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Article ; Online: Interferons in Viral Infections.

Sengupta, Pracheta / Chattopadhyay, Saurabh

2024 Volume 16, Issue 3

Abstract: Interferons (IFNs) are cytokines that inhibit viral replication in host cells by triggering innate immune responses through the transcriptional induction of various IFN-stimulated genes (ISGs) [ ... ]. ...

Abstract	Interferons (IFNs) are cytokines that inhibit viral replication in host cells by triggering innate immune responses through the transcriptional induction of various IFN-stimulated genes (ISGs) [...].
MeSH term(s)	Humans ; Interferons/genetics ; Cytokines ; Immunity, Innate ; Virus Diseases ; Virus Replication
Chemical Substances	Interferons (9008-11-1) ; Cytokines
Language	English
Publishing date	2024-03-14
Publishing country	Switzerland
Document type	Editorial
ZDB-ID	2516098-9
ISSN	1999-4915 ; 1999-4915
ISSN (online)	1999-4915
ISSN	1999-4915
DOI	10.3390/v16030451
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Article ; Online: Inflammatory Control of Viral Infection.

Chakravarty, Sukanya / Chakravarti, Ritu / Chattopadhyay, Saurabh

Viruses

2023 Volume 15, Issue 7

Abstract: Inflammatory responses during virus infection differentially impact the host. Managing inflammatory responses is essential in controlling viral infection and related diseases. Recently, we identified a cellular anti-inflammatory mechanism, RIKA ( ... ...

Abstract	Inflammatory responses during virus infection differentially impact the host. Managing inflammatory responses is essential in controlling viral infection and related diseases. Recently, we identified a cellular anti-inflammatory mechanism, RIKA (Repression of IRF3-mediated inhibition of NF-κB activity), which controls viral inflammation and pathogenesis. The RIKA function of IRF3 may be explored further in other inflammatory diseases beyond viral infection.
MeSH term(s)	Humans ; Signal Transduction ; NF-kappa B/metabolism ; Virus Diseases ; Inflammation ; Immunity, Innate
Chemical Substances	NF-kappa B
Language	English
Publishing date	2023-07-20
Publishing country	Switzerland
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	2516098-9
ISSN	1999-4915 ; 1999-4915
ISSN (online)	1999-4915
ISSN	1999-4915
DOI	10.3390/v15071579
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Article ; Online: Non-transcriptional IRF7 interacts with NF-κB to inhibit viral inflammation.

Fan, Shumin / Popli, Sonam / Chakravarty, Sukanya / Chakravarti, Ritu / Chattopadhyay, Saurabh

The Journal of biological chemistry

2024 Volume 300, Issue 4, Page(s) 107200

Abstract: Interferon (IFN) regulatory factors (IRF) are key transcription factors in cellular antiviral responses. IRF7, a virus-inducible IRF, expressed primarily in myeloid cells, is required for transcriptional induction of interferon α and antiviral genes. ... ...

Abstract	Interferon (IFN) regulatory factors (IRF) are key transcription factors in cellular antiviral responses. IRF7, a virus-inducible IRF, expressed primarily in myeloid cells, is required for transcriptional induction of interferon α and antiviral genes. IRF7 is activated by virus-induced phosphorylation in the cytoplasm, leading to its translocation to the nucleus for transcriptional activity. Here, we revealed a nontranscriptional activity of IRF7 contributing to its antiviral functions. IRF7 interacted with the pro-inflammatory transcription factor NF-κB-p65 and inhibited the induction of inflammatory target genes. Using knockdown, knockout, and overexpression strategies, we demonstrated that IRF7 inhibited NF-κB-dependent inflammatory target genes, induced by virus infection or toll-like receptor stimulation. A mutant IRF7, defective in transcriptional activity, interacted with NF-κB-p65 and suppressed NF-κB-induced gene expression. A single-action IRF7 mutant, active in anti-inflammatory function, but defective in transcriptional activity, efficiently suppressed Sendai virus and murine hepatitis virus replication. We, therefore, uncovered an anti-inflammatory function for IRF7, independent of transcriptional activity, contributing to the antiviral response of IRF7.
MeSH term(s)	Interferon Regulatory Factor-7/metabolism ; Interferon Regulatory Factor-7/genetics ; Humans ; Animals ; Sendai virus ; Mice ; Inflammation/metabolism ; Inflammation/genetics ; Transcription Factor RelA/metabolism ; Transcription Factor RelA/genetics ; HEK293 Cells ; Virus Replication ; NF-kappa B/metabolism ; NF-kappa B/genetics
Chemical Substances	Interferon Regulatory Factor-7 ; IRF7 protein, human ; Transcription Factor RelA ; NF-kappa B ; Irf7 protein, mouse
Language	English
Publishing date	2024-03-18
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2997-x
ISSN	1083-351X ; 0021-9258
ISSN (online)	1083-351X
ISSN	0021-9258
DOI	10.1016/j.jbc.2024.107200
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Article ; Online: How Different Pathologies Are Affected by IFIT Expression.

