---
_id: '10812'
abstract:
- lang: eng
text: Several promising strategies based on combining or cycling different antibiotics
have been proposed to increase efficacy and counteract resistance evolution, but
we still lack a deep understanding of the physiological responses and genetic
mechanisms that underlie antibiotic interactions and the clinical applicability
of these strategies. In antibiotic-exposed bacteria, the combined effects of physiological
stress responses and emerging resistance mutations (occurring at different time
scales) generate complex and often unpredictable dynamics. In this Review, we
present our current understanding of bacterial cell physiology and genetics of
responses to antibiotics. We emphasize recently discovered mechanisms of synergistic
and antagonistic drug interactions, hysteresis in temporal interactions between
antibiotics that arise from microbial physiology and interactions between antibiotics
and resistance mutations that can cause collateral sensitivity or cross-resistance.
We discuss possible connections between the different phenomena and indicate relevant
research directions. A better and more unified understanding of drug and genetic
interactions is likely to advance antibiotic therapy.
acknowledgement: The authors thank B. Kavčič and H. Schulenburg for constructive feedback
on the manuscript.
article_processing_charge: No
article_type: review
author:
- first_name: Roderich
full_name: Römhild, Roderich
id: 68E56E44-62B0-11EA-B963-444F3DDC885E
last_name: Römhild
orcid: 0000-0001-9480-5261
- first_name: Mark Tobias
full_name: Bollenbach, Mark Tobias
id: 3E6DB97A-F248-11E8-B48F-1D18A9856A87
last_name: Bollenbach
orcid: 0000-0003-4398-476X
- first_name: Dan I.
full_name: Andersson, Dan I.
last_name: Andersson
citation:
ama: Römhild R, Bollenbach MT, Andersson DI. The physiology and genetics of bacterial
responses to antibiotic combinations. Nature Reviews Microbiology. 2022;20:478-490.
doi:10.1038/s41579-022-00700-5
apa: Römhild, R., Bollenbach, M. T., & Andersson, D. I. (2022). The physiology
and genetics of bacterial responses to antibiotic combinations. Nature Reviews
Microbiology. Springer Nature. https://doi.org/10.1038/s41579-022-00700-5
chicago: Römhild, Roderich, Mark Tobias Bollenbach, and Dan I. Andersson. “The Physiology
and Genetics of Bacterial Responses to Antibiotic Combinations.” Nature Reviews
Microbiology. Springer Nature, 2022. https://doi.org/10.1038/s41579-022-00700-5.
ieee: R. Römhild, M. T. Bollenbach, and D. I. Andersson, “The physiology and genetics
of bacterial responses to antibiotic combinations,” Nature Reviews Microbiology,
vol. 20. Springer Nature, pp. 478–490, 2022.
ista: Römhild R, Bollenbach MT, Andersson DI. 2022. The physiology and genetics
of bacterial responses to antibiotic combinations. Nature Reviews Microbiology.
20, 478–490.
mla: Römhild, Roderich, et al. “The Physiology and Genetics of Bacterial Responses
to Antibiotic Combinations.” Nature Reviews Microbiology, vol. 20, Springer
Nature, 2022, pp. 478–90, doi:10.1038/s41579-022-00700-5.
short: R. Römhild, M.T. Bollenbach, D.I. Andersson, Nature Reviews Microbiology
20 (2022) 478–490.
date_created: 2022-03-04T04:33:49Z
date_published: 2022-08-01T00:00:00Z
date_updated: 2023-08-02T14:41:44Z
day: '01'
department:
- _id: CaGu
doi: 10.1038/s41579-022-00700-5
external_id:
isi:
- '000763891900001'
pmid:
- '35241807'
intvolume: ' 20'
isi: 1
keyword:
- General Immunology and Microbiology
- Microbiology
- Infectious Diseases
language:
- iso: eng
month: '08'
oa_version: None
page: 478-490
pmid: 1
publication: Nature Reviews Microbiology
publication_identifier:
eissn:
- 1740-1534
issn:
- 1740-1526
publication_status: published
publisher: Springer Nature
quality_controlled: '1'
scopus_import: '1'
status: public
title: The physiology and genetics of bacterial responses to antibiotic combinations
type: journal_article
user_id: 4359f0d1-fa6c-11eb-b949-802e58b17ae8
volume: 20
year: '2022'
...
