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Article ; Online: Mechanistic insights into bone remodelling dysregulation by human viral pathogens.

Caetano, Camila C S / Azamor, Tamiris / Meyer, Nikki M / Onwubueke, Chineme / Calabrese, Cassandra M / Calabrese, Leonard H / Visperas, Anabelle / Piuzzi, Nicolas S / Husni, M Elaine / Foo, Suan-Sin / Chen, Weiqiang

Nature microbiology

2024 Volume 9, Issue 2, Page(s) 322–335

Abstract: Bone-related diseases (osteopathologies) associated with human virus infections have increased around the globe. Recent findings have highlighted the intricate interplay between viral infection, the host immune system and the bone remodelling process. ... ...

Abstract	Bone-related diseases (osteopathologies) associated with human virus infections have increased around the globe. Recent findings have highlighted the intricate interplay between viral infection, the host immune system and the bone remodelling process. Viral infections can disrupt bone homeostasis, contributing to conditions such as arthritis and soft tissue calcifications. Osteopathologies can occur after arbovirus infections such as chikungunya virus, dengue virus and Zika virus, as well as respiratory viruses, such as severe acute respiratory syndrome coronavirus 2 and enteroviruses such as Coxsackievirus B. Here we explore how human viruses dysregulate bone homeostasis, detailing viral factors, molecular mechanisms, host immune response changes and bone remodelling that ultimately result in osteopathologies. We highlight model systems and technologies to advance mechanistic understanding of viral-mediated bone alterations. Finally, we propose potential prophylactic and therapeutic strategies, introduce 'osteovirology' as a research field highlighting the underestimated roles of viruses in bone-related diseases, and discuss research avenues for further investigation.
MeSH term(s)	Humans ; Dengue Virus ; Arbovirus Infections ; Chikungunya virus ; Zika Virus/physiology ; Zika Virus Infection
Language	English
Publishing date	2024-02-05
Publishing country	England
Document type	Journal Article ; Review
ISSN	2058-5276
ISSN (online)	2058-5276
DOI	10.1038/s41564-023-01586-6
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: Single-cell analysis of Kaposi's sarcoma-associated herpesvirus infection in three-dimensional air-liquid interface culture model.

Kyle L Jung / Un Yung Choi / Angela Park / Suan-Sin Foo / Stephanie Kim / Shin-Ae Lee / Jae U Jung

PLoS Pathogens, Vol 18, Iss 8, p e

2022 Volume 1010775

Abstract: The oral cavity is the major site for transmission of Kaposi's sarcoma-associated herpesvirus (KSHV), but how KSHV establishes infection and replication in the oral epithelia remains unclear. Here, we report a KSHV spontaneous lytic replication model ... ...

Abstract	The oral cavity is the major site for transmission of Kaposi's sarcoma-associated herpesvirus (KSHV), but how KSHV establishes infection and replication in the oral epithelia remains unclear. Here, we report a KSHV spontaneous lytic replication model using fully differentiated, three-dimensional (3D) oral epithelial organoids at an air-liquid interface (ALI). This model revealed that KSHV infected the oral epithelia when the basal epithelial cells were exposed by damage. Unlike two-dimensional (2D) cell culture, 3D oral epithelial organoid ALI culture allowed high levels of spontaneous KSHV lytic replication, where lytically replicating cells were enriched at the superficial layer of epithelial organoid. Single cell RNA sequencing (scRNAseq) showed that KSHV infection induced drastic changes of host gene expression in infected as well as uninfected cells at the different epithelial layers, resulting in altered keratinocyte differentiation and cell death. Moreover, we identified a unique population of infected cells containing lytic gene expression at the KSHV K2-K5 gene locus and distinct host gene expression compared to latent or lytic infected cells. This study demonstrates an in vitro 3D epithelial organoid ALI culture model that recapitulates KSHV infection in the oral cavity, where KSHV undergoes the epithelial differentiation-dependent spontaneous lytic replication with a unique cell population carrying distinct viral gene expression.
Keywords	Immunologic diseases. Allergy ; RC581-607 ; Biology (General) ; QH301-705.5
Subject code	570
Language	English
Publishing date	2022-08-01T00:00:00Z
Publisher	Public Library of Science (PLoS)
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: TXNIP-mediated crosstalk between oxidative stress and glucose metabolism.

