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Article: Advancements in Host-Based Interventions for Influenza Treatment.

Yip, Tsz-Fung / Selim, Aisha Sami Mohammed / Lian, Ida / Lee, Suki Man-Yan

2018 Volume 9, Page(s) 1547

Abstract: Influenza is a major acute respiratory infection that causes mortality and morbidity worldwide. Two classes of conventional antivirals, M2 ion channel blockers and neuraminidase inhibitors, are mainstays in managing influenza disease to lessen symptoms ... ...

Abstract	Influenza is a major acute respiratory infection that causes mortality and morbidity worldwide. Two classes of conventional antivirals, M2 ion channel blockers and neuraminidase inhibitors, are mainstays in managing influenza disease to lessen symptoms while minimizing hospitalization and death in patients with severe influenza. However, the development of viral resistance to both drug classes has become a major public health concern. Vaccines are prophylaxis mainstays but are limited in efficacy due to the difficulty in matching predicted dominant viral strains to circulating strains. As such, other potential interventions are being explored. Since viruses rely on host cellular functions to replicate, recent therapeutic developments focus on targeting host factors involved in virus replication. Besides controlling virus replication, potential targets for drug development include controlling virus-induced host immune responses such as the recently suggested involvement of innate lymphoid cells and NADPH oxidases in influenza virus pathogenesis and immune cell metabolism. In this review, we will discuss the advancements in novel host-based interventions for treating influenza disease.
Keywords	covid19
Language	English
Publishing date	2018
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2606827-8
ISSN	1664-3224
ISSN	1664-3224
DOI	10.3389/fimmu.2018.01547
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Article: Recognition of Double-Stranded RNA and Regulation of Interferon Pathway by Toll-Like Receptor 10.

Lee, Suki Man-Yan / Yip, Tsz-Fung / Yan, Sheng / Jin, Dong-Yan / Wei, Hong-Li / Guo, Rey-Ting / Peiris, Joseph Sriyal Malik

Frontiers in immunology

2018 Volume 9, Page(s) 516

Abstract: Toll-like receptor (TLR)-10 remains an orphan receptor without well-characterized ligands or functions. Here, we reveal that TLR10 is predominantly localized to endosomes and binds ... ...

Abstract	Toll-like receptor (TLR)-10 remains an orphan receptor without well-characterized ligands or functions. Here, we reveal that TLR10 is predominantly localized to endosomes and binds dsRNA
MeSH term(s)	Endosomes/metabolism ; Humans ; Interferons/metabolism ; RNA, Double-Stranded/metabolism ; Signal Transduction ; THP-1 Cells ; Toll-Like Receptor 10/metabolism ; Toll-Like Receptor 3/metabolism
Chemical Substances	RNA, Double-Stranded ; TLR10 protein, human ; TLR3 protein, human ; Toll-Like Receptor 10 ; Toll-Like Receptor 3 ; Interferons (9008-11-1)
Language	English
Publishing date	2018-03-16
Publishing country	Switzerland
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2606827-8
ISSN	1664-3224
ISSN	1664-3224
DOI	10.3389/fimmu.2018.00516
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Article ; Online: Targeting the host or the virus: current and novel concepts for antiviral approaches against influenza virus infection.

Lee, Suki Man-Yan / Yen, Hui-Ling

Antiviral research

2012 Volume 96, Issue 3, Page(s) 391–404

Abstract: Influenza epidemics and pandemics are constant threats to human health. The application of antiviral drugs provides an immediate and direct control of influenza virus infection. At present, the major strategy for managing patients with influenza is ... ...

