Pathophysiology of reinfection by exogenous HSV-1 is driven by heparanase dysfunction

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Abstract

Limited knowledge exists on exogenous DNA virus reinfections. Herpes simplex virus-1 (HSV-1), a prototype DNA virus, causes multiple human diseases including vision-threatening eye infections. While reinfection with an exogenous HSV-1 strain is considered plausible, little is known about the underlying mechanisms governing its pathophysiology in a host. Heparanase (HPSE), a host endoglycosidase, when up-regulated by HSV-1 infection dictates local inflammatory response by destabilizing tissue architecture. Here, we demonstrate that HSV-1 reinfection in mice causes notable pathophysiology in wild-type controls compared to the animals lacking HPSE. The endoglycosidase promotes infected cell survival and supports a pro-disease environment. In contrast, lack of HPSE strengthens intrinsic immunity by promoting cytokine expression, inducing necroptosis of infected cells, and decreasing leukocyte infiltration into the cornea. Collectively, we report that immunity from a recent prior infection fails to abolish disease manifestation during HSV-1 reinfection unless HPSE is rendered inactive.

Abstract

Immunity from a prior HSV-1 infection fails to abolish HSV-1 reinfection pathologies unless heparanase is rendered inactive.

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Most cited references 29

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Increased risk of SARS-CoV-2 reinfection associated with emergence of Omicron in South Africa

Juliet Pulliam, Cari van Schalkwyk, Nevashan Govender … (2022)

Here, we provide two methods for monitoring reinfection trends in routine surveillance data to identify signatures of changes in reinfection risk and apply these approaches to data from South Africa’s SARS-CoV-2 epidemic to date. While we found no evidence of increased reinfection risk associated with circulation of Beta (B.1.351) or Delta (B.1.617.2) variants, we find clear, population-level evidence to suggest immune evasion by the Omicron (B.1.1.529) variant in previously infected individuals in South Africa. Reinfections occurring between 01 November 2021 and 31 January 2022 were detected in individuals infected in all three previous waves, and there has been an increase in the risk of having a third infection since mid-November 2021.

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Necroptosis: a regulated inflammatory mode of cell death

Yogesh Dhuriya, Divakar Sharma (2018)

Programmed cell death has a vital role in embryonic development and tissue homeostasis. Necroptosis is an alternative mode of regulated cell death mimicking features of apoptosis and necrosis. Necroptosis requires protein RIPK3 (previously well recognized as regulator of inflammation, cell survival, and disease) and its substrate MLKL, the crucial players of this pathway. Necroptosis is induced by toll-like receptor, death receptor, interferon, and some other mediators. Shreds of evidence based on a mouse model reveals that deregulation of necroptosis has been found to be associated with pathological conditions like cancer, neurodegenerative diseases, and inflammatory diseases. In this timeline article, we are discussing the molecular mechanisms of necroptosis and its relevance to diseases.

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Herpesviruses: latency and reactivation – viral strategies and host response

Bjørn Grinde (2013)

Eight members of the Herpesviridae family commonly infect humans, and close to 100% of the adult population is infected with at least one of these. The five that cause the most health concerns are: herpes simplex virus (HSV) type 1 and 2, Epstein–Barr virus (EBV), cytomegalovirus (CMV), and varicella zoster virus (VZV). In addition, there are human herpes virus (HHV) types 6–8. The review starts by introducing possible viral strategies in general. The particular biology and host relationship of the various human herpesviruses, including their pathology, are examined subsequently. Factors that contribute to the maintenance of latency and reactivation of viral replication are discussed. There will be special reference to how these viruses exploit and contribute to pathology in the oral cavity. Reactivation does not necessarily imply clinical symptoms, as reflected in the asymptomatic shedding of EBV and CMV from oral mucosa. The immune response and the level of viral output are both important to the consequences experienced.