Kim, Stephanie / Ge, Jianning / Kim, Dokyun / Lee, Jae Jin / Choi, Youn Jung / Chen, Weiqiang / Bowman, James W / Foo, Suan-Sin / Chang, Lin-Chun / Liang, Qiming / Hara, Daiki / Choi, Inpyo / Kim, Myung Hee / Eoh, Hyungjin / Jung, Jae U

PloS one

2024 Volume 19, Issue 2, Page(s) e0292655

Abstract: Thioredoxin-interacting protein (TXNIP) has emerged as a key player in cancer and diabetes since it targets thioredoxin (TRX)-mediated redox regulation and glucose transporter (GLUT)-mediated metabolism. TXNIP consists of two arrestin (ARR, N-ARR and C- ... ...

Abstract	Thioredoxin-interacting protein (TXNIP) has emerged as a key player in cancer and diabetes since it targets thioredoxin (TRX)-mediated redox regulation and glucose transporter (GLUT)-mediated metabolism. TXNIP consists of two arrestin (ARR, N-ARR and C-ARR) domains at its amino-terminus and two PPxY (PY) motifs and a di-leucine (LL) motif for endocytosis at its carboxyl-terminus. Here, we report that TXNIP shuffles between TRX and GLUTs to regulate homeostasis of intracellular oxidative stress and glucose metabolism. While TXNIP functions as a gatekeeper of TRX by default, it robustly interacted with class I GLUTs through its C-ARR domain upon increase of intracellular reactive oxygen species. This interaction prompted the surface expression downregulation and lysosomal degradation of GLUTs by its carboxyl-terminal LL endocytic signaling motif to attenuate glucose uptake. Consequently, TXNIP expression significantly limited glucose uptake, leading to the suppression of glycolysis, hexosamine biosynthesis, and the pentose phosphate pathway. Our findings establish a fundamental link between ROS and glucose metabolism through TXNIP and provide a promising target for the drug development against GLUT-related metabolic disorders.
MeSH term(s)	Humans ; Carrier Proteins/genetics ; Carrier Proteins/metabolism ; Diabetes Mellitus ; Glucose/metabolism ; Oxidative Stress ; Reactive Oxygen Species/metabolism ; Thioredoxins/genetics ; Thioredoxins/metabolism ; Animals ; Mice
Chemical Substances	Carrier Proteins ; Glucose (IY9XDZ35W2) ; Reactive Oxygen Species ; Thioredoxins (52500-60-4) ; TXNIP protein, human ; Txnip protein, mouse
Language	English
Publishing date	2024-02-08
Publishing country	United States
Document type	Journal Article
ZDB-ID	2267670-3
ISSN	1932-6203 ; 1932-6203
ISSN (online)	1932-6203
ISSN	1932-6203
DOI	10.1371/journal.pone.0292655
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Article ; Online: Respiratory distress in SARS-CoV-2 exposed uninfected neonates followed in the COVID Outcomes in Mother-Infant Pairs (COMP) Study.

Man, Olivia M / Azamor, Tamiris / Cambou, Mary Catherine / Fuller, Trevon L / Kerin, Tara / Paiola, Sophia G / Cranston, Jessica S / Mok, Thalia / Rao, Rashmi / Chen, Weiqiang / Jung, Jae U / Martinez, Viviana Fajardo / Foo, Suan-Sin / Nielsen-Saines, Karin

Nature communications

2024 Volume 15, Issue 1, Page(s) 399

Abstract: Respiratory distress (RD) has been reported in SARS-CoV-2 exposed uninfected (SEU) term neonates. Prior studies suggest that prenatal exposure to Coronavirus Disease 19 (COVID-19) may activate an inflammatory cascade in the newborn airway. In this study, ...

