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Article ; Online: Interplay between group A

Su, Marcia Shu-Wei / Cheng, Yi-Lin / Lin, Yee-Shin / Wu, Jiunn-Jong

Microbiology and molecular biology reviews : MMBR

2024 Volume 88, Issue 1, Page(s) e0005222

Abstract: SUMMARYGroup ... ...

Abstract	SUMMARYGroup A
MeSH term(s)	Humans ; Streptococcus pyogenes ; Streptococcal Infections/pathology ; Immunity, Innate ; Virulence Factors ; Phagocytosis
Chemical Substances	Virulence Factors
Language	English
Publishing date	2024-03-07
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	1376131-6
ISSN	1098-5557 ; 1070-6275 ; 1092-2172
ISSN (online)	1098-5557 ; 1070-6275
ISSN	1092-2172
DOI	10.1128/mmbr.00052-22
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Article ; Online: VEGF-Mediated Augmentation of Autophagic and Lysosomal Activity in Endothelial Cells Defends against Intracellular Streptococcus pyogenes.

Lu, Shiou-Ling / Omori, Hiroko / Zhou, Yi / Lin, Yee-Shin / Liu, Ching-Chuan / Wu, Jiunn-Jong / Noda, Takeshi

mBio

2022 Volume 13, Issue 4, Page(s) e0123322

Abstract: Group A Streptococcus (GAS), a deleterious human-pathogenic bacterium, causes life-threatening diseases such as sepsis and necrotic fasciitis. We recently reported that GAS survives and replicates within blood vessel endothelial cells because these cells ...

Abstract	Group A Streptococcus (GAS), a deleterious human-pathogenic bacterium, causes life-threatening diseases such as sepsis and necrotic fasciitis. We recently reported that GAS survives and replicates within blood vessel endothelial cells because these cells are intrinsically defective in xenophagy. Because blood vessel endothelial cells are relatively germfree environments, specific stimulation may be required to sufficiently induce xenophagy. Here, we explored how vascular endothelial growth factor (VEGF) promoted xenophagy and lysosomal activity in endothelial cells. These effects were achieved by amplifying the activation of TFEB, a transcriptional factor crucial for lysosome/autophagy biogenesis, via cAMP-mediated calcium release. In a mouse model of local infection with GAS, the VEGF level was significantly elevated at the infection site. Interestingly, low serum VEGF levels were found in a mouse model of invasive bacteremia and in patients with severe GAS-induced sepsis. Moreover, the administration of VEGF improved the survival of GAS-infected mice. We propose a novel theory regarding GAS infection in endothelial cells, wherein VEGF concentrations in the systemic circulation play a critical role.
MeSH term(s)	Animals ; Autophagy ; Endothelial Cells/microbiology ; Humans ; Lysosomes ; Mice ; Sepsis ; Streptococcus pyogenes/metabolism ; Vascular Endothelial Growth Factor A/metabolism ; Vascular Endothelial Growth Factors/metabolism
Chemical Substances	Vascular Endothelial Growth Factor A ; Vascular Endothelial Growth Factors
Language	English
Publishing date	2022-07-05
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2557172-2
ISSN	2150-7511 ; 2161-2129
ISSN (online)	2150-7511
ISSN	2161-2129
DOI	10.1128/mbio.01233-22
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: Negative regulation of type I interferon signaling by integrin-linked kinase permits dengue virus replication.

Kao, Yi-Sheng / Wang, Li-Chiu / Chang, Po-Chun / Lin, Heng-Ming / Lin, Yee-Shin / Yu, Chia-Yi / Chen, Chien-Chin / Lin, Chiou-Feng / Yeh, Trai-Ming / Wan, Shu-Wen / Wang, Jen-Ren / Ho, Tzong-Shiann / Chu, Chien-Chou / Zhang, Bo-Cheng / Chang, Chih-Peng

PLoS pathogens

2023 Volume 19, Issue 3, Page(s) e1011241

Abstract: Dengue virus (DENV) infection can induce life-threatening dengue hemorrhagic fever/dengue shock syndrome in infected patients. DENV is a threat to global health due to its growing numbers and incidence of infection in the last 50 years. During infection, ...