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Author and article information

Contributors

Rahul K. Suryawanshi:

ORCID: https://orcid.org/0000-0001-8374-669X

Role: ConceptualizationRole: Formal analysisRole: InvestigationRole: MethodologyRole: Project administrationRole: ResourcesRole: ValidationRole: VisualizationRole: Writing - original draftRole: Writing - review & editing

Chandrashekhar D. Patil:

ORCID: https://orcid.org/0000-0002-5641-4523

Role: ConceptualizationRole: Data curationRole: Formal analysisRole: InvestigationRole: MethodologyRole: Project administrationRole: ResourcesRole: SupervisionRole: ValidationRole: VisualizationRole: Writing - original draftRole: Writing - review & editing

Alex Agelidis: Role: ConceptualizationRole: Formal analysisRole: InvestigationRole: MethodologyRole: SoftwareRole: ValidationRole: VisualizationRole: Writing - review & editing

Raghuram Koganti:

ORCID: https://orcid.org/0000-0002-6551-2475

Role: MethodologyRole: Writing - original draftRole: Writing - review & editing

Tejabhiram Yadavalli:

ORCID: https://orcid.org/0000-0001-8584-2685

Role: ConceptualizationRole: InvestigationRole: MethodologyRole: Writing - original draftRole: Writing - review & editing

Joshua M. Ames:

ORCID: https://orcid.org/0000-0002-9282-5637

Role: Methodology

Hemant Borase:

ORCID: https://orcid.org/0000-0003-2097-1018

Role: InvestigationRole: MethodologyRole: ValidationRole: Writing - original draft

Deepak Shukla:

ORCID: https://orcid.org/0000-0002-3039-6953

Role: ConceptualizationRole: Funding acquisitionRole: InvestigationRole: Project administrationRole: ResourcesRole: SupervisionRole: ValidationRole: Writing - original draftRole: Writing - review & editing

Journal

Journal ID (nlm-ta): Sci Adv

Journal ID (iso-abbrev): Sci Adv

Journal ID (publisher-id): sciadv

Journal ID (hwp): advances

Title: Science Advances

Publisher: American Association for the Advancement of Science

ISSN (Electronic): 2375-2548

Publication date Collection: April 2023

Publication date (Electronic, pub): 28 April 2023

Volume: 9

Issue: 17

Electronic Location Identifier: eadf3977

Affiliations

[ ¹ ]Department of Ophthalmology and Visual Sciences, University of Illinois at Chicago, Chicago, IL 60612, USA.

[ ² ]Department of Microbiology and Immunology, University of Illinois at Chicago, Chicago, IL 60612, USA.

Author notes

[†]

These authors contributed equally to this work.

[‡]

Present address: Gladstone Institutes, San Francisco, CA, USA.

[* ]Corresponding author. Email: dshukla@ 123456uic.edu

Author information

Rahul K. Suryawanshi https://orcid.org/0000-0001-8374-669X

Chandrashekhar D. Patil https://orcid.org/0000-0002-5641-4523

Raghuram Koganti https://orcid.org/0000-0002-6551-2475

Tejabhiram Yadavalli https://orcid.org/0000-0001-8584-2685

Joshua M. Ames https://orcid.org/0000-0002-9282-5637

Hemant Borase https://orcid.org/0000-0003-2097-1018

Deepak Shukla https://orcid.org/0000-0002-3039-6953

Article

Publisher ID: adf3977

DOI: 10.1126/sciadv.adf3977

PMC ID: 10146881

PubMed ID: 37115924

SO-VID: 950e8f85-0e58-4ff9-a16d-533ceb7bac74

Copyright © Copyright © 2023 The Authors, some rights reserved; exclusive licensee American Association for the Advancement of Science. No claim to original U.S. Government Works. Distributed under a Creative Commons Attribution License 4.0 (CC BY).

License:

This is an open-access article distributed under the terms of the Creative Commons Attribution license, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

History

Date received : 18 October 2022

Date accepted : 23 March 2023

Funding

Funded by: FundRef http://dx.doi.org/10.13039/100000002, National Institutes of Health;

Award ID: EY029426

Funded by: FundRef http://dx.doi.org/10.13039/100000002, National Institutes of Health;

Award ID: AI139768

Funded by: FundRef http://dx.doi.org/10.13039/100000002, National Institutes of Health;

Award ID: EY024710

Funded by: FundRef http://dx.doi.org/10.13039/100000053, National Eye Institute;

Award ID: EY001792

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Copyeditor Mjoy Azul

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Pathophysiology of reinfection by exogenous HSV-1 is driven by heparanase dysfunction

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UCL: UN SDG 01 No Poverty

Most cited references 29

Increased risk of SARS-CoV-2 reinfection associated with emergence of Omicron in South Africa

Necroptosis: a regulated inflammatory mode of cell death

Herpesviruses: latency and reactivation – viral strategies and host response

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