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Viruses
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Viruses and Eye Diseases
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Viruses and Eye Diseases

A special issue of Viruses (ISSN 1999-4915). This special issue belongs to the section "Human Virology and Viral Diseases".

Deadline for manuscript submissions: 28 February 2025 | Viewed by 2600

Special Issue Editors

Prof. Dr. Homayon Ghiasi

E-Mail Website
Guest Editor
Ophthalmology Viral Immunology and Vaccine Laboratory, Cedars-Sinai Health System, Los Angeles, CA 90048, USA
Interests: the role of HSV-1 in herpes induced corneal scarring; vaccine development against ocular HSV-1 infection; the role of viral infection and cytokines in CNS demyelination
Prof. Dr. Deepak Shukla

E-Mail Website
Guest Editor
1. Marion Schenk Esq. Professor of the Aging Eye Research and Director of Research, Department of Ophthalmology and Visual Sciences, College of Medicine, University of Illinois Chicago, Chicago, IL 60607, USA
2. Department of Microbiology and Immunology, College of Medicine, University of Illinois Chicago, Chicago, IL 60607, USA
Interests: herpes simplex virus infection; viral glycoproteins; antiviral agents; viral vaccines; ocular infection; heparan sulfate proteoglycans; heparanase
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

In recent years, there has been growing recognition of the intricate interplay between viruses and ocular health. Viral infections have emerged as significant contributors to a wide array of eye diseases, spanning from mild irritation to severe vision impairment and even blindness. From the cornea to the retina, viruses can infiltrate various tissues within the eye, causing inflammation, tissue damage, and vision loss.

One of the most well-known viruses that affects ocular health is the herpes simplex virus (HSV). HSV infection can manifest as herpetic keratitis, a potentially sight-threatening condition characterized by inflammation of the cornea. Additionally, varicella zoster virus (VZV), which causes chickenpox and shingles, can lead to herpes zoster ophthalmicus, involving painful skin lesions and potentially affecting the eye, leading to conditions such as keratitis, uveitis, and retinitis. Both of these viruses hide in sensory nerves for the lifetime of infected individuals and periodically reactivate to cause recurrent eye diseases.

Another significant viral culprit is adenovirus, which can cause epidemic keratoconjunctivitis, a highly contagious form of conjunctivitis characterized by redness, watery discharge, and foreign body sensation. Moreover, respiratory viruses such as influenza and adenovirus can also lead to viral conjunctivitis, further highlighting the systemic impact of viral infections on ocular health.

Beyond these commonly recognized viruses, emerging pathogens like Zika virus have been implicated in causing congenital eye abnormalities, including microphthalmia, optic nerve abnormalities, and chorioretinal atrophy, emphasizing the devastating consequences of viral infections during pregnancy.

In addition to direct tissue damage, viruses can also induce autoimmune responses within the eye, leading to conditions such as acute retinal necrosis (ARN) and progressive outer retinal necrosis (PORN). These conditions, often associated with viruses like cytomegalovirus (CMV) and herpesviruses, result in rapid and severe vision loss if left untreated.

Understanding the mechanisms underlying virus–ocular tissue interactions is paramount for devising effective prevention and treatment strategies against these diverse viral pathogens. In this Special Issue, we aim to explore the latest advances in virology, immunology, and ophthalmology, shedding light on the complex interplay between viruses and ocular health. Through a comprehensive examination of viral pathogenesis, host immune responses, and therapeutic interventions, we strive to advance our understanding of viral eye diseases and pave the way for improved clinical outcomes and vision preservation for patients worldwide. Join us as we delve into the multifaceted world of viruses and eye diseases, aiming to unravel mysteries and forge new pathways toward ocular health and well-being.