Abstract	Dengue virus (DENV) infection can induce life-threatening dengue hemorrhagic fever/dengue shock syndrome in infected patients. DENV is a threat to global health due to its growing numbers and incidence of infection in the last 50 years. During infection, DENV expresses ten structural and nonstructural proteins modulating cell responses to benefit viral replication. However, the lack of knowledge regarding the cellular proteins and their functions in enhancing DENV pathogenesis impedes the development of antiviral drugs and therapies against fatal DENV infection. Here, we identified that integrin-linked kinase (ILK) is a novel enhancing factor for DENV infection by suppressing type I interferon (IFN) responses. Mechanistically, ILK binds DENV NS1 and NS3, activates Akt and Erk, and induces NF-κB-driven suppressor of cytokine signaling 3 (SOCS3) expression. Elevated SOCS3 in DENV-infected cells inhibits phosphorylation of STAT1/2 and expression of interferon-stimulated genes (ISGs). Inhibiting ILK, Akt, or Erk activation abrogates SOCS3 expression. In DENV-infected mice, the treatment of an ILK inhibitor significantly reduces viral loads in the brains, disease severity, and mortality rate. Collectively, our results show that ILK is a potential therapeutic target against DENV infection.
MeSH term(s)	Animals ; Mice ; Dengue ; Dengue Virus/physiology ; Proto-Oncogene Proteins c-akt ; Virus Replication ; Interferon Type I/therapeutic use
Chemical Substances	integrin-linked kinase (EC 2.7.1.-) ; Proto-Oncogene Proteins c-akt (EC 2.7.11.1) ; Interferon Type I
Language	English
Publishing date	2023-03-17
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2205412-1
ISSN	1553-7374 ; 1553-7374
ISSN (online)	1553-7374
ISSN	1553-7374
DOI	10.1371/journal.ppat.1011241
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Article ; Online: Biomarkers of severe dengue disease - a review.

John, Daisy Vanitha / Lin, Yee-Shin / Perng, Guey Chuen

Journal of biomedical science

2015 Volume 22, Page(s) 83

Abstract: Dengue virus infection presents a wide spectrum of manifestations including asymptomatic condition, dengue fever (DF), or severe forms, such as dengue hemorrhagic fever (DHF) and dengue shock syndrome (DSS) in affected individuals. The early prediction ... ...

Abstract	Dengue virus infection presents a wide spectrum of manifestations including asymptomatic condition, dengue fever (DF), or severe forms, such as dengue hemorrhagic fever (DHF) and dengue shock syndrome (DSS) in affected individuals. The early prediction of severe dengue in patients without any warning signs who may later develop severe DHF is very important to choose appropriate intensive supportive therapy since available vaccines for immunization are yet to be approved. Severe dengue responses include T and B cell activation and apoptosis, cytokine storm, hematologic disorders and complement activation. Cytokines, complement and other unidentified factors may transiently act on the endothelium and alter normal fluid barrier function of the endothelial cells and cause plasma leakage. In this review, the host factors such as activated immune and endothelial cells and their products which can be utilized as biomarkers for severe dengue disease are discussed.
MeSH term(s)	B-Lymphocytes/metabolism ; Biomarkers/blood ; Cytokines/blood ; Dengue/blood ; Endothelium, Vascular/metabolism ; Humans ; Severity of Illness Index ; T-Lymphocytes/metabolism
Chemical Substances	Biomarkers ; Cytokines
Language	English
Publishing date	2015-10-14
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	1193378-1
ISSN	1423-0127 ; 1021-7770
ISSN (online)	1423-0127
ISSN	1021-7770
DOI	10.1186/s12929-015-0191-6
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Article ; Online: Regulation of autophagy, glucose uptake, and glycolysis under dengue virus infection.

Lee, Ying-Ray / Wu, Shan-Ying / Chen, Ruei-Yi / Lin, Yee-Shin / Yeh, Trai-Ming / Liu, Hsiao-Sheng

The Kaohsiung journal of medical sciences

2020 Volume 36, Issue 11, Page(s) 911–919

Abstract: We previously reported that dengue virus (DENV)-induced autophagy plays a promoting role in viral replication and pathogenesis both in vitro and in vivo. Although it is known that DENV infection increases glycolysis, which promotes viral replication, the ...