Abstract	Influenza epidemics and pandemics are constant threats to human health. The application of antiviral drugs provides an immediate and direct control of influenza virus infection. At present, the major strategy for managing patients with influenza is through targeting conserved viral proteins critical for viral replication. Two classes of conventional antiviral drugs, the M2 ion channel blockers and the neuraminidase inhibitors, are frequently used. In recent years, increasing levels of resistance to both drug classes has become a major public health concern, highlighting the urgent need for the development of alternative treatments. Novel classes of antiviral compounds or biomolecules targeting viral replication mechanism are under development, using approaches including high-throughput small-molecule screening platforms and structure-based designs. In response to influenza virus infection, host cellular mechanisms are triggered to defend against the invaders. At the same time, viruses as obligate intracellular pathogens have evolved to exploit cellular responses in support of their efficient replication, including antagonizing the host type I interferon response as well as activation of specific cellular pathways at different stages of the replication cycle. Numerous studies have highlighted the possibility of targeting virus-host interactions and host cellular mechanisms to develop new treatment regimens. This review aims to give an overview of current and novel concepts targeting the virus and the host for managing influenza.
MeSH term(s)	Amides/pharmacology ; Animals ; Antibodies, Viral/metabolism ; Antiviral Agents/pharmacology ; Cross Reactions ; Host-Pathogen Interactions ; Humans ; Immunomodulation ; Influenza A virus/drug effects ; Influenza A virus/pathogenicity ; Influenza A virus/physiology ; Orthomyxoviridae Infections/drug therapy ; Orthomyxoviridae Infections/virology ; Pyrazines/pharmacology ; Receptors, Cell Surface/antagonists & inhibitors ; Viral Matrix Proteins/antagonists & inhibitors ; Virus Attachment/drug effects ; Virus Internalization/drug effects ; Virus Replication
Chemical Substances	Amides ; Antibodies, Viral ; Antiviral Agents ; M2 protein, Influenza A virus ; Pyrazines ; Receptors, Cell Surface ; Viral Matrix Proteins ; sialic acid receptor ; favipiravir (EW5GL2X7E0)
Keywords	covid19
Language	English
Publishing date	2012-09-26
Publishing country	Netherlands
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	306628-9
ISSN	1872-9096 ; 0166-3542
ISSN (online)	1872-9096
ISSN	0166-3542
DOI	10.1016/j.antiviral.2012.09.013
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Article ; Online: Whole transcriptome analysis reveals differential gene expression profile reflecting macrophage polarization in response to influenza A H5N1 virus infection

Na Zhang / Yun-Juan Bao / Amy Hin-Yan Tong / Scott Zuyderduyn / Gary D. Bader / J. S. Malik Peiris / Si Lok / Suki Man-Yan Lee

BMC Medical Genomics, Vol 11, Iss 1, Pp 1-

2018 Volume 14

Abstract: Abstract Background Avian influenza A H5N1 virus can cause lethal disease in humans. The virus can trigger severe pneumonia and lead to acute respiratory distress syndrome. Data from clinical, in vitro and in vivo suggest that virus-induced cytokine ... ...

Abstract	Abstract Background Avian influenza A H5N1 virus can cause lethal disease in humans. The virus can trigger severe pneumonia and lead to acute respiratory distress syndrome. Data from clinical, in vitro and in vivo suggest that virus-induced cytokine dysregulation could be a contributory factor to the pathogenesis of human H5N1 disease. However, the precise mechanism of H5N1 infection eliciting the unique host response are still not well understood. Methods To obtain a better understanding of the molecular events at the earliest time points, we used RNA-Seq to quantify and compare the host mRNA and miRNA transcriptomes induced by the highly pathogenic influenza A H5N1 (A/Vietnam/3212/04) or low virulent H1N1 (A/Hong Kong/54/98) viruses in human monocyte-derived macrophages at 1-, 3-, and 6-h post infection. Results Our data reveals that two macrophage populations corresponding to M1 (classically activated) and M2 (alternatively activated) macrophage subtypes respond distinctly to H5N1 virus infection when compared to H1N1 virus or mock infection, a distinction that could not be made from previous microarray studies. When this confounding variable is considered in our statistical model, a clear set of dysregulated genes and pathways emerges specifically in H5N1 virus-infected macrophages at 6-h post infection, whilst was not found with H1N1 virus infection. Furthermore, altered expression of genes in these pathways, which have been previously implicated in viral host response, occurs specifically in the M1 subtype. We observe a significant up-regulation of genes in the RIG-I-like receptor signaling pathway. In particular, interferons, and interferon-stimulated genes are broadly affected. The negative regulators of interferon signaling, the suppressors of cytokine signaling, SOCS-1 and SOCS-3, were found to be markedly up-regulated in the initial round of H5N1 virus replication. Elevated levels of these suppressors could lead to the eventual suppression of cellular antiviral genes, contributing to pathophysiology ...
Keywords	Influenza A virus ; H5N1 ; Macrophage polarization ; Transcriptomics ; RNA-Seq ; Internal medicine ; RC31-1245 ; Genetics ; QH426-470
Subject code	570
Language	English
Publishing date	2018-02-01T00:00:00Z
Publisher	BMC
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Whole transcriptome analysis reveals differential gene expression profile reflecting macrophage polarization in response to influenza A H5N1 virus infection.

Zhang, Na / Bao, Yun-Juan / Tong, Amy Hin-Yan / Zuyderduyn, Scott / Bader, Gary D / Malik Peiris, J S / Lok, Si / Lee, Suki Man-Yan

BMC medical genomics

2018 Volume 11, Issue 1, Page(s) 20

Abstract: Background: Avian influenza A H5N1 virus can cause lethal disease in humans. The virus can trigger severe pneumonia and lead to acute respiratory distress syndrome. Data from clinical, in vitro and in vivo suggest that virus-induced cytokine ... ...