Abstract	Respiratory distress (RD) has been reported in SARS-CoV-2 exposed uninfected (SEU) term neonates. Prior studies suggest that prenatal exposure to Coronavirus Disease 19 (COVID-19) may activate an inflammatory cascade in the newborn airway. In this study, we examine the relationship between maternal COVID-19 vaccination and neonatal RD using a longitudinal cohort of mother-infant pairs in Los Angeles, CA. Two-hundred and twenty-one mothers with laboratory confirmed SARS-CoV-2 during pregnancy and 227 exposed fetuses are enrolled in our study. Maternal disease severity and neonatal RD variables were defined based on current accepted clinical criteria. To explore the multifactorial associations between maternal COVID-19 parameters and infant RD, we utilize a multivariable logistic regression model and a proteomic sub-analysis to propose a pathway for the development of RD following in utero exposure to SARS-CoV-2. Unusually high rates of RD are observed in SEU infants (17%). The odds ratio of RD is 3.06 (95% CI:1.08-10.21) in term neonates born to unvaccinated individuals versus those born to individuals vaccinated prior to maternal infection. Proteomic analysis reveals a robust inflammatory response associated with ciliary dysregulation and enhanced IgE production among SEU neonates with RD. Maternal vaccination against COVID-19 reduces the frequency of neonatal RD.
MeSH term(s)	Infant ; Infant, Newborn ; Female ; Pregnancy ; Humans ; SARS-CoV-2 ; COVID-19 ; COVID-19 Vaccines ; Mothers ; Proteomics ; Dyspnea ; Respiratory Distress Syndrome
Chemical Substances	COVID-19 Vaccines
Language	English
Publishing date	2024-01-24
Publishing country	England
Document type	Journal Article
ZDB-ID	2553671-0
ISSN	2041-1723 ; 2041-1723
ISSN (online)	2041-1723
ISSN	2041-1723
DOI	10.1038/s41467-023-44549-5
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Article ; Online: Single-cell analysis of Kaposi's sarcoma-associated herpesvirus infection in three-dimensional air-liquid interface culture model.

Jung, Kyle L / Choi, Un Yung / Park, Angela / Foo, Suan-Sin / Kim, Stephanie / Lee, Shin-Ae / Jung, Jae U

PLoS pathogens

2022 Volume 18, Issue 8, Page(s) e1010775

Abstract	The oral cavity is the major site for transmission of Kaposi's sarcoma-associated herpesvirus (KSHV), but how KSHV establishes infection and replication in the oral epithelia remains unclear. Here, we report a KSHV spontaneous lytic replication model using fully differentiated, three-dimensional (3D) oral epithelial organoids at an air-liquid interface (ALI). This model revealed that KSHV infected the oral epithelia when the basal epithelial cells were exposed by damage. Unlike two-dimensional (2D) cell culture, 3D oral epithelial organoid ALI culture allowed high levels of spontaneous KSHV lytic replication, where lytically replicating cells were enriched at the superficial layer of epithelial organoid. Single cell RNA sequencing (scRNAseq) showed that KSHV infection induced drastic changes of host gene expression in infected as well as uninfected cells at the different epithelial layers, resulting in altered keratinocyte differentiation and cell death. Moreover, we identified a unique population of infected cells containing lytic gene expression at the KSHV K2-K5 gene locus and distinct host gene expression compared to latent or lytic infected cells. This study demonstrates an in vitro 3D epithelial organoid ALI culture model that recapitulates KSHV infection in the oral cavity, where KSHV undergoes the epithelial differentiation-dependent spontaneous lytic replication with a unique cell population carrying distinct viral gene expression.
MeSH term(s)	Acquired Immunodeficiency Syndrome ; Gene Expression Regulation, Viral ; Herpesviridae Infections ; Herpesvirus 8, Human/physiology ; Humans ; Single-Cell Analysis ; Virus Latency ; Virus Replication
Language	English
Publishing date	2022-08-17
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
ZDB-ID	2205412-1
ISSN	1553-7374 ; 1553-7374
ISSN (online)	1553-7374
ISSN	1553-7374
DOI	10.1371/journal.ppat.1010775
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Article: Immunometabolic rewiring in long COVID patients with chronic headache.