Abstract	We previously reported that dengue virus (DENV)-induced autophagy plays a promoting role in viral replication and pathogenesis both in vitro and in vivo. Although it is known that DENV infection increases glycolysis, which promotes viral replication, the role of glucose metabolism together with autophagic activity in DENV replication remains unclear. In this study, we reveal that DENV2 infection increased autophagic activity, glucose uptake, protein levels of glucose transporter-1 (GLUT1), and glycolysis rate-limiting enzyme hexokinase-2 (HK2) in cells. Furthermore, the protein levels of LC3-II and HK2 were increased in the brain tissues of the DENV2-infected suckling mice. However, DENV2 infection decreased ATP level and showed no effect on mRNA expression of HK2 and phosphofructokinase, as well as lactate production, indicating that DENV2-regulated glycolytic flux occurs at the post-transcriptional level and is lactate pathway-independent. Moreover, amiodarone-induced autophagic activity, glucose uptake, HK2 level, and viral titer were reversed by the autophagy inhibitor spautin-1 or silencing of Atg5 gene expression. Intriguingly, blocking of glycolysis, HK2 protein level, and viral titer were accordingly decreased, but autophagic activity was increased, suggesting the existence of another regulation mechanism that influences the relationship between glycolysis and autophagy. This is the first report to reveal that DENV2-induced autophagy positively regulates glycolysis and viral replication in vitro and in vivo. Our findings open a new avenue wherein metabolic modulation could be used as a target for the treatment of DENV infection.
MeSH term(s)	A549 Cells ; Amiodarone/pharmacology ; Animals ; Animals, Newborn ; Autophagy/drug effects ; Autophagy/genetics ; Autophagy-Related Protein 5/antagonists & inhibitors ; Autophagy-Related Protein 5/genetics ; Autophagy-Related Protein 5/metabolism ; Benzylamines/pharmacology ; Biological Transport ; Brain/metabolism ; Brain/pathology ; Brain/virology ; Chlorocebus aethiops ; Dengue/genetics ; Dengue/metabolism ; Dengue/pathology ; Dengue/virology ; Dengue Virus/genetics ; Dengue Virus/growth & development ; Dengue Virus/metabolism ; Gene Expression Regulation ; Glucose/metabolism ; Glucose Transporter Type 1/genetics ; Glucose Transporter Type 1/metabolism ; Glycolysis/drug effects ; Glycolysis/genetics ; Hexokinase/genetics ; Hexokinase/metabolism ; Host-Pathogen Interactions/genetics ; Humans ; Mice ; Mice, Inbred ICR ; Microtubule-Associated Proteins/genetics ; Microtubule-Associated Proteins/metabolism ; Phosphofructokinases/genetics ; Phosphofructokinases/metabolism ; Quinazolines/pharmacology ; Signal Transduction ; Vero Cells ; Virus Replication/drug effects ; Virus Replication/genetics
Chemical Substances	Atg5 protein, mouse ; Autophagy-Related Protein 5 ; Benzylamines ; Glucose Transporter Type 1 ; Map1lc3b protein, mouse ; Microtubule-Associated Proteins ; Quinazolines ; Slc2a1 protein, mouse ; spautin-1 ; Phosphofructokinases (EC 2.7.1 -) ; Hexokinase (EC 2.7.1.1) ; hexokinase 2, mouse (EC 2.7.1.1) ; Glucose (IY9XDZ35W2) ; Amiodarone (N3RQ532IUT)
Language	English
Publishing date	2020-08-12
Publishing country	China (Republic : 1949- )
Document type	Journal Article
ZDB-ID	639302-0
ISSN	2410-8650 ; 0257-5655
ISSN (online)	2410-8650
ISSN	0257-5655
DOI	10.1002/kjm2.12271
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Article: Autophagy regulates vinorelbine sensitivity due to continued Keap1-mediated ROS generation in lung adenocarcinoma cells.

Wu, Yan-Wei / Lin, Chiou-Feng / Lin, Yee-Shin / Su, Wu-Chou / Chiu, Wei-Hsin

Cell death discovery

2018 Volume 4, Page(s) 33

Abstract: Autophagy is one of the induced mechanisms in metastatic cancer to escape death due to starvation, hypoxia, metabolic stresses, chemotherapy, and radiation. Some publications have revealed that chemotherapy combined with autophagy inhibitor will overcome ...