Abstract	Background: Avian influenza A H5N1 virus can cause lethal disease in humans. The virus can trigger severe pneumonia and lead to acute respiratory distress syndrome. Data from clinical, in vitro and in vivo suggest that virus-induced cytokine dysregulation could be a contributory factor to the pathogenesis of human H5N1 disease. However, the precise mechanism of H5N1 infection eliciting the unique host response are still not well understood. Methods: To obtain a better understanding of the molecular events at the earliest time points, we used RNA-Seq to quantify and compare the host mRNA and miRNA transcriptomes induced by the highly pathogenic influenza A H5N1 (A/Vietnam/3212/04) or low virulent H1N1 (A/Hong Kong/54/98) viruses in human monocyte-derived macrophages at 1-, 3-, and 6-h post infection. Results: Our data reveals that two macrophage populations corresponding to M1 (classically activated) and M2 (alternatively activated) macrophage subtypes respond distinctly to H5N1 virus infection when compared to H1N1 virus or mock infection, a distinction that could not be made from previous microarray studies. When this confounding variable is considered in our statistical model, a clear set of dysregulated genes and pathways emerges specifically in H5N1 virus-infected macrophages at 6-h post infection, whilst was not found with H1N1 virus infection. Furthermore, altered expression of genes in these pathways, which have been previously implicated in viral host response, occurs specifically in the M1 subtype. We observe a significant up-regulation of genes in the RIG-I-like receptor signaling pathway. In particular, interferons, and interferon-stimulated genes are broadly affected. The negative regulators of interferon signaling, the suppressors of cytokine signaling, SOCS-1 and SOCS-3, were found to be markedly up-regulated in the initial round of H5N1 virus replication. Elevated levels of these suppressors could lead to the eventual suppression of cellular antiviral genes, contributing to pathophysiology of H5N1 virus infection. Conclusions: Our study provides important mechanistic insights into the understanding of H5N1 viral pathogenesis and the multi-faceted host immune responses. The dysregulated genes could be potential candidates as therapeutic targets for treating H5N1 disease.
MeSH term(s)	Gene Expression Profiling ; Humans ; Immunity, Innate/genetics ; Influenza A Virus, H1N1 Subtype/physiology ; Influenza A Virus, H5N1 Subtype/physiology ; Macrophages/cytology ; Macrophages/immunology ; Macrophages/metabolism ; Macrophages/virology ; MicroRNAs/genetics
Chemical Substances	MicroRNAs
Language	English
Publishing date	2018-02-23
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ISSN	1755-8794
ISSN (online)	1755-8794
DOI	10.1186/s12920-018-0335-0
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Article ; Online: A novel biparatopic hybrid antibody-ACE2 fusion that blocks SARS-CoV-2 infection

Miao, Xiaoniu / Luo, Yi / Huang, Xi / Lee, Suki M. Y. / Yuan, Zhijun / Tang, Yongzhou / Chen, Liandi / Wang, Chao / Wu, Fan / Xu, Yifeng / Jiang, Wenchao / Gao, Wei / Song, Xuedong / Yan, Yao / Pang, Tuling / Chen, Cheng / Zou, Yuefeng / Fu, Weihui / Wan, Liping /

Gilbert-Jaramillo, Javier / Knight, Michael / Tan, Tiong Kit / Rijal, Pramila / Townsend, Alain / Sun, Joanne / Liu, Xiaolin / James, William / Tsun, Andy / Xu, Yingda

mAbs

implications for therapy

2020 Volume 12, Issue 1, Page(s) 1804241

Keywords	Immunology ; Immunology and Allergy ; covid19
Language	English
Publisher	Informa UK Limited
Publishing country	uk
Document type	Article ; Online
ZDB-ID	2537838-7
ISSN	1942-0870 ; 1942-0862
ISSN (online)	1942-0870
ISSN	1942-0862
DOI	10.1080/19420862.2020.1804241
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: A novel biparatopic hybrid antibody-ACE2 fusion that blocks SARS-CoV-2 infection: implications for therapy.

