Evidence map›Paper›PMID 32611319›Full record

ArticleBMC microbiology2020

Eravacycline susceptibility was impacted by genetic mutation of 30S ribosome subunits, and branched-chain amino acid transport system II carrier protein, Na/Pi cotransporter family protein in Staphylococcus aureus.

Zhanwen Wang, Zhiwei Lin, Bing Bai, Guangjian Xu, Peiyu Li, Zhijian Yu, Qiwen Deng, Yongpeng Shang, Jinxin Zheng

Open access · goldAbstract read
In one paragraph

Article in BMC microbiology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
0.1field-weighted citation impact, top 42% 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

8 citing papers in PubMed, 12 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Mechanisms ofInternational journal of molecular sciences · 2025
    Article
  5. Review
  6. Emergence of eravacycline heteroresistance in carbapenem-resistantFrontiers in cellular and infection microbiology · 2024
    Article
  7. Frontiers in microbiology · 2022
    Article
  8. Article
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

9 authors at 2 institutions in 1 country.

Zhanwen WangDepartment of Infectious Diseases and Shenzhen key laboratory for endogenous infections, Shenzhen Nanshan people's Hospital and the 6th Affiliated Hospital of Shenzhen University Health Science Center, No 89, Taoyuan Road, Nanshan District, Shenzhen, 518052, China.
Zhiwei LinDepartment of Infectious Diseases and Shenzhen key laboratory for endogenous infections, Shenzhen Nanshan people's Hospital and the 6th Affiliated Hospital of Shenzhen University Health Science Center, No 89, Taoyuan Road, Nanshan District, Shenzhen, 518052, China.
Bing BaiDepartment of Infectious Diseases and Shenzhen key laboratory for endogenous infections, Shenzhen Nanshan people's Hospital and the 6th Affiliated Hospital of Shenzhen University Health Science Center, No 89, Taoyuan Road, Nanshan District, Shenzhen, 518052, China.
Guangjian XuDepartment of Infectious Diseases and Shenzhen key laboratory for endogenous infections, Shenzhen Nanshan people's Hospital and the 6th Affiliated Hospital of Shenzhen University Health Science Center, No 89, Taoyuan Road, Nanshan District, Shenzhen, 518052, China.
Peiyu LiDepartment of Infectious Diseases and Shenzhen key laboratory for endogenous infections, Shenzhen Nanshan people's Hospital and the 6th Affiliated Hospital of Shenzhen University Health Science Center, No 89, Taoyuan Road, Nanshan District, Shenzhen, 518052, China.
Zhijian YuDepartment of Infectious Diseases and Shenzhen key laboratory for endogenous infections, Shenzhen Nanshan people's Hospital and the 6th Affiliated Hospital of Shenzhen University Health Science Center, No 89, Taoyuan Road, Nanshan District, Shenzhen, 518052, China.
Qiwen DengDepartment of Infectious Diseases and Shenzhen key laboratory for endogenous infections, Shenzhen Nanshan people's Hospital and the 6th Affiliated Hospital of Shenzhen University Health Science Center, No 89, Taoyuan Road, Nanshan District, Shenzhen, 518052, China.
Yongpeng ShangDepartment of Infectious Diseases and Shenzhen key laboratory for endogenous infections, Shenzhen Nanshan people's Hospital and the 6th Affiliated Hospital of Shenzhen University Health Science Center, No 89, Taoyuan Road, Nanshan District, Shenzhen, 518052, China. 16111010064@fudan.edu.cn.
Jinxin ZhengDepartment of Infectious Diseases and Shenzhen key laboratory for endogenous infections, Shenzhen Nanshan people's Hospital and the 6th Affiliated Hospital of Shenzhen University Health Science Center, No 89, Taoyuan Road, Nanshan District, Shenzhen, 518052, China. jinxinzheng@fudan.edu.cn.
Shenzhen University Health Science Center · CNGuangdong Medical College · CN

Funding

National Natural Science Foundation of China 81902033Natural Science Foundation of Guangdong Province 2020A1515010052Sanming Project of Medicine in Shenzhen SMGC201705029Science and Technology Planning Project of Shenzhen Municipality JCYJ20180302144431923Science and Technology Planning Project of Shenzhen Municipality JCYJ20180302144721183
6 · The paper itself

Abstract

backgroundOur previous research indicated the excellent in vitro antibacterial activity of Eravacycline (Erava) and its heteroresistance frequency against clinical Staphylococcus aureus isolates. In this study, we further aimed to investigate the mechanisms of Erava resistance and heteroresistance in S. aureus. Eight parental S. aureus isolates were induced under Erava pressure in vitro and the Erava-resistant isolates were selected and identified. Then, the genetic mutations of 30S ribosomal subunits were analyzed by PCR and sequence alignment. RT-qPCR analysis were performed to compare the relative expression of eight candidate genes impacting the susceptibility of tetracycline (Tet) between the resistant or heteroresistant and parental isolates. Furthermore, the in vitro overexpression vectors of three selected candidate genes were constructed to test their impact on the heteroresistance and resistance of Erava in S. aureus.

resultsThe MICs elevation in Erava-induced resistant S. aureus isolates were identified and the increasing MICs values of another two Tet class antibiotics, including both omadacycline (Omada) and tigecycline (Tige) were also tested. Genetic mutations in 30S ribosomal protein S10 were found frequently in Erava-derived resistant isolates. RT-qPCR analysis and the in vitro overexpression experiments indicated that USA300HOU_RS00550 (an Na/Pi cotransporter family protein) and USA300HOU_RS01625 (a branched-chain amino acid transport system II carrier protein) contributed to Erava heteroresistance in S. aureus.

conclusionGenetic mutation of 30S ribosome subunits contributed to Erava resistance, and the transcriptional overexpression of USA300HOU_RS01625 and USA300HOU_RS00550 also participated in the occurrence of Erava heteroresistance in S. aureus.

Indexed as

Drug Resistance, BacterialAnti-Bacterial AgentsBacterial ProteinsChinaHumansMicrobial Sensitivity TestsMutationRibosome Subunits, Small, BacterialStaphylococcal InfectionsStaphylococcus aureusTetracyclinesTigecyclineAnti-Bacterial AgentsBacterial ProteinseravacyclineomadacyclineTetracyclinesTigecyclineAntimicrobial activityAntimicrobial agentEravacyclineStaphylococcus aureus

Identifiers

PMID32611319
PMCPMC7329441
OpenAlexW3038307258

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.