Foo, Suan-Sin / Chen, Weiqiang / Jung, Kyle L / Azamor, Tamiris / Choi, Un Yung / Zhang, Pengfei / Comhair, Suzy Aa / Erzurum, Serpil C / Jehi, Lara / Jung, Jae U

bioRxiv : the preprint server for biology

2023

Abstract: Almost 20% of patients with COVID-19 experience long-term effects, known as post-COVID condition or long COVID. Among many lingering neurologic symptoms, chronic headache is the most common. Despite this health concern, the etiology of long COVID ... ...

Abstract	Almost 20% of patients with COVID-19 experience long-term effects, known as post-COVID condition or long COVID. Among many lingering neurologic symptoms, chronic headache is the most common. Despite this health concern, the etiology of long COVID headache is still not well characterized. Here, we present a longitudinal multi-omics analysis of blood leukocyte transcriptomics, plasma proteomics and metabolomics of long COVID patients with chronic headache. Long COVID patients experienced a state of hyper-inflammation prior to chronic headache onset and maintained persistent inflammatory activation throughout the progression of chronic headache. Metabolomic analysis also revealed augmented arginine and lipid metabolisms, skewing towards a nitric oxide-based pro-inflammation. Furthermore, metabolisms of neurotransmitters including serotonin, dopamine, glutamate, and GABA were markedly dysregulated during the progression of long COVID headache. Overall, these findings illustrate the immuno-metabolomics landscape of long COVID patients with chronic headache, which may provide insights to potential therapeutic interventions.
Language	English
Publishing date	2023-03-06
Publishing country	United States
Document type	Preprint
DOI	10.1101/2023.03.06.531302
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: OASL phase condensation induces amyloid-like fibrillation of RIPK3 to promote virus-induced necroptosis.

Lee, Shin-Ae / Chang, Lin-Chun / Jung, WooRam / Bowman, James W / Kim, Dokyun / Chen, Weiqiang / Foo, Suan-Sin / Choi, Youn Jung / Choi, Un Yung / Bowling, Anna / Yoo, Ji-Seung / Jung, Jae U

Nature cell biology

2023 Volume 25, Issue 1, Page(s) 92–107

Abstract: RIPK3-ZBP1-MLKL-mediated necroptosis is a proinflammatory cell death process that is crucial for antiviral host defence. RIPK3 self-oligomerization and autophosphorylation are prerequisites for executing necroptosis, yet the underlying mechanism of virus- ...