Abstract	Autophagy is one of the induced mechanisms in metastatic cancer to escape death due to starvation, hypoxia, metabolic stresses, chemotherapy, and radiation. Some publications have revealed that chemotherapy combined with autophagy inhibitor will overcome drug resistance. We modified AS2 cells with PTEN overexpression, mTOR knockdown, or Keap1 knockdown, and made modification of A549 cells with PTEN knockdown, Atg5 knockdown, and Keap1 overexpression. Our study was aimed toward an exploration of how autophagy modulates Keap1, ROS generation, and vinorelbine-induced apoptosis in these cell lines. We found that lung cancer PC14PE6/AS2 (AS2) had higher mTOR and Akt and also lower PTEN expression than A549 cells. Descended autophagy was demonstrated with more decreased p62 accumulation and LC3 II conversion in AS2 cells as compared to A549 cells. The A549 cells had lower Keap1/Nrf2 and more active anti-oxidant response element (ARE) activity than the AS2 cells. We modified AS2 cells with PTEN overexpression, mTOR knockdown, Keap1 knockdown, and revealed amplified p62 and LC3 expression accompanied with decreased Akt, Keap1, ROS, and vinorelbine-induced apoptosis. Declined p62, LC3 expression were accompanied with increased Akt, Keap1, ROS, and vinorelbine-induced apoptosis after modification of A549 cells with PTEN knockdown, Atg5 knockdown, and Keap1 overexpression. Keap1 overexpression lowered ARE levels in A549 cells, and ARE level exhibited up-growth in Keap1 knockdown AS2 cells. The autophagy inhibitor caused more ROS generation and vinorelbine-induced apoptosis in the A549 and CL1-5 cells. According to these findings, autophagy regulates vinorelbine sensitivity by continuing Keap1-mediated ROS generation in lung adenocarcinoma cells.
Language	English
Publishing date	2018-09-12
Publishing country	United States
Document type	Journal Article
ISSN	2058-7716
ISSN	2058-7716
DOI	10.1038/s41420-018-0098-6
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Article ; Online: Erratum for Cheng et al., "Group A

Cheng, Yi-Lin / Kuo, Chih-Feng / Lu, Shiou-Ling / Omori, Hiroko / Wu, Ya-Na / Hsieh, Cheng-Lu / Noda, Takeshi / Wu, Shang-Rung / Anderson, Robert / Lin, Chiou-Feng / Chen, Chia-Ling / Wu, Jiunn-Jong / Lin, Yee-Shin

mBio

2021 Volume 12, Issue 4, Page(s) e0225021

Language	English
Publishing date	2021-08-31
Publishing country	United States
Document type	Journal Article ; Published Erratum
ZDB-ID	2557172-2
ISSN	2150-7511 ; 2161-2129
ISSN (online)	2150-7511
ISSN	2161-2129
DOI	10.1128/mBio.02250-21
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Article: Autophagy Drives Galectin-1 Secretion From Tumor-Associated Macrophages Facilitating Hepatocellular Carcinoma Progression.

Davuluri, Goutham Venkata Naga / Chen, Chien-Chin / Chiu, Yen-Cheng / Tsai, Hung-Wen / Chiu, Hung-Chih / Chen, Yuh-Ling / Tsai, Pei-Jane / Kuo, Wan-Ting / Tsao, Nina / Lin, Yee-Shin / Chang, Chih-Peng

Frontiers in cell and developmental biology

2021 Volume 9, Page(s) 741820

Abstract: Galectin-1 (Gal-1) is a secretory lectin with pro-tumor activities and is associated strongly with hepatocellular carcinoma (HCC) development. Although Gal-1 is a well-known soluble pro-tumor factor in the tumor microenvironment (TME), the secretion mode ...