---
_id: '12119'
abstract:
- lang: eng
text: Intravascular neutrophils and platelets collaborate in maintaining host integrity,
but their interaction can also trigger thrombotic complications. We report here
that cooperation between neutrophil and platelet lineages extends to the earliest
stages of platelet formation by megakaryocytes in the bone marrow. Using intravital
microscopy, we show that neutrophils “plucked” intravascular megakaryocyte extensions,
termed proplatelets, to control platelet production. Following CXCR4-CXCL12-dependent
migration towards perisinusoidal megakaryocytes, plucking neutrophils actively
pulled on proplatelets and triggered myosin light chain and extracellular-signal-regulated
kinase activation through reactive oxygen species. By these mechanisms, neutrophils
accelerate proplatelet growth and facilitate continuous release of platelets in
steady state. Following myocardial infarction, plucking neutrophils drove excessive
release of young, reticulated platelets and boosted the risk of recurrent ischemia.
Ablation of neutrophil plucking normalized thrombopoiesis and reduced recurrent
thrombosis after myocardial infarction and thrombus burden in venous thrombosis.
We establish neutrophil plucking as a target to reduce thromboischemic events.
acknowledgement: "We thank Coung Kieu and Dominik van den Heuvel for excellent technical
assistance. This work was supported by the German Research Foundation (PE2704/2-1,
PE2704/3-1 to T.P., SFB 1123-project B06 to S.M., SFB1525 project A07 to D.S, TRR
332 project A7 to C.S., PO 2247/2-1 to A.P., SFB1116-project B11 to A.P. and B12
to M.K.), LMU Munich’s Institutional\r\nStrategy LMUexcellent within the framework
of the German Excellence Initiative (No. 806 32 006 to T.P.), and by the German
Centre for Cardiovascular Research (DZHK) to T.P. (Postdoc Start-up grant No. 100378833).
This project has received funding from the European Research Council (ERC) under
the European Union’s Horizon 2020 research and innovation program (grant agreement
No. 833440 to S.M.). F.G. received funding from the European Union’s\r\nHorizon
2020 research and innovation program under the Marie Sk1odowska-Curie grant agreement
no. 747687. A.H. was funded by RTI2018-095497-B-I00 from Ministerio de Ciencia e
Innovacio´ n (MICINN), HR17_00527 from Fundacion La Caixa, and Transatlantic Network
of Excellence (TNE-18CVD04) from the Leducq Foundation. The CNIC is supported by
the MICINN and the Pro CNIC Foundation and is a Severo Ochoa Center of Excellence
(CEX2020-001041-S). A.P. was supported by the Forschungskommission of the Medical
Faculty of the Heinrich-Heine-Universität Düsseldorf (No. 18-2019 to A.P.). C.G.
was supported by the Helmholtz Alliance ‘Aging and Metabolic Programming, AMPro,’
by the German Federal\r\nMinistry of Education and Research to the German Center
for Diabetes Research (DZD), and by the Bavarian State Ministry of Health and Care
through the research project DigiMed Bayern."