Miao, Xiaoniu / Luo, Yi / Huang, Xi / Lee, Suki M Y / Yuan, Zhijun / Tang, Yongzhou / Chen, Liandi / Wang, Chao / Wu, Fan / Xu, Yifeng / Jiang, Wenchao / Gao, Wei / Song, Xuedong / Yan, Yao / Pang, Tuling / Chen, Cheng / Zou, Yuefeng / Fu, Weihui / Wan, Liping /

Gilbert-Jaramillo, Javier / Knight, Michael / Tan, Tiong Kit / Rijal, Pramila / Townsend, Alain / Sun, Joanne / Liu, Xiaolin / James, William / Tsun, Andy / Xu, Yingda

mAbs

2020 Volume 12, Issue 1, Page(s) 1804241

Abstract: In the absence of a proven effective vaccine preventing infection by SARS-CoV-2, or a proven drug to treat COVID-19, the positive results of passive immune therapy using convalescent serum provide a strong lead. We have developed a new class of ... ...

Abstract	In the absence of a proven effective vaccine preventing infection by SARS-CoV-2, or a proven drug to treat COVID-19, the positive results of passive immune therapy using convalescent serum provide a strong lead. We have developed a new class of tetravalent, biparatopic therapy, 89C8-ACE2. It combines the specificity of a monoclonal antibody (89C8) that recognizes the relatively conserved N-terminal domain of the viral Spike (S) glycoprotein, and the ectodomain of ACE2, which binds to the receptor-binding domain of S. This molecule shows exceptional performance
MeSH term(s)	Angiotensin-Converting Enzyme 2 ; Antibodies, Monoclonal/pharmacology ; Antibodies, Neutralizing/pharmacology ; Antibodies, Viral/pharmacology ; Betacoronavirus/drug effects ; COVID-19 ; Coronavirus Infections ; Drug Design ; Drug Discovery ; Humans ; Pandemics ; Peptidyl-Dipeptidase A/drug effects ; Pneumonia, Viral ; Recombinant Proteins ; SARS-CoV-2 ; Spike Glycoprotein, Coronavirus/drug effects
Chemical Substances	Antibodies, Monoclonal ; Antibodies, Neutralizing ; Antibodies, Viral ; Recombinant Proteins ; Spike Glycoprotein, Coronavirus ; spike protein, SARS-CoV-2 ; Peptidyl-Dipeptidase A (EC 3.4.15.1) ; ACE2 protein, human (EC 3.4.17.23) ; Angiotensin-Converting Enzyme 2 (EC 3.4.17.23)
Keywords	covid19
Language	English
Publishing date	2020-08-17
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2537838-7
ISSN	1942-0870 ; 1942-0870
ISSN (online)	1942-0870
ISSN	1942-0870
DOI	10.1080/19420862.2020.1804241
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: A novel biparatopic antibody-ACE2 fusion that blocks SARS-CoV-2 infection: implications for therapy

Miao, Xiaoniu / Luo, Yi / Huang, Xi / Lee, Suki M. Y. / Yuan, Zhijun / Tang, Yongzhou / Chen, Liandi / Wang, Chao / Jiang, Wenchao / Gao, Wei / Song, Xuedong / Yan, Yao / Pang, Tuling / Zou, Yuefeng / Fu, Weihui / Wan, Liping / Gilbert-Jaramillo, Javier / Knight, Michael / Tan, Tiong Kit /

Rijal, Pramila / Townsend, Alain / Sun, Joanne / Liu, Xiaolin / James, William / Tsun, Andy / Xu, Yingda

bioRxiv

Abstract: In the absence of a proven effective vaccine preventing infection by SARS-CoV-2, or a proven drug to treat COVID-19, the positive results of passive immune therapy using convalescent serum provides a strong lead. We have developed a new class of ... ...

Abstract	In the absence of a proven effective vaccine preventing infection by SARS-CoV-2, or a proven drug to treat COVID-19, the positive results of passive immune therapy using convalescent serum provides a strong lead. We have developed a new class of tetravalent, biparatopic therapy, 89C8-ACE2. It combines the specificity of a monoclonal antibody (89C8) that recognizes the relatively conserved N-terminal domain (NTD) of the viral S glycoprotein, and the ectodomain of ACE2, which binds to the receptor-binding domain (RBD) of S. This molecule shows exceptional performance in vitro, inhibiting the interaction of recombinant S1 to ACE2 and transduction of ACE2-overexpressing cells by S-pseudotyped lentivirus with IC50s substantially below 100 pM, and with potency approximately 100-fold greater than ACE2-Fc itself. Moreover, 89C8-ACE2 was able to neutralize authentic virus infection in a standard assay at low nanomolar concentrations, making this class of molecule a promising lead for therapeutic applications.
Keywords	covid19
Publisher	BioRxiv; WHO
Document type	Article ; Online
DOI	10.1101/2020.06.14.147868
Database	COVID19

