Modified vaccinia virus Ankara multiplies in rat IEC-6 cells and limited production of mature virions occurs in other mammalian cell lines

Okeke, Malachy Ifeanyi; Nilssen, Øivind; Traavik, Terje

doi:10.1099/vir.0.81479-0

Cited by 30 publications

(37 citation statements)

References 37 publications

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“…Thus, IEC-6 cells are semipermissive for MVA by the categories defined in a previous report (9). However, in contrast to previous observations (35), IEC-6 cells were clearly not fully permissive for MVA B . All CVA mutants replicated with an efficiency similar to that of CVA B in this rat cell line (Fig.…”

Section: Cloning Of the Cva And Mva Genomes As Bacs And Reactivation contrasting

confidence: 61%

“…The block in viral replication occurs very late during assembly of mature and infectious viral particles (42,48). With the notable exception of the Syrian hamster cell line BHK-21 and the recently described rat cell line IEC-6, MVA has a very limited ability to productively replicate in mammalian cells (9,16,35). The genetic basis of the particular host range restriction of MVA is still not well defined.…”

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confidence: 99%

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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

Meisinger-Henschel

Späth

Lukassen

et al. 2010

J Virol

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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.

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Section: Cloning Of the Cva And Mva Genomes As Bacs And Reactivation contrasting

confidence: 61%

mentioning

confidence: 99%

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

Meisinger-Henschel

Späth

Lukassen

et al. 2010

J Virol

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“…During this passaging the virus lost 15% of its genome, with 25 of its approximately 177 genes exhibiting mutations, deletions and/or truncations [46]. MVA has a restricted host range with severely limited replication efficiency in most mammalian cell lines [47][48][49]. MVA is currently being used as a viral vector for the development of recombinant vaccines for numerous other pathogens including: HIV, malaria, HPV, CMV, leishmania, TB and others [50][51][52][53][54][55][56].…”

Section: Smallpox Vaccinesmentioning

confidence: 99%

T‐Cell epitope discovery for variola and vaccinia viruses

Kennedy

2006

Reviews in Medical Virology

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Variola major, the causative agent of smallpox, afflicted mankind throughout history until the worldwide World Health Organisation WHO vaccination campaign successfully eradicated the disease. Unfortunately, recent concerns about bioterrorism have renewed scientific interest in this virus. One essential component of our biodefense and preparedness efforts is an understanding of poxvirus immunity. To this end a number of laboratories have sought to discover T- and B-Cell epitopes from select agents such as variola virus. This review focuses on the efforts to identify CD8(+) T-Cell epitopes from poxviruses as a means to develop new vaccines and therapeutics. A wide variety of techniques have been employed by several research groups to provide complementary information regarding cellular immune responses to poxviruses. In the last several years well over 100 T-Cell epitopes have been identified and the work rapidly continues. The information gleaned from these studies will not only give us a greater understanding of immunity to variola virus and other viruses, but also provide a foundation for next generation vaccines and additional tools with which to study host-pathogen interactions.

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“…This suggested the production of MVA particles despite its much reduced replication capability. Although MVA is generally known to be highly attenuated, several cell lines other than CEF (chicken embryo fibroblasts) and BHK21 (baby hamster kidney cells) but including Vero-B4 have been shown to be semi-permissive (Okeke et al, 2006). At a titer of > 10 7 MVA gene copies/ ml, Vero-B4 cells started to detach from PI18 onwards and eventually died off.…”

Section: Vaccinia Virus (Vv) and Modified Vaccinia Ankara (Mva)mentioning

confidence: 99%