article_processing_charge: No
article_type: original
author:
- first_name: Tobias
full_name: Petzold, Tobias
last_name: Petzold
- first_name: Zhe
full_name: Zhang, Zhe
last_name: Zhang
- first_name: Iván
full_name: Ballesteros, Iván
last_name: Ballesteros
- first_name: Inas
full_name: Saleh, Inas
last_name: Saleh
- first_name: Amin
full_name: Polzin, Amin
last_name: Polzin
- first_name: Manuela
full_name: Thienel, Manuela
last_name: Thienel
- first_name: Lulu
full_name: Liu, Lulu
last_name: Liu
- first_name: Qurrat
full_name: Ul Ain, Qurrat
last_name: Ul Ain
- first_name: Vincent
full_name: Ehreiser, Vincent
last_name: Ehreiser
- first_name: Christian
full_name: Weber, Christian
last_name: Weber
- first_name: Badr
full_name: Kilani, Badr
last_name: Kilani
- first_name: Pontus
full_name: Mertsch, Pontus
last_name: Mertsch
- first_name: Jeremias
full_name: Götschke, Jeremias
last_name: Götschke
- first_name: Sophie
full_name: Cremer, Sophie
last_name: Cremer
- first_name: Wenwen
full_name: Fu, Wenwen
last_name: Fu
- first_name: Michael
full_name: Lorenz, Michael
last_name: Lorenz
- first_name: Hellen
full_name: Ishikawa-Ankerhold, Hellen
last_name: Ishikawa-Ankerhold
- first_name: Elisabeth
full_name: Raatz, Elisabeth
last_name: Raatz
- first_name: Shaza
full_name: El-Nemr, Shaza
last_name: El-Nemr
- first_name: Agnes
full_name: Görlach, Agnes
last_name: Görlach
- first_name: Esther
full_name: Marhuenda, Esther
last_name: Marhuenda
- first_name: Konstantin
full_name: Stark, Konstantin
last_name: Stark
- first_name: Joachim
full_name: Pircher, Joachim
last_name: Pircher
- first_name: David
full_name: Stegner, David
last_name: Stegner
- first_name: Christian
full_name: Gieger, Christian
last_name: Gieger
- first_name: Marc
full_name: Schmidt-Supprian, Marc
last_name: Schmidt-Supprian
- first_name: Florian R
full_name: Gärtner, Florian R
id: 397A88EE-F248-11E8-B48F-1D18A9856A87
last_name: Gärtner
orcid: 0000-0001-6120-3723
- first_name: Isaac
full_name: Almendros, Isaac
last_name: Almendros
- first_name: Malte
full_name: Kelm, Malte
last_name: Kelm
- first_name: Christian
full_name: Schulz, Christian
last_name: Schulz
- first_name: Andrés
full_name: Hidalgo, Andrés
last_name: Hidalgo
- first_name: Steffen
full_name: Massberg, Steffen
last_name: Massberg
citation:
ama: Petzold T, Zhang Z, Ballesteros I, et al. Neutrophil “plucking” on megakaryocytes
drives platelet production and boosts cardiovascular disease. Immunity.
2022;55(12):2285-2299.e7. doi:10.1016/j.immuni.2022.10.001
apa: Petzold, T., Zhang, Z., Ballesteros, I., Saleh, I., Polzin, A., Thienel, M.,
… Massberg, S. (2022). Neutrophil “plucking” on megakaryocytes drives platelet
production and boosts cardiovascular disease. Immunity. Elsevier. https://doi.org/10.1016/j.immuni.2022.10.001
chicago: Petzold, Tobias, Zhe Zhang, Iván Ballesteros, Inas Saleh, Amin Polzin,
Manuela Thienel, Lulu Liu, et al. “Neutrophil ‘Plucking’ on Megakaryocytes Drives
Platelet Production and Boosts Cardiovascular Disease.” Immunity. Elsevier,
2022. https://doi.org/10.1016/j.immuni.2022.10.001.
ieee: T. Petzold et al., “Neutrophil ‘plucking’ on megakaryocytes drives
platelet production and boosts cardiovascular disease,” Immunity, vol.
55, no. 12. Elsevier, p. 2285–2299.e7, 2022.
ista: Petzold T, Zhang Z, Ballesteros I, Saleh I, Polzin A, Thienel M, Liu L, Ul
Ain Q, Ehreiser V, Weber C, Kilani B, Mertsch P, Götschke J, Cremer S, Fu W, Lorenz
M, Ishikawa-Ankerhold H, Raatz E, El-Nemr S, Görlach A, Marhuenda E, Stark K,
Pircher J, Stegner D, Gieger C, Schmidt-Supprian M, Gärtner FR, Almendros I, Kelm
M, Schulz C, Hidalgo A, Massberg S. 2022. Neutrophil “plucking” on megakaryocytes
drives platelet production and boosts cardiovascular disease. Immunity. 55(12),
2285–2299.e7.
mla: Petzold, Tobias, et al. “Neutrophil ‘Plucking’ on Megakaryocytes Drives Platelet
Production and Boosts Cardiovascular Disease.” Immunity, vol. 55, no. 12,
Elsevier, 2022, p. 2285–2299.e7, doi:10.1016/j.immuni.2022.10.001.
short: T. Petzold, Z. Zhang, I. Ballesteros, I. Saleh, A. Polzin, M. Thienel, L.