Abstract	Galectin-1 (Gal-1) is a secretory lectin with pro-tumor activities and is associated strongly with hepatocellular carcinoma (HCC) development. Although Gal-1 is a well-known soluble pro-tumor factor in the tumor microenvironment (TME), the secretion mode of Gal-1 is not clearly defined. On the other hand, in addition to cancer cells, Gal-1 is widely expressed in tumor stromal cells, including tumor-associated macrophages (TAMs). TAMs are a significant component of stromal cells in TME; however, their contributions in producing Gal-1 to TME are still not explored. Here we reveal that TAMs can actively secrete Gal-1 in response to stimuli of HCC cells. Gal-1 produced by TAMs leads to an increase of the systemic level of Gal-1 and HCC tumor growth in mice. Mechanistically, TLR2-dependent secretory autophagy is found to be responsible for Gal-1 secretion from TAMs. Gal-1 acts as a cargo of autophagosomes to fuse with multivesicular bodies via Rab11 and VAMP7-mediated vesicle trafficking before being secreted. This autophagy-regulated Gal-1 secretion in TAMs correlates to poor overall survival and progression-free survival rates of HCC patients. Our findings uncover the secretion mode of Gal-1 via secretory autophagy and highlight the pathological role of TAM-produced Gal-1 in HCC progression.
Language	English
Publishing date	2021-09-06
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2737824-X
ISSN	2296-634X
ISSN	2296-634X
DOI	10.3389/fcell.2021.741820
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Article ; Online: Mast cell-macrophage dynamics in modulation of dengue virus infection in skin.

Chu, Ya-Ting / Wan, Shu-Wen / Anderson, Robert / Lin, Yee-Shin

Immunology

2015 Volume 146, Issue 1, Page(s) 163–172

Abstract: Dengue virus (DENV) infection causes dengue fever, dengue haemorrhagic fever, or dengue shock syndrome. Mast cells have been speculated to play a role in DENV disease although their precise roles are unclear. In this study, we used mast cell-deficient ... ...

Abstract	Dengue virus (DENV) infection causes dengue fever, dengue haemorrhagic fever, or dengue shock syndrome. Mast cells have been speculated to play a role in DENV disease although their precise roles are unclear. In this study, we used mast cell-deficient Kit(W-sh/W-sh) mice to investigate the involvement of mast cells after intradermal DENV infection. An approximately two- to three-fold higher level of DENV NS3 antigen was detected at the skin inoculation site in DENV-infected Kit(W-sh/W-sh) mice than in DENV-infected wild-type (WT) mice (using a dose of 1 × 10(9) plaque-forming units/mouse). Moreover, as an indicator of heightened pathogenesis, a more prolonged bleeding time was observed in DENV-infected Kit(W-sh/W-sh) mice than in WT mice. Monocytes/macrophages are considered to be important targets for DENV infection, so we investigated the susceptibility and chemokine response of DENV-infected peritoneal macrophages from Kit(W-sh/W-sh) and WT mice both ex vivo and in vivo. There was a tendency for higher DENV infection and higher secretion of CCL2 (MCP-1) from peritoneal macrophages isolated from Kit(W-sh/W-sh) mice than those from WT mice. In vivo studies using intradermal inoculation of DENV showed about twofold higher levels of infiltrating macrophages and CCL2 (MCP-1) at the inoculation site in both mock control and DENV-inoculated Kit(W-sh/W-sh) mice than in corresponding WT mice. In summary, compared with WT mice, Kit(W-sh/W-sh) mice show enhanced DENV infection and macrophage infiltration at the skin inoculation site as well as increased DENV-associated bleeding time. The results indicate an intriguing interplay between mast cells and tissue macrophages to restrict DENV replication in the skin.
MeSH term(s)	Animals ; Antibodies, Viral/immunology ; Chemokine CCL2/secretion ; Chemokine CCL5/metabolism ; Chemokine CXCL10/metabolism ; Dengue/immunology ; Dengue/pathology ; Dengue/virology ; Dengue Virus/immunology ; Disease Models, Animal ; Macrophages, Peritoneal/immunology ; Mast Cells/cytology ; Mast Cells/immunology ; Mice ; Mice, Inbred C57BL ; Mice, Transgenic ; RNA Helicases/immunology ; RNA Helicases/metabolism ; RNA, Viral/biosynthesis ; RNA, Viral/genetics ; Serine Endopeptidases/immunology ; Serine Endopeptidases/metabolism ; Skin/immunology ; Skin/virology ; Viral Nonstructural Proteins/immunology ; Viral Nonstructural Proteins/metabolism
Chemical Substances	Antibodies, Viral ; Ccl2 protein, mouse ; Ccl5 protein, mouse ; Chemokine CCL2 ; Chemokine CCL5 ; Chemokine CXCL10 ; Cxcl10 protein, mouse ; NS3 protein, flavivirus ; RNA, Viral ; Viral Nonstructural Proteins ; Serine Endopeptidases (EC 3.4.21.-) ; RNA Helicases (EC 3.6.4.13)
Language	English
Publishing date	2015-09
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	80124-0
ISSN	1365-2567 ; 0019-2805 ; 0953-4954
ISSN (online)	1365-2567
ISSN	0019-2805 ; 0953-4954
DOI	10.1111/imm.12492
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Article ; Online: Dengue virus nonstructural protein 1 activates platelets via Toll-like receptor 4, leading to thrombocytopenia and hemorrhage.

