Parvoviral target cell specificity: Acquisition of fibrotropism by a mutant of the lymphotropic strain of minute virus of mice involves multiple amino acid substitutions within the capsid

Ball-Goodrich, Lisa J.; Moir, Robyn D.; Tattersall, Peter

doi:10.1016/0042-6822(91)90834-x

Cited by 25 publications

(24 citation statements)

References 19 publications

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“…However, a recombinant virus containing only that region of MVM(p) in an MVM(i) genetic background has been reported to generate pinpoint-sized plaques, whereas viruses containing a large region of the MVM(p) genome, including the NS gene of MVM(p) in addition to the minimum region responsible for the fibrotropism, generated wild-type plaques in mouse fibroblasts (Gardiner & Tattersall, 1988b). A similar observation has been reported on analysis of the determinants of fibrotropism of hr 101, an extended host range variant of MVM(i) (Ball-Goodrich et al, 1991). These reports seem to support our finding in the CPV/MEV system that the NS gene is involved in the full expression of the growth properties of CPV in canine cells.…”

Section: Discussionsupporting

confidence: 92%

Mapping of determinants of the host range for canine cells in the genome of canine parvovirus using canine parvovirus/mink enteritis virus chimeric viruses

Horiuchi¹,

Gotō

Ishiguro³

et al. 1994

Journal of General Virology

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Feline panleukopenia virus (FPLV), mink enteritis virus (MEV) and canine parvovirus (CPV) are more than 98 % similar in DNA and predicted amino acid sequences, but they show different host-cell specificities; CPV is able to replicate in canine cells in culture, whereas FPLV and MEV cannot or replicate only to a low titre. To map the genomic region responsible for the host range of CPV in vitro, CPV/MEV chimeric viruses were generated by transfecting infectious CPV/MEV chimeric plasmids into a cultured feline kidney cell line, and their host cell ranges were analysed. The 60 to 91 map units (m.u.) region of the CPV genome, which contains a part of the capsid protein (VP) gene encoding from amino acid 91 (in the VP2 sequence) to the carboxy terminus of VP protein, was required to impart the ability to replicate in canine cells to MEV, although the chimeric virus containing the 60 to 91 m.u. region of the CPV genome in the MEV background did not replicate in canine cells as efficiently as did CPV derived from the infectious plasmid of CPV. Not only the VP gene, but also a part of the NS gene of CPV were considered to participate in the full expression of the ability to replicate in canine cells. Within the 60 to 91 m.u. region, five of nine amino acid changes between MEV-Abashiri and CPV-Y1 were thought to be phylogenetically CPV-common; however, a recombinant virus containing all five amino acid changes of CPV in the MEV background replicated minimally in canine cells.

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Section: Discussionsupporting

confidence: 92%

Mapping of determinants of the host range for canine cells in the genome of canine parvovirus using canine parvovirus/mink enteritis virus chimeric viruses

Horiuchi¹,

Gotō

Ishiguro³

et al. 1994

Journal of General Virology

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“…In the minute virus of mice (MVM), two strains can be distinguished on the basis of their tropisms for lymphoid and fibroblastic cells. MVM (p) can infect fibroblasts, while MVM (i) infects erythropoetic progenitor cells and lymphoid cells, including T cells (3,7,29). The fibrotropic phenotype of MVM (p) was controlled by a combination of residues 317 and 321 in VP2, which determine the host cell specificity in a coordinated manner (4).…”

Section: Vol 77 2003mentioning

confidence: 99%

Combinations of Two Capsid Regions Controlling Canine Host Range Determine Canine Transferrin Receptor Binding by Canine and Feline Parvoviruses

Hueffer

Govindasamy

Agbandje‐McKenna

et al. 2003

J Virol

133

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Feline panleukopenia virus (FPV) and its host range variant, canine parvovirus (CPV), can bind the feline transferrin receptor (TfR), while only CPV binds to the canine TfR. Introducing two CPV-specific changes into FPV (at VP2 residues 93 and 323) endowed that virus with the canine TfR binding property and allowed canine cell infection, although neither change alone altered either property. In CPV the reciprocal changes of VP2 residue 93 or 323 to the FPV sequences individually resulted in modest reductions in infectivity for canine cells. Changing both residues in CPV to the FPV amino acids blocked the canine cell infection, but that virus was still able to bind the canine TfR at low levels. This shows that both CPV-specific changes control canine TfR binding but that binding is not always sufficient to mediate infection.