Liu, Q. Ul Ain, V. Ehreiser, C. Weber, B. Kilani, P. Mertsch, J. Götschke, S.
Cremer, W. Fu, M. Lorenz, H. Ishikawa-Ankerhold, E. Raatz, S. El-Nemr, A. Görlach,
E. Marhuenda, K. Stark, J. Pircher, D. Stegner, C. Gieger, M. Schmidt-Supprian,
F.R. Gärtner, I. Almendros, M. Kelm, C. Schulz, A. Hidalgo, S. Massberg, Immunity
55 (2022) 2285–2299.e7.
date_created: 2023-01-12T11:56:54Z
date_published: 2022-12-13T00:00:00Z
date_updated: 2023-08-03T14:21:51Z
day: '13'
ddc:
- '570'
department:
- _id: MiSi
doi: 10.1016/j.immuni.2022.10.001
ec_funded: 1
external_id:
isi:
- '000922019600003'
pmid:
- '36272416'
file:
- access_level: open_access
checksum: 073267a9c0ad9f85a650053bc7b23777
content_type: application/pdf
creator: dernst
date_created: 2023-01-23T10:18:48Z
date_updated: 2023-01-23T10:18:48Z
file_id: '12341'
file_name: 2022_Immunity_Petzold.pdf
file_size: 5299475
relation: main_file
success: 1
file_date_updated: 2023-01-23T10:18:48Z
has_accepted_license: '1'
intvolume: ' 55'
isi: 1
issue: '12'
keyword:
- Infectious Diseases
- Immunology
- Immunology and Allergy
language:
- iso: eng
license: https://creativecommons.org/licenses/by-nc-nd/4.0/
month: '12'
oa: 1
oa_version: Published Version
page: 2285-2299.e7
pmid: 1
project:
- _id: 260AA4E2-B435-11E9-9278-68D0E5697425
call_identifier: H2020
grant_number: '747687'
name: Mechanical Adaptation of Lamellipodial Actin Networks in Migrating Cells
publication: Immunity
publication_identifier:
issn:
- 1074-7613
publication_status: published
publisher: Elsevier
quality_controlled: '1'
scopus_import: '1'
status: public
title: Neutrophil “plucking” on megakaryocytes drives platelet production and boosts
cardiovascular disease
tmp:
image: /images/cc_by_nc_nd.png
legal_code_url: https://creativecommons.org/licenses/by-nc-nd/4.0/legalcode
name: Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International
(CC BY-NC-ND 4.0)
short: CC BY-NC-ND (4.0)
type: journal_article
user_id: 4359f0d1-fa6c-11eb-b949-802e58b17ae8
volume: 55
year: '2022'
...
---
_id: '12131'
abstract:
- lang: eng
text: Replication-incompetent adenoviral vectors have been extensively used as a
platform for vaccine design, with at least four anti-COVID-19 vaccines authorized
to date. These vaccines elicit neutralizing antibody responses directed against
SARS-CoV-2 Spike protein and confer significant level of protection against SARS-CoV-2
infection. Immunization with adenovirus-vectored vaccines is known to be accompanied
by the production of anti-vector antibodies, which may translate into reduced
efficacy of booster or repeated rounds of revaccination. Here, we used blood samples
from patients who received an adenovirus-based Gam-COVID-Vac vaccine to address
the question of whether anti-vector antibodies may influence the magnitude of
SARS-CoV-2-specific humoral response after booster vaccination. We observed that
rAd26-based prime vaccination with Gam-COVID-Vac induced the development of Ad26-neutralizing
antibodies, which persisted in circulation for at least 9 months. Our analysis
further indicates that high pre-boost Ad26 neutralizing antibody titers do not
appear to affect the humoral immunogenicity of the Gam-COVID-Vac boost. The titers
of anti-SARS-CoV-2 RBD IgGs and antibodies, which neutralized both the wild type
and the circulating variants of concern of SARS-CoV-2 such as Delta and Omicron,
were independent of the pre-boost levels of Ad26-neutralizing antibodies. Thus,
our results support the development of repeated immunization schedule with adenovirus-based
COVID-19 vaccines.
