptors encoded by three genetic loci, tva, tvb, and tvc (1, 2). The tva locus encodes a protein belonging to the family of low-density lipoprotein receptors and determines susceptibility to the subgroup A ASLVs (3, 4). The tumor necrosis factor receptor-related protein encoded by the tvb locus confers susceptibility to subgroup B, D, and E ASLVs (5-7). Finally, subgroup C ASLVs utilize the Tvc protein of the butyrophilin family with two immunoglobulin-like domains (8). The complete resistance or decreased susceptibility of host chicken cells to a particular ASLV subgroup can then be caused by premature termination or a frameshift in the receptor-encoding loci (8-10), decreased receptor expression and display (11), and even single amino acid substitutions in the receptor sequence (9, 12).Subgroup J avian leukosis virus (ALV-J), the prototype virus isolate of which is HPRS-103, is an independent envelope subgroup which does not interfere with subgroups A to E and cannot be neutralized by antisera raised against subgroups A to E (13). ALV-J was originally d...

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Section: Discussionmentioning

confidence: 99%

Nonconserved Tryptophan 38 of the Cell Surface Receptor for Subgroup J Avian Leukosis Virus Discriminates Sensitive from Resistant Avian Species

Kučerová

Plachý

Reinišová

et al. 2013

J Virol

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“…QT6 is a quail fibroblast cell line obtained by chemical mutagenesis (76). The 1757 duck cell line was derived from a duck sarcoma induced by avian leukosis virus (ALV) (82). All other cell lines used are of chicken origin.…”

Section: Methodsmentioning

confidence: 99%

Interferon Regulatory Factor 4 Contributes to Transformation of v-Rel-Expressing Fibroblasts

Hrdličková

Nehyba

Bose

2001

Molecular and Cellular Biology

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“…North American and Asian duck populations share wintering grounds, and at least two reports indicate the presence of ALV-J in ducks and partridges (17,18). Avian leukosis viruses of other subgroups can infect ducks and establish persistent infections in these heterologous hosts (38,39). On the other hand, we reported that NHE1 receptors of duck species are restrictive, and in vitro infection of duck embryo fibroblasts with ALV-J was inefficient (21).…”

Section: Discussionmentioning

confidence: 86%

Identification of New World Quails Susceptible to Infection with Avian Leukosis Virus Subgroup J

Plachý

Reinišová

Kučerová

et al. 2017

J Virol

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The J subgroup of avian leukosis virus (ALV-J) infects domestic chickens, jungle fowl, and turkeys. This virus enters the host cell through a receptor encoded by the tvj locus and identified as Na ϩ /H ϩ exchanger 1. The resistance to avian leukosis virus subgroup J in a great majority of galliform species has been explained by deletions or substitutions of the critical tryptophan 38 in the first extracellular loop of Na ϩ /H ϩ exchanger 1. Because there are concerns of transspecies virus transmission, we studied natural polymorphisms and susceptibility/resistance in wild galliforms and found the presence of tryptophan 38 in four species of New World quails. The embryo fibroblasts of New World quails are susceptible to infection with avian leukosis virus subgroup J, and the cloned Na ϩ /H ϩ exchanger 1 confers susceptibility on the otherwise resistant host. New World quails are also susceptible to new avian leukosis virus subgroup J variants but resistant to subgroups A and B and weakly susceptible to subgroups C and D of avian sarcoma/leukosis virus due to obvious defects of the respective receptors. Our results suggest that the avian leukosis virus subgroup J could be transmitted to New World quails and establish a natural reservoir of circulating virus with a potential for further evolution.IMPORTANCE Since its spread in broiler chickens in China and Southeast Asia in 2000, ALV-J remains a major enzootic challenge for the poultry industry. Although the virus diversifies rapidly in the poultry, its spillover and circulation in wild bird species has been prevented by the resistance of most species to ALV-J. It is, nevertheless, important to understand the evolution of the virus and its potential host range in wild birds. Because resistance to avian retroviruses is due particularly to receptor incompatibility, we studied Na ϩ /H ϩ exchanger 1, the receptor for ALV-J. In New World quails, we found a receptor compatible with virus entry, and we confirmed the susceptibilities of four New World quail species in vitro. We propose that a prospective molecular epidemiology study be conducted to identify species with the potential to become reservoirs for ALV-J.KEYWORDS ALV-J, antiretroviral resistance, Na ϩ /H ϩ exchanger, New World quail, retroviral receptor T he range of hosts susceptible to a given retrovirus results from the process of coevolution between the viral envelope glycoproteins and host cell receptors. Selection forces imposed by the retrovirus drive the positive selection of receptors toward variants with decreased or even abrogated binding to retroviral envelopes. Vice versa, the highly error prone replication of retroviruses enables the rapid evolution of new strains with the capacity to bind to the variant receptors or even to quite new cell surface molecules. The results of these processes acting over evolutionary time are visible particularly in avian sarcoma/leukosis viruses (ASLVs), murine leukemia viruses (MLV), and feline leukemia viruses, where closely related virus subgroups differ in

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Ducks: a new experimental host system for studying persistent infection with avian leukaemia retroviruses

Cited by 14 publications

References 37 publications

Nonconserved Tryptophan 38 of the Cell Surface Receptor for Subgroup J Avian Leukosis Virus Discriminates Sensitive from Resistant Avian Species

Nonconserved Tryptophan 38 of the Cell Surface Receptor for Subgroup J Avian Leukosis Virus Discriminates Sensitive from Resistant Avian Species

Interferon Regulatory Factor 4 Contributes to Transformation of v-Rel-Expressing Fibroblasts

Identification of New World Quails Susceptible to Infection with Avian Leukosis Virus Subgroup J

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