Abstract	RIPK3-ZBP1-MLKL-mediated necroptosis is a proinflammatory cell death process that is crucial for antiviral host defence. RIPK3 self-oligomerization and autophosphorylation are prerequisites for executing necroptosis, yet the underlying mechanism of virus-induced RIPK3 activation remains elusive. Interferon-inducible 2'-5' oligoadenylate synthetase-like (OASL) protein is devoid of enzymatic function but displays potent antiviral activity. Here we describe a role of OASL as a virus-induced necroptosis promoter that scaffolds the RIPK3-ZBP1 non-canonical necrosome via liquid-like phase condensation. This liquid-like platform of OASL recruits RIPK3 and ZBP1 via protein-protein interactions to provide spatial segregation for RIPK3 nucleation. This process facilitates the amyloid-like fibril formation and activation of RIPK3 and thereby MLKL phosphorylation for necroptosis. Mice deficient in Oasl1 exhibit severely impaired necroptosis and attenuated inflammation after viral infection, resulting in uncontrolled viral dissemination and lethality. Our study demonstrates an interferon-induced innate response whereby OASL scaffolds RIPK3-ZBP1 assembly via its phase-separated liquid droplets to facilitate necroptosis-mediated antiviral immunity.
MeSH term(s)	Animals ; Mice ; Protein Kinases/genetics ; Protein Kinases/metabolism ; Necroptosis ; Cell Death ; Antiviral Agents ; Interferons/metabolism ; Receptor-Interacting Protein Serine-Threonine Kinases/metabolism ; Apoptosis ; RNA-Binding Proteins/metabolism
Chemical Substances	Protein Kinases (EC 2.7.-) ; Antiviral Agents ; Interferons (9008-11-1) ; Receptor-Interacting Protein Serine-Threonine Kinases (EC 2.7.11.1) ; Zbp1 protein, mouse ; RNA-Binding Proteins ; Ripk3 protein, mouse (EC 2.7.11.1)
Language	English
Publishing date	2023-01-05
Publishing country	England
Document type	Journal Article
ZDB-ID	1474722-4
ISSN	1476-4679 ; 1465-7392
ISSN (online)	1476-4679
ISSN	1465-7392
DOI	10.1038/s41556-022-01039-y
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Article ; Online: Neuromotor repertoires in infants exposed to maternal COVID-19 during pregnancy: a cohort study.

Fajardo Martinez, Viviana / Zhang, Dajie / Paiola, Sophia / Mok, Thalia / Cambou, Mary C / Kerin, Tara / Rao, Rashmi / Brasil, Patricia / Ferreira, Fatima / Fuller, Trevon / Bhattacharya, Debika / Foo, Suan-Sin / Chen, Weiqiang / Jung, Jae / Einspieler, Christa / Marschik, Peter B / Nielsen-Saines, Karin

BMJ open

2023 Volume 13, Issue 1, Page(s) e069194

Abstract: Objective: To evaluate neuromotor repertoires and developmental milestones in infants exposed to antenatal COVID-19.: Design: Longitudinal cohort study.: Setting: Hospital-based study in Los Angeles, USA and Rio de Janeiro, Brazil between March ... ...

Abstract	Objective: To evaluate neuromotor repertoires and developmental milestones in infants exposed to antenatal COVID-19. Design: Longitudinal cohort study. Setting: Hospital-based study in Los Angeles, USA and Rio de Janeiro, Brazil between March 2020 and December 2021. Participants: Infants born to mothers with COVID-19 during pregnancy and prepandemic control infants from the Graz University Database. Interventions: General movement assessment (GMA) videos between 3 and 5 months post-term age were collected and clinical assessments/developmental milestones evaluated at 6-8 months of age. Cases were matched by gestational age, gender and post-term age to prepandemic neurotypical unexposed controls from the database. Main outcome measures: Motor Optimality Scores Revised (MOS-R) at 3-5 months. Presence of developmental delay (DD) at 6-8 months. Results: 239 infants were enrolled; 124 cases (83 in the USA/41 in Brazil) and 115 controls. GMA was assessed in 115 cases and 115 controls; 25% were preterm. Median MOS-R in cases was 23 (IQR 21-24, range 9-28) vs 25 (IQR 24-26, range 20-28) in controls, p<0.001. Sixteen infants (14%) had MOS-R scores <20 vs zero controls, p<0.001. At 6-8 months, 13 of 109 case infants (12%) failed to attain developmental milestones; all 115 control infants had normal development. The timing of maternal infection in pregnancy (first, second or third trimester) or COVID-19 disease severity (NIH categories asymptomatic, mild/moderate or severe/critical) was not associated with suboptimal MOS-R or DD. Maternal fever in pregnancy was associated with DD (OR 3.7; 95% CI 1.12 to 12.60) but not suboptimal MOS-R (OR 0.25; 95% CI 0.04 to 0.96). Conclusions: Compared with prepandemic controls, infants exposed to antenatal COVID-19 more frequently had suboptimal neuromotor development.
MeSH term(s)	Infant, Newborn ; Infant ; Humans ; Pregnancy ; Female ; Cohort Studies ; Longitudinal Studies ; Brazil ; COVID-19 ; Pregnancy Complications, Infectious
Language	English
Publishing date	2023-01-23
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2599832-8
ISSN	2044-6055 ; 2044-6055
ISSN (online)	2044-6055
ISSN	2044-6055
DOI	10.1136/bmjopen-2022-069194
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Article ; Online: Immunometabolic rewiring in long COVID patients with chronic headache