acknowledgement: We thank Sergey Kulemzin, Grigory Efimov, Yuri Lebedin, Alexander
Taranin and Rudolf Valenta for providing reagents. Figures were created with the
help of BioRender.com. This work was supported by the Russian Science Foundation
(Project 21-15-00286). Byazrova M.G. was supported by the RUDN University Strategic
Academic Leadership Program.
article_number: '145'
article_processing_charge: No
article_type: original
author:
- first_name: Maria G.
full_name: Byazrova, Maria G.
last_name: Byazrova
- first_name: Ekaterina A.
full_name: Astakhova, Ekaterina A.
last_name: Astakhova
- first_name: Aygul
full_name: Minnegalieva, Aygul
id: 87DF77F0-1D9A-11EA-B6AE-CE443DDC885E
last_name: Minnegalieva
- first_name: Maria M.
full_name: Sukhova, Maria M.
last_name: Sukhova
- first_name: Artem A.
full_name: Mikhailov, Artem A.
last_name: Mikhailov
- first_name: Alexey G.
full_name: Prilipov, Alexey G.
last_name: Prilipov
- first_name: Andrey A.
full_name: Gorchakov, Andrey A.
last_name: Gorchakov
- first_name: Alexander V.
full_name: Filatov, Alexander V.
last_name: Filatov
citation:
ama: Byazrova MG, Astakhova EA, Minnegalieva A, et al. Anti-Ad26 humoral immunity
does not compromise SARS-COV-2 neutralizing antibody responses following Gam-COVID-Vac
booster vaccination. npj Vaccines. 2022;7. doi:10.1038/s41541-022-00566-x
apa: Byazrova, M. G., Astakhova, E. A., Minnegalieva, A., Sukhova, M. M., Mikhailov,
A. A., Prilipov, A. G., … Filatov, A. V. (2022). Anti-Ad26 humoral immunity does
not compromise SARS-COV-2 neutralizing antibody responses following Gam-COVID-Vac
booster vaccination. Npj Vaccines. Springer Nature. https://doi.org/10.1038/s41541-022-00566-x
chicago: Byazrova, Maria G., Ekaterina A. Astakhova, Aygul Minnegalieva, Maria M.
Sukhova, Artem A. Mikhailov, Alexey G. Prilipov, Andrey A. Gorchakov, and Alexander
V. Filatov. “Anti-Ad26 Humoral Immunity Does Not Compromise SARS-COV-2 Neutralizing
Antibody Responses Following Gam-COVID-Vac Booster Vaccination.” Npj Vaccines.
Springer Nature, 2022. https://doi.org/10.1038/s41541-022-00566-x.
ieee: M. G. Byazrova et al., “Anti-Ad26 humoral immunity does not compromise
SARS-COV-2 neutralizing antibody responses following Gam-COVID-Vac booster vaccination,”
npj Vaccines, vol. 7. Springer Nature, 2022.
ista: Byazrova MG, Astakhova EA, Minnegalieva A, Sukhova MM, Mikhailov AA, Prilipov
AG, Gorchakov AA, Filatov AV. 2022. Anti-Ad26 humoral immunity does not compromise
SARS-COV-2 neutralizing antibody responses following Gam-COVID-Vac booster vaccination.
npj Vaccines. 7, 145.
mla: Byazrova, Maria G., et al. “Anti-Ad26 Humoral Immunity Does Not Compromise
SARS-COV-2 Neutralizing Antibody Responses Following Gam-COVID-Vac Booster Vaccination.”
Npj Vaccines, vol. 7, 145, Springer Nature, 2022, doi:10.1038/s41541-022-00566-x.
short: M.G. Byazrova, E.A. Astakhova, A. Minnegalieva, M.M. Sukhova, A.A. Mikhailov,
A.G. Prilipov, A.A. Gorchakov, A.V. Filatov, Npj Vaccines 7 (2022).