Franco, Justin H / Chattopadhyay, Saurabh / Pan, Zhixing K

Viruses

2023 Volume 15, Issue 2

Abstract: The type-I interferon (IFN) system represents the first line of defense against viral pathogens. Recognition of the virus initiates complex signaling pathways that result in the transcriptional induction of IFNs, which are then secreted. Secreted IFNs ... ...

Abstract	The type-I interferon (IFN) system represents the first line of defense against viral pathogens. Recognition of the virus initiates complex signaling pathways that result in the transcriptional induction of IFNs, which are then secreted. Secreted IFNs stimulate nearby cells and result in the production of numerous proinflammatory cytokines and antiviral factors. Of particular note, IFN-induced tetratricopeptide repeat (IFIT) proteins have been thoroughly studied because of their antiviral activity against different viral pathogens. Although classically studied as an antiviral protein, IFIT expression has recently been investigated in the context of nonviral pathologies, such as cancer and sepsis. In oral squamous cell carcinoma (OSCC), IFIT1 and IFIT3 promote metastasis, while IFIT2 exhibits the opposite effect. The role of IFIT proteins during bacterial/fungal sepsis is still under investigation, with studies showing conflicting roles for IFIT2 in disease severity. In the setting of viral sepsis, IFIT proteins play a key role in clearing viral infection. As a result, many viral pathogens, such as SARS-CoV-2, employ mechanisms to inhibit the type-I IFN system and promote viral replication. In cancers that are characterized by upregulated IFIT proteins, medications that decrease IFIT expression may reduce metastasis and improve survival rates. Likewise, in cases of viral sepsis, therapeutics that increase IFIT expression may improve viral clearance and reduce the risk of septic shock. By understanding the effect of IFIT proteins in different pathologies, novel therapeutics can be developed to halt disease progression.
MeSH term(s)	Humans ; Carcinoma, Squamous Cell ; Mouth Neoplasms ; Tetratricopeptide Repeat ; COVID-19 ; SARS-CoV-2 ; Sepsis ; Viremia ; Antiviral Agents ; Interferon Type I
Chemical Substances	Antiviral Agents ; Interferon Type I
Language	English
Publishing date	2023-01-25
Publishing country	Switzerland
Document type	Journal Article ; Review ; Research Support, N.I.H., Extramural
ZDB-ID	2516098-9
ISSN	1999-4915 ; 1999-4915
ISSN (online)	1999-4915
ISSN	1999-4915
DOI	10.3390/v15020342
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Article ; Online: Critically ill patients: Histopathological evidence of thyroid dysfunction.

Saha, Dipti / Chattopadhyay, Saurabh / Dutta, Sayak Sovan / Roy, Anup Kumar

Journal of critical care

2023 Volume 78, Page(s) 154384

Abstract: Purpose: Critical illness is characterized by severe biphasic physical and metabolic stress as result of systemic inflammatory response syndrome and/or multiple organ dysfunction syndrome, and is frequently associated with non-thyroidal illness. Purpose ...