Foo, Suan-Sin / Chen, Weiqiang / Jung, Kyle L / Azamor, Tamiris / Choi, Un Yung / Zhang, Pengfei / Comhair, Suzy AA / Erzurum, Serpil C / Jehi, Lara / Jung, Jae U

bioRxiv

Abstract	Almost 20% of patients with COVID-19 experience long-term effects, known as post-COVID condition or long COVID. Among many lingering neurologic symptoms, chronic headache is the most common. Despite this health concern, the etiology of long COVID headache is still not well characterized. Here, we present a longitudinal multi-omics analysis of blood leukocyte transcriptomics, plasma proteomics and metabolomics of long COVID patients with chronic headache. Long COVID patients experienced a state of hyper-inflammation prior to chronic headache onset and maintained persistent inflammatory activation throughout the progression of chronic headache. Metabolomic analysis also revealed augmented arginine and lipid metabolisms, skewing towards a nitric oxide-based pro-inflammation. Furthermore, metabolisms of neurotransmitters including serotonin, dopamine, glutamate, and GABA were markedly dysregulated during the progression of long COVID headache. Overall, these findings illustrate the immuno-metabolomics landscape of long COVID patients with chronic headache, which may provide insights to potential therapeutic interventions.
Keywords	covid19
Language	English
Publishing date	2023-03-06
Publisher	Cold Spring Harbor Laboratory
Document type	Article ; Online
DOI	10.1101/2023.03.06.531302
Database	COVID19

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Article ; Online: Lung-specific MCEMP1 functions as an adaptor for KIT to promote SCF-mediated mast cell proliferation.

Nature communications

2023 Volume 14, Issue 1, Page(s) 2045

Abstract: Lung mast cells are important in host defense, and excessive proliferation or activation of these cells can cause chronic inflammatory disorders like asthma. Two parallel pathways induced by KIT-stem cell factor (SCF) and FcεRI-immunoglobulin E ... ...

Abstract	Lung mast cells are important in host defense, and excessive proliferation or activation of these cells can cause chronic inflammatory disorders like asthma. Two parallel pathways induced by KIT-stem cell factor (SCF) and FcεRI-immunoglobulin E interactions are critical for the proliferation and activation of mast cells, respectively. Here, we report that mast cell-expressed membrane protein1 (MCEMP1), a lung-specific surface protein, functions as an adaptor for KIT, which promotes SCF-mediated mast cell proliferation. MCEMP1 elicits intracellular signaling through its cytoplasmic immunoreceptor tyrosine-based activation motif and forms a complex with KIT to enhance its autophosphorylation and activation. Consequently, MCEMP1 deficiency impairs SCF-induced peritoneal mast cell proliferation in vitro and lung mast cell expansion in vivo. Mcemp1-deficient mice exhibit reduced airway inflammation and lung impairment in chronic asthma mouse models. This study shows lung-specific MCEMP1 as an adaptor for KIT to facilitate SCF-mediated mast cell proliferation.
MeSH term(s)	Animals ; Mice ; Asthma ; Cell Proliferation ; Lung/metabolism ; Proto-Oncogene Proteins c-kit/metabolism ; Stem Cell Factor/metabolism
Chemical Substances	Proto-Oncogene Proteins c-kit (EC 2.7.10.1) ; Stem Cell Factor ; Mcemp1 protein, mouse
Language	English
Publishing date	2023-04-11
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2553671-0
ISSN	2041-1723 ; 2041-1723
ISSN (online)	2041-1723
ISSN	2041-1723
DOI	10.1038/s41467-023-37873-3
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