date_created: 2023-01-12T12:02:54Z
date_published: 2022-11-15T00:00:00Z
date_updated: 2023-08-04T08:52:40Z
day: '15'
ddc:
- '570'
department:
- _id: FyKo
doi: 10.1038/s41541-022-00566-x
external_id:
isi:
- '000884278600004'
pmid:
- '36379998'
file:
- access_level: open_access
checksum: ddaac096381565b2b4b7dcc34cdbc4ee
content_type: application/pdf
creator: dernst
date_created: 2023-01-23T11:22:09Z
date_updated: 2023-01-23T11:22:09Z
file_id: '12347'
file_name: 2022_njpVaccines_Byazrova.pdf
file_size: 1856046
relation: main_file
success: 1
file_date_updated: 2023-01-23T11:22:09Z
has_accepted_license: '1'
intvolume: ' 7'
isi: 1
keyword:
- Pharmacology (medical)
- Infectious Diseases
- Pharmacology
- Immunology
- SARS-COV-2
- COVID
language:
- iso: eng
month: '11'
oa: 1
oa_version: Published Version
pmid: 1
publication: npj Vaccines
publication_identifier:
issn:
- 2059-0105
publication_status: published
publisher: Springer Nature
quality_controlled: '1'
scopus_import: '1'
status: public
title: Anti-Ad26 humoral immunity does not compromise SARS-COV-2 neutralizing antibody
responses following Gam-COVID-Vac booster vaccination
tmp:
image: /images/cc_by.png
legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
short: CC BY (4.0)
type: journal_article
user_id: 4359f0d1-fa6c-11eb-b949-802e58b17ae8
volume: 7
year: '2022'
...
---
_id: '12173'
abstract:
- lang: eng
text: With increasing urbanization and industrialization, the prevalence of inflammatory
bowel diseases (IBDs) has steadily been rising over the past two decades. IBD
involves flares of gastrointestinal (GI) inflammation accompanied by microbiota
perturbations. However, microbial mechanisms that trigger such flares remain elusive.
Here, we analyzed the association of the emerging pathogen atypical enteropathogenic
E. coli (aEPEC) with IBD disease activity. The presence of diarrheagenic E. coli
was assessed in stool samples from 630 IBD patients and 234 age- and sex-matched
controls without GI symptoms. Microbiota was analyzed with 16S ribosomal RNA gene
amplicon sequencing, and 57 clinical aEPEC isolates were subjected to whole-genome
sequencing and in vitro pathogenicity experiments including biofilm formation,
epithelial barrier function and the ability to induce pro-inflammatory signaling.
The presence of aEPEC correlated with laboratory, clinical and endoscopic disease
activity in ulcerative colitis (UC), as well as microbiota dysbiosis. In vitro,
aEPEC strains induce epithelial p21-activated kinases, disrupt the epithelial
barrier and display potent biofilm formation. The effector proteins espV and espG2
distinguish aEPEC cultured from UC and Crohn’s disease patients, respectively.
EspV-positive aEPEC harbor more virulence factors and have a higher pro-inflammatory
potential, which is counteracted by 5-ASA. aEPEC may tip a fragile immune–microbiota
homeostasis and thereby contribute to flares in UC. aEPEC isolates from UC patients
display properties to disrupt the epithelial barrier and to induce pro-inflammatory
signaling in vitro.
acknowledgement: "We would like to acknowledge Anita Krnjic, Christina Gmainer, Marion
Nehr, Helga Mock, and Sena Ecin for technical support in conducting the experiments.\r\nThis
study was supported by the Austrian Science Fund (P 32302) and the Vienna Science
and Technology Fund (LS18- 053; Austrian Science Fund (FWF)) [P 32302]."
article_number: e2143218
article_processing_charge: No
article_type: original
author:
- first_name: Maximilian
full_name: Baumgartner, Maximilian
last_name: Baumgartner
- first_name: Rebecca
full_name: Zirnbauer, Rebecca
last_name: Zirnbauer
- first_name: Sabine
full_name: Schlager, Sabine
last_name: Schlager
- first_name: Daniel
full_name: Mertens, Daniel
last_name: Mertens
- first_name: Nikolaus
full_name: Gasche, Nikolaus
last_name: Gasche
- first_name: Barbara
full_name: Sladek, Barbara
last_name: Sladek
- first_name: Craig
full_name: Herbold, Craig
last_name: Herbold
- first_name: Olga
full_name: Bochkareva, Olga
last_name: Bochkareva
- first_name: Vera
full_name: Emelianenko, Vera
id: 20152b9d-927a-11ed-8107-be36d740812d
last_name: Emelianenko
- first_name: Harald
full_name: Vogelsang, Harald
last_name: Vogelsang
- first_name: Michaela
full_name: Lang, Michaela
last_name: Lang
- first_name: Anton
full_name: Klotz, Anton
last_name: Klotz
- first_name: Birgit
full_name: Moik, Birgit
last_name: Moik
- first_name: Athanasios
full_name: Makristathis, Athanasios
last_name: Makristathis
- first_name: David
full_name: Berry, David
last_name: Berry
- first_name: Stefanie
full_name: Dabsch, Stefanie
last_name: Dabsch
- first_name: Vineeta
full_name: Khare, Vineeta
last_name: Khare
- first_name: Christoph
full_name: Gasche, Christoph
last_name: Gasche
citation:
ama: Baumgartner M, Zirnbauer R, Schlager S, et al. Atypical enteropathogenic E.