Chao, Chiao-Hsuan / Wu, Wei-Chueh / Lai, Yen-Chung / Tsai, Pei-Jane / Perng, Guey-Chuen / Lin, Yee-Shin / Yeh, Trai-Ming

PLoS pathogens

2019 Volume 15, Issue 4, Page(s) e1007625

Abstract: Dengue virus (DENV) infection, the most common mosquito-transmitted viral infection, can cause a range of diseases from self-limiting dengue fever to life-threatening dengue hemorrhagic fever and shock syndrome. Thrombocytopenia is a major characteristic ...

Abstract	Dengue virus (DENV) infection, the most common mosquito-transmitted viral infection, can cause a range of diseases from self-limiting dengue fever to life-threatening dengue hemorrhagic fever and shock syndrome. Thrombocytopenia is a major characteristic observed in both mild and severe dengue disease and is significantly correlated with the progression of dengue severity. Previous studies have shown that DENV nonstructural protein 1 (NS1), which can be secreted into patients' blood, can stimulate immune cells via Toll-like receptor 4 (TLR4) and can cause endothelial leakage. However, it is unclear whether DENV NS1 can directly induce platelet activation or cause thrombocytopenia during DENV infection. In this study, we first demonstrated that DENV but not Zika virus cell culture supernatant could induce P-selectin expression and phosphatidylserine (PS) exposure in human platelets, both of which were abolished when NS1 was depleted from the DENV supernatant. Similar results were found using recombinant NS1 from all four serotypes of DENV, and those effects were blocked in the presence of anti-NS1 F(ab')2, anti-TLR4 antibody, a TLR4 antagonist (Rhodobacter sphaeroides lipopolysaccharide, LPS-Rs) and a TLR4 signaling inhibitor (TAK242), but not polymyxin B (an LPS inhibitor). Moreover, the activation of platelets by DENV NS1 promoted subthreshold concentrations of adenosine diphosphate (ADP)-induced platelet aggregation and enhanced platelet adhesion to endothelial cells and phagocytosis by macrophages. Finally, we demonstrated that DENV-induced thrombocytopenia and hemorrhage were attenuated in TLR4 knockout and wild-type mice when NS1 was depleted from DENV supernatant. Taken together, these results suggest that the binding of DENV NS1 to TLR4 on platelets can trigger its activation, which may contribute to thrombocytopenia and hemorrhage during dengue infection.
MeSH term(s)	Animals ; Blood Platelets/immunology ; Blood Platelets/metabolism ; Blood Platelets/pathology ; Cells, Cultured ; Dengue/complications ; Dengue/metabolism ; Dengue/virology ; Dengue Virus/immunology ; Hemorrhage/etiology ; Hemorrhage/metabolism ; Hemorrhage/pathology ; Humans ; Lipopolysaccharides/toxicity ; Macrophages/immunology ; Macrophages/metabolism ; Macrophages/pathology ; Mice ; Mice, Inbred C3H ; Mice, Inbred C57BL ; Phagocytosis ; Thrombocytopenia/etiology ; Thrombocytopenia/metabolism ; Thrombocytopenia/pathology ; Toll-Like Receptor 4/metabolism ; Viral Nonstructural Proteins/metabolism
Chemical Substances	Lipopolysaccharides ; Toll-Like Receptor 4 ; Viral Nonstructural Proteins
Language	English
Publishing date	2019-04-22
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2205412-1
ISSN	1553-7374 ; 1553-7366
ISSN (online)	1553-7374
ISSN	1553-7366
DOI	10.1371/journal.ppat.1007625
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