Abstract	Purpose: Critical illness is characterized by severe biphasic physical and metabolic stress as result of systemic inflammatory response syndrome and/or multiple organ dysfunction syndrome, and is frequently associated with non-thyroidal illness. Purpose of this study is to better understand the cytomorphological basis of NTI by performing histopathological examinations of thyroid gland on autopsies of patients who died from critical illness. Methods: Histopathological examination of thyroid gland of 58 critically ill patients was performed in our hospital. The cases included 24 cases of burn injury, 24 cases of traumatic brain injury, and 10 cases of cerebral stroke. Thyroid samples obtained during autopsy were preserved in formol saline and stained with hematoxylin and eosin. The sections were visualized under light microscopy. Results: Out of 58 cases examined, 21 patients showed normal thyroid findings, and rest of the cases had unusual thyroid findings in the histopathological study. The principal finding was distortion of thyroid follicular architecture. Other findings include mononuclear cell infiltration, clumping of thyroglobulin, and exhaustion of thyroid follicles. Conclusion: Critical illness produces metabolically damaging effects on thyroid gland, which functionally corresponds to a state of low T3 syndrome. These changes are more pronounced in BI and cerebral stroke than in TBI.
MeSH term(s)	Humans ; Critical Illness ; Euthyroid Sick Syndromes/diagnosis ; Autopsy ; Death
Language	English
Publishing date	2023-07-25
Publishing country	United States
Document type	Journal Article
ZDB-ID	632818-0
ISSN	1557-8615 ; 0883-9441
ISSN (online)	1557-8615
ISSN	0883-9441
DOI	10.1016/j.jcrc.2023.154384
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Article ; Online: Autophagic checks and balances of cellular immune responses.

Chakravarty, Sukanya / Fan, Shumin / Chakravarti, Ritu / Chattopadhyay, Saurabh

Autophagy reports

2022 Volume 1, Issue 1, Page(s) 83–87

Abstract: IRF3 (interferon regulatory factor 3) is a critical component of the antiviral innate immune response. IRF3 deficiency causes detrimental effects to the host during virus infection. Dysregulation of IRF3 functions is associated with viral, inflammatory, ... ...

Abstract	IRF3 (interferon regulatory factor 3) is a critical component of the antiviral innate immune response. IRF3 deficiency causes detrimental effects to the host during virus infection. Dysregulation of IRF3 functions is associated with viral, inflammatory, and hepatic diseases. Both transcriptional and pro-apoptotic activities of IRF3 are involved in the exacerbated inflammation and apoptosis in liver injury induced by ethanol and high-fat diets. Therefore, regulation of IRF3 activities has consequences, and it is a potential therapeutic target for infectious and inflammatory diseases. We recently revealed that IRF3 is degraded by a small molecule, auranofin, by activating the cellular macroautophagy/autophagy pathway. Autophagy is a catabolic pathway that contributes to cellular homeostasis and antiviral host defense. Degradation of IRF3 by autophagy may be a novel strategy used by the viruses to their benefit. In addition, IRF3 functions are harmful in other diseases, including liver injury and bacterial infection. A better understanding of the role of autophagy in regulating IRF3 functions has significant implications in developing therapeutic strategies. Therefore, autophagy provides checks and balances in the innate immune response.
Language	English
Publishing date	2022-03-31
Publishing country	United States
Document type	Journal Article
ISSN	2769-4127
ISSN (online)	2769-4127
DOI	10.1080/27694127.2022.2058677
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Article ; Online: Retinoic Acid-Mediated Inhibition of Mouse Coronavirus Replication Is Dependent on IRF3 and CaMKK.

Franco, Justin H / Harris, Ryan A / Ryan, William G / Taylor, Roger Travis / McCullumsmith, Robert E / Chattopadhyay, Saurabh / Pan, Zhixing K

Viruses

2024 Volume 16, Issue 1

Abstract: The ongoing COVID-19 pandemic has revealed the shortfalls in our understanding of how to treat coronavirus infections. With almost 7 million case fatalities of COVID-19 globally, the catalog of FDA-approved antiviral therapeutics is limited compared to ... ...