coli are associated with disease activity in ulcerative colitis. Gut Microbes.
2022;14(1). doi:10.1080/19490976.2022.2143218
apa: Baumgartner, M., Zirnbauer, R., Schlager, S., Mertens, D., Gasche, N., Sladek,
B., … Gasche, C. (2022). Atypical enteropathogenic E. coli are associated with
disease activity in ulcerative colitis. Gut Microbes. Taylor & Francis.
https://doi.org/10.1080/19490976.2022.2143218
chicago: Baumgartner, Maximilian, Rebecca Zirnbauer, Sabine Schlager, Daniel Mertens,
Nikolaus Gasche, Barbara Sladek, Craig Herbold, et al. “Atypical Enteropathogenic
E. Coli Are Associated with Disease Activity in Ulcerative Colitis.” Gut Microbes.
Taylor & Francis, 2022. https://doi.org/10.1080/19490976.2022.2143218.
ieee: M. Baumgartner et al., “Atypical enteropathogenic E. coli are associated
with disease activity in ulcerative colitis,” Gut Microbes, vol. 14, no.
1. Taylor & Francis, 2022.
ista: Baumgartner M, Zirnbauer R, Schlager S, Mertens D, Gasche N, Sladek B, Herbold
C, Bochkareva O, Emelianenko V, Vogelsang H, Lang M, Klotz A, Moik B, Makristathis
A, Berry D, Dabsch S, Khare V, Gasche C. 2022. Atypical enteropathogenic E. coli
are associated with disease activity in ulcerative colitis. Gut Microbes. 14(1),
e2143218.
mla: Baumgartner, Maximilian, et al. “Atypical Enteropathogenic E. Coli Are Associated
with Disease Activity in Ulcerative Colitis.” Gut Microbes, vol. 14, no.
1, e2143218, Taylor & Francis, 2022, doi:10.1080/19490976.2022.2143218.
short: M. Baumgartner, R. Zirnbauer, S. Schlager, D. Mertens, N. Gasche, B. Sladek,
C. Herbold, O. Bochkareva, V. Emelianenko, H. Vogelsang, M. Lang, A. Klotz, B.
Moik, A. Makristathis, D. Berry, S. Dabsch, V. Khare, C. Gasche, Gut Microbes
14 (2022).
date_created: 2023-01-12T12:11:36Z
date_published: 2022-11-22T00:00:00Z
date_updated: 2023-08-04T09:10:18Z
day: '22'
ddc:
- '570'
department:
- _id: FyKo
doi: 10.1080/19490976.2022.2143218
external_id:
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intvolume: ' 14'
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keyword:
- Infectious Diseases
- Microbiology (medical)
- Gastroenterology
- Microbiology
language:
- iso: eng
month: '11'
oa: 1
oa_version: Published Version
publication: Gut Microbes
publication_identifier:
eissn:
- 1949-0984
issn:
- 1949-0976
publication_status: published
publisher: Taylor & Francis
quality_controlled: '1'
scopus_import: '1'
status: public
title: Atypical enteropathogenic E. coli are associated with disease activity in ulcerative
colitis
tmp:
image: /images/cc_by.png
legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
short: CC BY (4.0)
type: journal_article
user_id: 4359f0d1-fa6c-11eb-b949-802e58b17ae8
volume: 14
year: '2022'
...
