Evidence map›Paper›PMID 28971351›Full record

ArticleVirologica Sinica2017

Attenuated phenotypes and analysis of a herpes simplex virus 1 strain with partial deletion of the UL7, UL41 and LAT genes.

Xingli Xu, Yingqiu Guo, Shengtao Fan, Pingfang Cui, Min Feng, Lichun Wang, Ying Zhang, Yun Liao, Xiaolong Zhang, Qihan Li

Erratum issuedOpen access · bronzeAbstract read
In one paragraph

Article in Virologica Sinica, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
1.6field-weighted citation impact, top 17% 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

11 citing papers in PubMed, 13 citations in OpenAlex.

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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

10 authors at 1 institution in 1 country.

Xingli XuInstitute of Medical Biology, Chinese Academy of Medical Sciences and Peking Union Medical College, Yunnan Key Laboratory of Vaccine Research and Development of Severe Infectious Disease, Kunming, 650118, China.
Yingqiu GuoInstitute of Medical Biology, Chinese Academy of Medical Sciences and Peking Union Medical College, Yunnan Key Laboratory of Vaccine Research and Development of Severe Infectious Disease, Kunming, 650118, China.
Shengtao FanInstitute of Medical Biology, Chinese Academy of Medical Sciences and Peking Union Medical College, Yunnan Key Laboratory of Vaccine Research and Development of Severe Infectious Disease, Kunming, 650118, China.
Pingfang CuiInstitute of Medical Biology, Chinese Academy of Medical Sciences and Peking Union Medical College, Yunnan Key Laboratory of Vaccine Research and Development of Severe Infectious Disease, Kunming, 650118, China.
Min FengInstitute of Medical Biology, Chinese Academy of Medical Sciences and Peking Union Medical College, Yunnan Key Laboratory of Vaccine Research and Development of Severe Infectious Disease, Kunming, 650118, China.
Lichun WangInstitute of Medical Biology, Chinese Academy of Medical Sciences and Peking Union Medical College, Yunnan Key Laboratory of Vaccine Research and Development of Severe Infectious Disease, Kunming, 650118, China.
Ying ZhangInstitute of Medical Biology, Chinese Academy of Medical Sciences and Peking Union Medical College, Yunnan Key Laboratory of Vaccine Research and Development of Severe Infectious Disease, Kunming, 650118, China.
Yun LiaoInstitute of Medical Biology, Chinese Academy of Medical Sciences and Peking Union Medical College, Yunnan Key Laboratory of Vaccine Research and Development of Severe Infectious Disease, Kunming, 650118, China.
Xiaolong ZhangInstitute of Medical Biology, Chinese Academy of Medical Sciences and Peking Union Medical College, Yunnan Key Laboratory of Vaccine Research and Development of Severe Infectious Disease, Kunming, 650118, China.
Qihan LiInstitute of Medical Biology, Chinese Academy of Medical Sciences and Peking Union Medical College, Yunnan Key Laboratory of Vaccine Research and Development of Severe Infectious Disease, Kunming, 650118, China. liqihan@imbcams.com.cn.ORCID http://orcid.org/0000-0002-8932-4516
Chinese Academy of Medical Sciences & Peking Union Medical College · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

We previously constructed a herpes simplex virus 1 (HSV-1) UL7 mutant virus (M1) and showed that a partial deletion mutation of the UL7 gene led to a lower proliferative rate and an attenuated phenotype. Using the M1 mutant, we further modified the UL41 gene, which encodes another tegument protein, and the latency-associated transcript (LAT) gene. Observations of the resulting mutants with modified UL7 and UL41 (M2) or UL7, UL41 and LAT (M3) genes indicated attenuated phenotypes, with lower proliferative ratios in various cells, non-lethal infections in mice and lower viral loads in nervous tissues compared with the wild-type strain. Furthermore, no LAT stable intron could be detected in the trigeminal ganglion of M3-infected animals. The results obtained with the three HSV-1 mutants indicate that the M3 mutant is an attenuated strain with low pathogenicity during both acute and latent infections. Together, the results support the use of the M3 mutant as a candidate for the development of an HSV-1 vaccine.

Indexed as

Adaptor Proteins, Signal TransducingAnimalsCell LineCell Line, TumorClustered Regularly Interspaced Short Palindromic RepeatsHEK293 CellsHerpesvirus 1, HumanHumansImmunohistochemistryIn Situ HybridizationIntronsMembrane ProteinsMiceMice, Inbred BALB CMutationNerve TissueAdaptor Proteins, Signal TransducingLAT protein, humanMembrane ProteinsUl41 protein, Human herpesvirus 1UL7 protein, human herpesvirus 1Viral Matrix ProteinsViral Proteinsherpes simplex virus 1 (HSV-1)LATmutantUL41UL7

Identifiers

PMID28971351
PMCPMC6598894
OpenAlexW2761172677

What OpenQuestion holds

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Registered trials

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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.