Abstract	The ongoing COVID-19 pandemic has revealed the shortfalls in our understanding of how to treat coronavirus infections. With almost 7 million case fatalities of COVID-19 globally, the catalog of FDA-approved antiviral therapeutics is limited compared to other medications, such as antibiotics. All-trans retinoic acid (RA), or activated vitamin A, has been studied as a potential therapeutic against coronavirus infection because of its antiviral properties. Due to its impact on different signaling pathways, RA's mechanism of action during coronavirus infection has not been thoroughly described. To determine RA's mechanism of action, we examined its effect against a mouse coronavirus, mouse hepatitis virus strain A59 (MHV). We demonstrated that RA significantly decreased viral titers in infected mouse L929 fibroblasts and RAW 264.7 macrophages. The reduced viral titers were associated with a corresponding decrease in MHV nucleocapsid protein expression. Using interferon regulatory factor 3 (IRF3) knockout RAW 264.7 cells, we demonstrated that RA-induced suppression of MHV required IRF3 activity. RNA-seq analysis of wildtype and IRF3 knockout RAW cells showed that RA upregulated calcium/calmodulin (CaM) signaling proteins, such as CaM kinase kinase 1 (CaMKK1). When treated with a CaMKK inhibitor, RA was unable to upregulate IRF activation during MHV infection. In conclusion, our results demonstrate that RA-induced protection against coronavirus infection depends on IRF3 and CaMKK.
MeSH term(s)	Animals ; Mice ; Amino Acids ; Antiviral Agents/pharmacology ; Calcium-Calmodulin-Dependent Protein Kinase Kinase/metabolism ; Interferon Regulatory Factor-3/metabolism ; Tretinoin/pharmacology ; Virus Replication/drug effects ; Murine hepatitis virus/drug effects ; Murine hepatitis virus/physiology ; RAW 264.7 Cells ; L Cells
Chemical Substances	Amino Acids ; Antiviral Agents ; Calcium-Calmodulin-Dependent Protein Kinase Kinase (EC 2.7.11.17) ; Interferon Regulatory Factor-3 ; Tretinoin (5688UTC01R)
Language	English
Publishing date	2024-01-18
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2516098-9
ISSN	1999-4915 ; 1999-4915
ISSN (online)	1999-4915
ISSN	1999-4915
DOI	10.3390/v16010140
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Article ; Online: Interferon-stimulated gene TDRD7 interacts with AMPK and inhibits its activation to suppress viral replication and pathogenesis.

Chakravarty, Sukanya / Subramanian, Gayatri / Popli, Sonam / Veleeparambil, Manoj / Fan, Shumin / Chakravarti, Ritu / Chattopadhyay, Saurabh

mBio

2023 Volume 14, Issue 5, Page(s) e0061123

Abstract: Importance: Virus infection triggers induction of interferon (IFN)-stimulated genes (ISGs), which ironically inhibit viruses themselves. We identified Tudor domain-containing 7 (TDRD7) as a novel antiviral ISG, which inhibits viral replication by ... ...

Abstract	Importance: Virus infection triggers induction of interferon (IFN)-stimulated genes (ISGs), which ironically inhibit viruses themselves. We identified Tudor domain-containing 7 (TDRD7) as a novel antiviral ISG, which inhibits viral replication by interfering with autophagy pathway. Here, we present a molecular basis for autophagy inhibitory function of TDRD7. TDRD7 interacted with adenosine monophosphate (AMP)-activated protein kinase (AMPK), the kinase that initiates autophagy, to inhibit its activation. We identified domains required for the interaction; deleting AMPK-interacting domain blocked antiAMPK and antiviral activities of TDRD7. We used primary cells and mice to evaluate the TDRD7-AMPK antiviral pathway. TDRD7-deficient primary mouse cells exhibited enhanced AMPK activation and viral replication. Finally, TDRD7 knockout mice showed increased susceptibility to respiratory virus infection. Therefore, our study revealed a new antiviral pathway of IFN and its contribution to host response. Our results have therapeutic potential; a TDRD7-derived peptide may be an effective AMPK inhibitor with application as antiviral agent.
MeSH term(s)	Animals ; Mice ; Interferons/metabolism ; AMP-Activated Protein Kinases/metabolism ; Virus Replication/genetics ; Antiviral Agents/pharmacology ; Virus Diseases ; Immunity, Innate ; Ribonucleoproteins/genetics
Chemical Substances	Interferons (9008-11-1) ; AMP-Activated Protein Kinases (EC 2.7.11.31) ; Antiviral Agents ; TDRD7 protein, mouse ; Ribonucleoproteins
Language	English
Publishing date	2023-09-15
Publishing country	United States
Document type	Journal Article
ZDB-ID	2557172-2
ISSN	2150-7511 ; 2161-2129
ISSN (online)	2150-7511
ISSN	2161-2129
DOI	10.1128/mbio.00611-23
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Article ; Online: Biochemical Analysis of Caspase-8-dependent Proteolysis of IRF3 in Virus-infected Cells.

