Evidence map›Paper›PMID 31236440›Full record

ArticleMolecular therapy oncolytics2019

Partial Deletion of Glycoprotein B5R Enhances Vaccinia Virus Neutralization Escape while Preserving Oncolytic Function.

Motomu Nakatake, Hajime Kurosaki, Nozomi Kuwano, Kosuke Horita, Mai Ito, Hiromichi Kono, Tomotaka Okamura, Kosei Hasegawa, Yasuhiro Yasutomi, Takafumi Nakamura

Open access · goldAbstract read
In one paragraph

Article in Molecular therapy oncolytics, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
2.3field-weighted citation impact, top 11% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

19 citing papers in PubMed, 23 citations in OpenAlex.

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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

10 authors at 3 institutions in 1 country.

Motomu NakatakeDivision of Molecular Medicine, Department of Biomedical Science, Graduate School of Medical Sciences, Tottori University, 86 Nishi-cho, Yonago 683-8503, Japan.
Hajime KurosakiDivision of Molecular Medicine, Department of Biomedical Science, Graduate School of Medical Sciences, Tottori University, 86 Nishi-cho, Yonago 683-8503, Japan.
Nozomi KuwanoDivision of Molecular Medicine, Department of Biomedical Science, Graduate School of Medical Sciences, Tottori University, 86 Nishi-cho, Yonago 683-8503, Japan.
Kosuke HoritaDivision of Molecular Medicine, Department of Biomedical Science, Graduate School of Medical Sciences, Tottori University, 86 Nishi-cho, Yonago 683-8503, Japan.
Mai ItoDivision of Molecular Medicine, Department of Biomedical Science, Graduate School of Medical Sciences, Tottori University, 86 Nishi-cho, Yonago 683-8503, Japan.
Hiromichi KonoDivision of Molecular Medicine, Department of Biomedical Science, Graduate School of Medical Sciences, Tottori University, 86 Nishi-cho, Yonago 683-8503, Japan.
Tomotaka OkamuraLaboratory of Immunoregulation and Vaccine Research, Tsukuba Primate Research Center, National Institutes of Biomedical Innovation, Health and Nutrition, Tsukuba, Ibaraki 305-0843, Japan.
Kosei HasegawaDepartment of Gynecologic Oncology, Saitama Medical University International Medical Center, 1397-1, Yamane, Hidaka-City, Saitama 350-1298, Japan.
Yasuhiro YasutomiLaboratory of Immunoregulation and Vaccine Research, Tsukuba Primate Research Center, National Institutes of Biomedical Innovation, Health and Nutrition, Tsukuba, Ibaraki 305-0843, Japan.
Takafumi NakamuraDivision of Molecular Medicine, Department of Biomedical Science, Graduate School of Medical Sciences, Tottori University, 86 Nishi-cho, Yonago 683-8503, Japan.
Tottori University · JPNational Institute of Biomedical Innovation, Health and Nutrition · JPSaitama Medical University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Vaccinia virus (VV) has been utilized in oncolytic virotherapy, but it risks a host antiviral immune response. VV has an extracellular enveloped virus (EEV) form consisting of a normal virion covered with a host-derived outer membrane that enables its spread via circulation while evading host immune mechanisms. However, the immune resistance of EEV is only partial, owing to expression of the surface protein B5R, which has four short consensus repeat (SCR) domains that are targeted by host immune factors. To engineer a more effective virus for oncolytic virotherapy, we developed an enhanced immune-evading oncolytic VV by removing the SCRs from the attenuated strain LC16mO. Although deletion of only the SCRs preserved viral replication, progeny production, and oncolytic activity, deletion of whole B5R led to attenuation of the virus. Importantly, SCR-deleted EEV had higher neutralization resistance than did B5R-wild-type EEV against VV-immunized animal serum; moreover, it retained oncolytic function, thereby prolonging the survival of tumor-bearing mice treated with anti-VV antibody. These results demonstrate that partial SCR deletion increases neutralization escape without affecting the oncolytic potency of VV, making it useful for the treatment of tumors under the anti-virus antibody existence.

Indexed as

anti-virus antibodyB5REEVneutralization escapeoncolytic vaccinia virus

Identifiers

PMID31236440
PMCPMC6580015
OpenAlexW2946710272

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.