scholarly journals Marker Rescue of the Host Range Restriction Defects of Modified Vaccinia Virus Ankara

Virology ◽  
1998 ◽  
Vol 251 (2) ◽  
pp. 334-342 ◽  
Author(s):  
Linda S. Wyatt ◽  
Miles W. Carroll ◽  
Claus-Peter Czerny ◽  
Michael Merchlinsky ◽  
Jerry R. Sisler ◽  
...  
Keyword(s):  
Vaccinia Virus ◽  
Host Range ◽  
Range Restriction ◽  
Marker Rescue ◽  
Modified Vaccinia Virus Ankara ◽  
Host Range Restriction

scholarly journals Host-Range Restriction of Vaccinia Virus E3L Deletion Mutant Can Be Overcome In Vitro, but Not In Vivo, by Expression of the Influenza Virus NS1 Protein

PLoS ONE ◽  
2011 ◽  
Vol 6 (12) ◽  
pp. e28677 ◽  
Author(s):  
Susana Guerra ◽  
Fernando Abaitua ◽  
Luis Martínez-Sobrido ◽  
Mariano Esteban ◽  
Adolfo García-Sastre ◽  
...  
Keyword(s):  
Influenza Virus ◽  
Vaccinia Virus ◽  
Host Range ◽  
Deletion Mutant ◽  
Ns1 Protein ◽  
Range Restriction ◽  
Host Range Restriction

scholarly journals Introduction of the Six Major Genomic Deletions of Modified Vaccinia Virus Ankara (MVA) into the Parental Vaccinia Virus Is Not Sufficient To Reproduce an MVA-Like Phenotype in Cell Culture and in Mice

2010 ◽  
Vol 84 (19) ◽  
pp. 9907-9919 ◽  
Author(s):  
Christine Meisinger-Henschel ◽  
Michaela Späth ◽  
Susanne Lukassen ◽  
Michael Wolferstätter ◽  
Heike Kachelriess ◽  
...  
Keyword(s):  
Cell Culture ◽  
Vaccinia Virus ◽  
Host Range ◽  
Cell Lines ◽  
Moderate Degree ◽  
Range Restriction ◽  
Genomic Deletions ◽  
Artificial Chromosomes ◽  
Modified Vaccinia Virus Ankara

ABSTRACT Modified vaccinia virus Ankara (MVA) has a highly restricted host range in cell culture and is apathogenic in vivo. MVA was derived from the parental chorioallantois vaccinia virus Ankara (CVA) by more than 570 passages in chicken embryo fibroblast (CEF) cells. During CEF cell passaging, six major deletions comprising 24,668 nucleotides occurred in the CVA genome. We have cloned both the MVA and the parental CVA genome as bacterial artificial chromosomes (BACs) and have sequentially introduced the six major MVA deletions into the cloned CVA genome. Reconstituted mutant CVA viruses containing up to six major MVA deletions showed no detectable replication restriction in 12 of 14 mammalian cell lines tested; the exceptions were rabbit cell lines RK13 and SIRC. In mice, CVA mutants with up to three deletions showed slightly enhanced virulence, suggesting that gene deletion in replicating vaccinia virus (VACV) can result in gain of fitness in vivo. CVA mutants containing five or all six deletions were still pathogenic, with a moderate degree of attenuation. Deletion V was mainly responsible for the attenuated phenotype of these mutants. In conclusion, loss or truncation of all 31 open reading frames in the six major deletions is not sufficient to reproduce the specific MVA phenotype of strong attenuation and highly restricted host range. Mutations in viral genes outside or in association with the six major deletions appear to contribute significantly to this phenotype. Host range restriction and avirulence of MVA are most likely a cooperative effect of gene deletions and mutations involving the major deletions.

Host-range restriction of vaccinia virus E3L-specific deletion mutants

Virus Genes ◽  
1996 ◽  
Vol 12 (1) ◽  
pp. 89-94 ◽  
Author(s):  
Elizabeth Beattie ◽  
Elizabeth B. Kauffman ◽  
Hector Martinez ◽  
Marion E. Perkus ◽  
Bertram L. Jacobs ◽  
...  
Keyword(s):  
Vaccinia Virus ◽  
Host Range ◽  
Deletion Mutants ◽  
Range Restriction ◽  
Host Range Restriction ◽  
Specific Deletion

scholarly journals Transient Host Range Selection for Genetic Engineering of Modified Vaccinia Virus Ankara

BioTechniques ◽  
2000 ◽  
Vol 28 (6) ◽  
pp. 1137-1148 ◽  
Author(s):  
C. Staib ◽  
I. Drexler ◽  
M. Ohlmann ◽  
S. Wintersperger ◽  
V. Erfle ◽  
...  
Keyword(s):  
Genetic Engineering ◽  
Vaccinia Virus ◽  
Host Range ◽  
Modified Vaccinia Virus Ankara ◽  
Selection For ◽  
Range Selection

scholarly journals Analysis of Host Range Restriction Determinants in the Rabbit Model: Comparison of Homologous and Heterologous Rotavirus Infections

1998 ◽  
Vol 72 (3) ◽  
pp. 2341-2351 ◽  
Author(s):  
Max Ciarlet ◽  
Mary K. Estes ◽  
Christopher Barone ◽  
Robert F. Ramig ◽  
Margaret E. Conner
Keyword(s):  
Host Range ◽  
Model Comparison ◽  
Rabbit Model ◽  
Productive Infection ◽  
Complete Protection ◽  
Range Restriction ◽  
Rotavirus Infection ◽  
Replication Efficiency ◽  
Host Range Restriction ◽  
Rotavirus Infections