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Article: A novel biparatopic hybrid antibody-ACE2 fusion that blocks SARS-CoV-2 infection: implications for therapy

Gilbert-Jaramillo, Javier / Knight, Michael / Tan, Tiong Kit / Rijal, Pramila / Townsend, Alain / Sun, Joanne / Liu, Xiaolin / James, William / Tsun, Andy / Xu, Yingda

MAbs

Abstract	In the absence of a proven effective vaccine preventing infection by SARS-CoV-2, or a proven drug to treat COVID-19, the positive results of passive immune therapy using convalescent serum provide a strong lead. We have developed a new class of tetravalent, biparatopic therapy, 89C8-ACE2. It combines the specificity of a monoclonal antibody (89C8) that recognizes the relatively conserved N-terminal domain of the viral Spike (S) glycoprotein, and the ectodomain of ACE2, which binds to the receptor-binding domain of S. This molecule shows exceptional performance in vitro, inhibiting the interaction of recombinant S1 to ACE2 and transduction of ACE2-overexpressing cells by S-pseudotyped lentivirus with IC50s substantially below 100 pM, and with potency approximately 100-fold greater than ACE2-Fc itself. Moreover, 89C8-ACE2 was able to neutralize authentic viral infection in a standard 96-h co-incubation assay at low nanomolar concentrations, making this class of molecule a promising lead for therapeutic applications.
Keywords	covid19
Publisher	WHO
Document type	Article
Note	WHO #Covidence: #720912
Database	COVID19

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Article ; Online: Toll-like receptor 10 is involved in induction of innate immune responses to influenza virus infection.

Lee, Suki M Y / Kok, Kin-Hang / Jaume, Martial / Cheung, Timothy K W / Yip, Tsz-Fung / Lai, Jimmy C C / Guan, Yi / Webster, Robert G / Jin, Dong-Yan / Peiris, J S Malik

Proceedings of the National Academy of Sciences of the United States of America

2014 Volume 111, Issue 10, Page(s) 3793–3798

Abstract: Toll-like receptors (TLRs) play key roles in innate immune recognition of pathogen-associated molecular patterns of invading microbes. Among the 10 TLR family members identified in humans, TLR10 remains an orphan receptor without known agonist or ... ...

Abstract	Toll-like receptors (TLRs) play key roles in innate immune recognition of pathogen-associated molecular patterns of invading microbes. Among the 10 TLR family members identified in humans, TLR10 remains an orphan receptor without known agonist or function. TLR10 is a pseudogene in mice and mouse models are noninformative in this regard. Using influenza virus infection in primary human peripheral blood monocyte-derived macrophages and a human monocytic cell line, we now provide previously unidentified evidence that TLR10 plays a role in innate immune responses following viral infection. Influenza virus infection increased TLR10 expression and TLR10 contributed to innate immune sensing of viral infection leading to cytokine induction, including proinflammatory cytokines and interferons. TLR10 induction is more pronounced following infection with highly pathogenic avian influenza H5N1 virus compared with a low pathogenic H1N1 virus. Induction of TLR10 by virus infection requires active virus replication and de novo protein synthesis. Culture supernatants of virus-infected cells modestly up-regulate TLR10 expression in nonvirus-infected cells. Signaling via TLR10 was activated by the functional RNA-protein complex of influenza virus leading to robust induction of cytokine expression. Taken together, our findings identify TLR10 as an important innate immune sensor of viral infection and its role in innate immune defense and immunopathology following viral and bacterial pathogens deserves attention.
MeSH term(s)	Animals ; Blotting, Western ; DNA Primers/genetics ; Dogs ; Enzyme-Linked Immunosorbent Assay ; Fluorescent Antibody Technique ; Humans ; Immunity, Innate/immunology ; Influenza A Virus, H1N1 Subtype/immunology ; Influenza A Virus, H5N1 Subtype/immunology ; Influenza, Human/immunology ; Macrophages ; Madin Darby Canine Kidney Cells ; Mice ; Organic Chemicals ; RNA, Small Interfering/genetics ; Reverse Transcriptase Polymerase Chain Reaction ; Toll-Like Receptor 10/immunology ; Toll-Like Receptor 10/metabolism
Chemical Substances	DNA Primers ; Organic Chemicals ; RNA, Small Interfering ; Toll-Like Receptor 10 ; SYBR Green I (163795-75-3)
Language	English
Publishing date	2014-02-24
Publishing country	United States
Document type	Comparative Study ; Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	209104-5
ISSN	1091-6490 ; 0027-8424
ISSN (online)	1091-6490
ISSN	0027-8424
DOI	10.1073/pnas.1324266111
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