---
_id: '10103'
abstract:
- lang: eng
text: The small cellular molecule inositol hexakisphosphate (IP6) has been known
for ~20 years to promote the in vitro assembly of HIV-1 into immature virus-like
particles. However, the molecular details underlying this effect have been determined
only recently, with the identification of the IP6 binding site in the immature
Gag lattice. IP6 also promotes formation of the mature capsid protein (CA) lattice
via a second IP6 binding site, and enhances core stability, creating a favorable
environment for reverse transcription. IP6 also enhances assembly of other retroviruses,
from both the Lentivirus and the Alpharetrovirus genera. These findings suggest
that IP6 may have a conserved function throughout the family Retroviridae. Here,
we discuss the different steps in the viral life cycle that are influenced by
IP6, and describe in detail how IP6 interacts with the immature and mature lattices
of different retroviruses.
acknowledgement: We thank Volker M. Vogt for his critical comments in preparation
of the review.
article_number: '1853'
article_processing_charge: Yes
article_type: original
author:
- first_name: Martin
full_name: Obr, Martin
id: 4741CA5A-F248-11E8-B48F-1D18A9856A87
last_name: Obr
orcid: 0000-0003-1756-6564
- first_name: Florian KM
full_name: Schur, Florian KM
id: 48AD8942-F248-11E8-B48F-1D18A9856A87
last_name: Schur
orcid: 0000-0003-4790-8078
- first_name: Robert A.
full_name: Dick, Robert A.
last_name: Dick
citation:
ama: Obr M, Schur FK, Dick RA. A structural perspective of the role of IP6 in immature
and mature retroviral assembly. Viruses. 2021;13(9). doi:10.3390/v13091853
apa: Obr, M., Schur, F. K., & Dick, R. A. (2021). A structural perspective of
the role of IP6 in immature and mature retroviral assembly. Viruses. MDPI.
https://doi.org/10.3390/v13091853
chicago: Obr, Martin, Florian KM Schur, and Robert A. Dick. “A Structural Perspective
of the Role of IP6 in Immature and Mature Retroviral Assembly.” Viruses.
MDPI, 2021. https://doi.org/10.3390/v13091853.
ieee: M. Obr, F. K. Schur, and R. A. Dick, “A structural perspective of the role
of IP6 in immature and mature retroviral assembly,” Viruses, vol. 13, no.
9. MDPI, 2021.
ista: Obr M, Schur FK, Dick RA. 2021. A structural perspective of the role of IP6
in immature and mature retroviral assembly. Viruses. 13(9), 1853.
mla: Obr, Martin, et al. “A Structural Perspective of the Role of IP6 in Immature
and Mature Retroviral Assembly.” Viruses, vol. 13, no. 9, 1853, MDPI, 2021,
doi:10.3390/v13091853.
short: M. Obr, F.K. Schur, R.A. Dick, Viruses 13 (2021).
date_created: 2021-10-07T09:13:29Z
date_published: 2021-09-17T00:00:00Z
date_updated: 2023-08-14T07:21:51Z
day: '17'
ddc:
- '616'
department:
- _id: FlSc
doi: 10.3390/v13091853
external_id:
isi:
- '000699841100001'
pmid:
- '34578434'
file:
- access_level: open_access
checksum: bcfd72a12977d48e22df3d0cc55aacf1
content_type: application/pdf
creator: cchlebak
date_created: 2021-10-08T10:38:15Z
date_updated: 2021-10-08T10:38:15Z
file_id: '10115'
file_name: 2021_Viruses_Obr.pdf
file_size: 4146796
relation: main_file
success: 1
file_date_updated: 2021-10-08T10:38:15Z
has_accepted_license: '1'
intvolume: ' 13'
isi: 1
issue: '9'
keyword:
- virology
- infectious diseases
language:
- iso: eng
month: '09'
oa: 1
oa_version: Published Version
pmid: 1
project:
- _id: 26736D6A-B435-11E9-9278-68D0E5697425
call_identifier: FWF
grant_number: P31445
name: Structural conservation and diversity in retroviral capsid
publication: Viruses
publication_identifier:
issn:
- 1999-4915
publication_status: published
publisher: MDPI
quality_controlled: '1'
status: public
title: A structural perspective of the role of IP6 in immature and mature retroviral
assembly
tmp:
image: /images/cc_by.png
legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
short: CC BY (4.0)
type: journal_article
user_id: 4359f0d1-fa6c-11eb-b949-802e58b17ae8
volume: 13
year: '2021'
...