ABSTRACT The main limitation of both the rabbit and mouse models of rotavirus infection is that human rotavirus (HRV) strains do not replicate efficiently in either animal. The identification of individual genes necessary for conferring replication competence in a heterologous host is important to an understanding of the host range restriction of rotavirus infections. We recently reported the identification of the P type of the spike protein VP4 of four lapine rotavirus strains as being P[14]. To determine whether VP4 is involved in host range restriction in rabbits, we evaluated infection in rotavirus antibody-free rabbits inoculated orally with two P[14] HRVs, PA169 (G6) and HAL1166 (G8), and with several other HRV strains and animal rotavirus strains of different P and G types. We also evaluated whether the parental rhesus rotavirus (RRV) (P5B[3], G3) and the derived RRV-HRV reassortant candidate vaccine strains RRV × D (G1), RRV × DS-1 (G2), and RRV × ST3 (G4) would productively infect rabbits. Based on virus shedding, limited replication was observed with the P[14] HRV strains and with the SA11 Cl3 (P[2], G3) and SA11 4F (P6[1], G3) animal rotavirus strains, compared to the homologous ALA strain (P[14], G3). However, even limited infection provided complete protection from rotavirus infection when rabbits were challenged orally 28 days postinoculation (DPI) with 103 50% infective doses of ALA rabbit rotavirus. Other HRVs did not productively infect rabbits and provided no significant protection from challenge, in spite of occasional seroconversion. Simian RRV replicated as efficiently as lapine ALA rotavirus in rabbits and provided complete protection from ALA challenge. Live attenuated RRV reassortant vaccine strains resulted in no, limited, or productive infection of rabbits, but all rabbits were completely protected from heterotypic ALA challenge. The altered replication efficiency of the reassortants in rabbits suggests a role for VP7 in host range restriction. Also, our results suggest that VP4 may be involved in, but is not exclusively responsible for, host range restriction in the rabbit model. The replication efficiency of rotavirus in rabbits also is not controlled by the product of gene 5 (NSP1) alone, since a reassortant rotavirus with ALA gene 5 and all other genes from SA11 was more severely replication restricted than either parental rotavirus strain.

scholarly journals Repair of a previously uncharacterized second host-range gene contributes to full replication of modified vaccinia virus Ankara (MVA) in human cells

2020 ◽  
Vol 117 (7) ◽  
pp. 3759-3767 ◽  
Author(s):  
Chen Peng ◽  
Bernard Moss
Keyword(s):  
Vaccinia Virus ◽  
Host Range ◽  
Cell Lines ◽  
Chicken Embryo ◽  
A549 Cells ◽  
Human Cells ◽  
Modified Vaccinia Virus Ankara ◽  
Core Proteins ◽  
Embryo Fibroblasts ◽  
Chicken Embryo Fibroblasts

Modified vaccinia virus Ankara (MVA), a widely used vaccine vector for expression of genes of unrelated pathogens, is safe, immunogenic, and can incorporate large amounts of added DNA. MVA was derived by extensively passaging the chorioallantois vaccinia virus Ankara (CVA) vaccine strain in chicken embryo fibroblasts during which numerous mutations and deletions occurred with loss of replicative ability in most mammalian cells. Restoration of the deleted C12L gene, encoding serine protease inhibitor 1, enhances replication of MVA in human MRC-5 cells but only slightly in other human cells. Here we show that repair of the inactivated C16L/B22R gene of MVA enhances replication in numerous human cell lines. This previously uncharacterized gene is present at both ends of the genome of many orthopoxviruses and is highly conserved in most, including smallpox and monkeypox viruses. The C16L/B22R gene is expressed early in infection from the second methionine of the previously annotated Copenhagen strain open reading frame (ORF) as a 17.4-kDa protein. The C16/B22 and C12 proteins together promote MVA replication in human cells to levels that are comparable to titers in chicken embryo fibroblasts. Both proteins enhance virion assembly, but C16/B22 increases proteolytic processing of core proteins in A549 cells consistent with higher infectious virus titers. Furthermore, human A549 cells expressing codon-optimized C16L/B22R and C12L genes support higher levels of MVA replication than cell lines expressing neither or either alone. Identification of the genes responsible for the host-range defect of MVA may allow more rational engineering of vaccines for efficacy, safety, and propagation.

scholarly journals Host Range Restriction of Epstein-Barr Virus and Related Lymphocryptoviruses

2015 ◽  
Vol 89 (17) ◽  
pp. 9133-9136 ◽  
Author(s):  
Janine Mühe ◽  
Fred Wang
Keyword(s):  
B Cells ◽  
Host Range ◽  
Epstein Barr Virus ◽  
Nonhuman Primates ◽  
Range Restriction ◽  
Barr Virus ◽  
Epstein Barr ◽  
Multiple Species ◽  
High Degree ◽  
Host Range Restriction

Epstein-Barr-related herpesviruses, or lymphocryptoviruses (LCV), naturally infect humans and nonhuman primates (NHP), but their host range is not well characterized. Using LCV and B cells from multiple species of Hominidae and Cercopithecidae, we show that LCV can immortalize B cells from some nonnative species but that growth transformation is restricted to B cells from their own family of hominoids or Old World NHP, suggesting a high degree of LCV adaptation to their natural primate host.

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