Subramanian, Gayatri / Pan, Karen / Chakravarti, Ritu / Chattopadhyay, Saurabh

Bio-protocol

2019 Volume 6, Issue 22

Language	English
Publishing date	2019-05-08
Publishing country	United States
Document type	Journal Article
ZDB-ID	2833269-6
ISSN	2331-8325 ; 2331-8325
ISSN (online)	2331-8325
ISSN	2331-8325
DOI	10.21769/BioProtoc.2018
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Article ; Online: Small secretory proteins of immune cells can modulate gynecological cancers.

Kumar, Niranjan / Vyas, Akanksha / Agnihotri, Saurabh Kumar / Chattopadhyay, Naibedya / Sachdev, Monika

Seminars in cancer biology

2022 Volume 86, Issue Pt 3, Page(s) 513–531

Abstract: Small secretory proteins of immune cells are mostly Cytokines, which include chemokines, interleukins, interferons, lymphokines and tumor necrosis factors but not hormones or growth factors. These secretory proteins are the molecular messengers and ... ...

Abstract	Small secretory proteins of immune cells are mostly Cytokines, which include chemokines, interleukins, interferons, lymphokines and tumor necrosis factors but not hormones or growth factors. These secretory proteins are the molecular messengers and primarily involved in autocrine, paracrine and endocrine signaling as immunomodulating agents. Hence, these proteins actually regulate the cells of immune system to communicate with one another to produce a synchronized, robust, still self-regulated response to a specific antigen. Chemokines are smaller secreted proteins that control overall immune cell movement and location; these chemokines are divided into 4 subgroups, namely, CXC, CC, CX3C and C according to the position of 4 conserved cysteine residues. Complete characterization of cytokines and chemokines can exploit their vast signaling networks to develop cancer treatments. These secretory proteins like IL-6, IL-10, IL-12, TNFα, CCL2, CXCL4 & CXCL8 are predominantly expressed in most of the gynecological cancers, which directly stimulate immune effector cells and stromal cells at the tumor site and augment tumor cell recognition by cytotoxic T-cells. Hence; these secretory proteins are the major regulators, which can actually modulate all kinds of gynecological cancers. Furthermore, advancements in adoptive T-cell treatment have relied on the use of multiple cytokines/chemokines to establish a highly regulated environment for anti-tumor T cell growth. A number of in vitro studies as well as animal models and clinical subjects have also shown that cytokines/chemokines have broad antitumor activity, which has been translated into a number of cancer therapy approaches. This review will focus on the foremost cytokines & chemokines involved in the majority of the gynecological malignancies and discuss their basic biology as well as clinical applications.
MeSH term(s)	Animals ; Humans ; Chemokines/metabolism ; Chemokines/therapeutic use ; Cytokines/metabolism ; Neoplasms/etiology ; Neoplasms/drug therapy ; Cell Communication ; Interleukins
Chemical Substances	Chemokines ; Cytokines ; Interleukins
Language	English
Publishing date	2022-02-09
Publishing country	England
Document type	Journal Article ; Review ; Research Support, Non-U.S. Gov't
ZDB-ID	1033980-2
ISSN	1096-3650 ; 1044-579X
ISSN (online)	1096-3650
ISSN	1044-579X
DOI	10.1016/j.semcancer.2022.02.008
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