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“…The major viral determinant of this host range resides within the capsid. The primary block to restrictive infections is intracellular, following binding to cells but before deposition of viral DNA in the nucleus (1,3,4,11,12,20).Characterization of MVMp and MVMi has also led to the identification of another determinant that affects viral replication in a host cell-dependent manner. Analysis of MVMi virus selected for growth on fibroblasts and analysis of the replication of engineered MVMi and MVMp chimeras on murine lymphocytes have demonstrated that a region encompassing the large-intron 3Ј splice site and P38 TATA box also plays a role in the efficiency of viral DNA replication in these two cell types (7, 12).…”

mentioning

confidence: 99%

mentioning

confidence: 99%

Replication of Minute Virus of Mice DNA Is Critically Dependent on Accumulated Levels of NS2

Choi

Newman

Burger

et al. 2005

J Virol

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Following transfection of murine fibroblasts, the lymphotropic strain of minute virus of mice (MVMi) does not efficiently produce progeny single-strand DNA (ssDNA). However, changing a single nucleotide in the MVMi 3 splice site to that found in the fibrotropic strain MVMp enabled full DNA replication and production of ssDNA. This change enhanced excision of the large intron and the production of NS2, likely by improving interaction, in fibroblasts with the branch point-binding U2 snRNA. One function of NS2 involves interaction with the nuclear export protein Crm1. The defect in production of MVMi ssDNA in fibroblasts can also be overcome by introducing a mutation in MVMi NS2 that enhances its interaction with Crm1. Although MVMi contains a 3 splice site that performs poorly in fibroblasts, MVMi generated at least as much R2 and NS2 in murine lymphocytes as did MVMp in fibroblasts. Therefore, it appears that MVMp has acquired a mutation that improves the excision of the large intron, as it adapted to fibroblasts to accommodate the need for NS2 for replication in these cells, and that the ratio of NS1 to NS2 may play a larger role in the host range of MVM than previously appreciated.Two strains of minute virus of mice, fibrotropic strain MVMp and lymphotropic strain MVMi, are reciprocally restricted for growth in murine cells (2,10,15,23,25,26). MVMp productively infects murine fibroblasts but not murine lymphocytes, while MVMi does the opposite. The major viral determinant of this host range resides within the capsid. The primary block to restrictive infections is intracellular, following binding to cells but before deposition of viral DNA in the nucleus (1,3,4,11,12,20).Characterization of MVMp and MVMi has also led to the identification of another determinant that affects viral replication in a host cell-dependent manner. Analysis of MVMi virus selected for growth on fibroblasts and analysis of the replication of engineered MVMi and MVMp chimeras on murine lymphocytes have demonstrated that a region encompassing the large-intron 3Ј splice site and P38 TATA box also plays a role in the efficiency of viral DNA replication in these two cell types (7, 12). The role that this region plays in replication has not been well characterized, but in both cases, differences in the ratio of mRNA R1 to R2, which encode NS1 and NS2, respectively, have been observed (4, 7, 11). The importance of the NS region in cell type-specific replication has also been noted for cells of neuronal origin (22).Previous studies in our lab have shown that even minor alterations of the MVM large-intron 3Ј splice site can have significant effects on the steady-state ratio of R1 to R2 and, hence, on the ratio of the viral nonstructural proteins NS1 and NS2 (19,28). Differences between MVMi and MVMp in this area have been previously noted, and ways in which these differences might affect RNA processing in the two strains have been discussed previously (19). Recently, two reports have In this study we have shown that, following transfection of mur...

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Parvoviral target cell specificity: Acquisition of fibrotropism by a mutant of the lymphotropic strain of minute virus of mice involves multiple amino acid substitutions within the capsid

Cited by 25 publications

References 19 publications

Mapping of determinants of the host range for canine cells in the genome of canine parvovirus using canine parvovirus/mink enteritis virus chimeric viruses

Mapping of determinants of the host range for canine cells in the genome of canine parvovirus using canine parvovirus/mink enteritis virus chimeric viruses

Combinations of Two Capsid Regions Controlling Canine Host Range Determine Canine Transferrin Receptor Binding by Canine and Feline Parvoviruses

Replication of Minute Virus of Mice DNA Is Critically Dependent on Accumulated Levels of NS2

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