Prof. Dr. Homayon Ghiasi
Prof. Dr. Deepak Shukla
Guest Editors

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Viruses is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2600 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • ocular health
  • herpesviruses
  • herpes simplex virus (HSV)
  • varicella zoster virus (VZV)
  • adenovirus
  • respiratory viruses
  • Zika virus
  • cytomegalovirus (CMV)
  • virus–ocular tissue interactions

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Published Papers (3 papers)

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Research

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11 pages, 1594 KiB  
Article
Heparanase 2 Modulation Inhibits HSV-2 Replication by Regulating Heparan Sulfate
by James Hopkins, Ipsita Volety, Farreh Qatanani and Deepak Shukla
Viruses 2024, 16(12), 1832; https://doi.org/10.3390/v16121832 - 26 Nov 2024
Viewed by 396
Abstract
The host enzyme heparanase (HPSE) facilitates the release of herpes simplex virus type 2 (HSV-2) from target cells by cleaving the viral attachment receptor heparan sulfate (HS) from infected cell surfaces. HPSE 2, an isoform of HPSE, binds to but does not possess [...] Read more.
The host enzyme heparanase (HPSE) facilitates the release of herpes simplex virus type 2 (HSV-2) from target cells by cleaving the viral attachment receptor heparan sulfate (HS) from infected cell surfaces. HPSE 2, an isoform of HPSE, binds to but does not possess the enzymatic activity needed to cleave cell surface HS. Our study demonstrates that HSV-2 infection significantly elevates HPSE 2 protein levels, impacting two distinct stages of viral replication. We show that higher HPSE 2 negatively affects HSV-2 replication which may be through the regulation of cell surface HS. By acting as a competitive inhibitor of HPSE, HPSE 2 may be interfering with HPSE’s interactions with HS. We demonstrate that the enhanced expression of HPSE 2, either via viral infection or plasmid transfection, reduces HPSE’s ability to cleave HS, thereby hindering viral egress. Conversely, low HPSE 2 levels achieved through siRNA transfection allow HPSE to cleave more HS, reducing viral entry. Altogether, we propose a hypothetical model in which the modulation of HPSE 2 impedes HSV-2 replication by regulating HS availability on the cell surface. This dual role of HPSE 2 in viral replication and potential tumor suppression underscores its significance in cellular processes and viral pathogenesis. Full article
(This article belongs to the Special Issue Viruses and Eye Diseases)
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21 pages, 3280 KiB  
Article
Presence of CD80 and Absence of LAT in Modulating Cellular Infiltration and HSV-1 Latency
by Ujjaldeep Jaggi and Homayon Ghiasi
Viruses 2024, 16(9), 1379; https://doi.org/10.3390/v16091379 - 29 Aug 2024
Viewed by 713
Abstract
CD80 is the best-known costimulatory molecule for effective T cell functions. Many different reports have summarized the role of CD80 in HSV-1 and its functions in maintaining adaptive immunity, which is the main player in causing herpes stromal keratitis (HSK). To determine the [...] Read more.
CD80 is the best-known costimulatory molecule for effective T cell functions. Many different reports have summarized the role of CD80 in HSV-1 and its functions in maintaining adaptive immunity, which is the main player in causing herpes stromal keratitis (HSK). To determine the effects of absence or overexpression of CD80 in HSV-1 infection, we infected CD80-/- and WT mice with a recombinant HSV-1 expressing murine CD80 (HSV-CD80) in place of the latency associated transcript (LAT). Parental dLAT2903 virus lacking LAT was used as a control. After infection, critical components of infection like virus replication, eye disease, early cellular infiltrates into the corneas and trigeminal ganglia (TG), latency-reactivation in the infected mice were determined. Our findings reveal that the absence of CD80 in the CD80-/- mice infected with both viruses did not affect the viral titers in the mice eyes or eye disease, but it played a significant role in critical components of HSV-induced immunopathology. The WT mice infected with dLAT2903 virus had significantly higher levels of latency compared with the CD80-/- mice infected with dLAT2903 virus, while levels of latency as determined by gB DNA expression were similar between the WT and CD80-/- mice infected with HSV-CD80 virus. In contrast to the differences in the levels of latency between the infected groups, the absence of CD80 expression in the CD80-/- mice or its overexpression by HSV-CD80 virus did not have any effect on the time of reactivation. Furthermore, the absence of CD80 expression contributed to more inflammation in the CD80-/--infected mice. Overall, this study suggests that in the absence of CD80, inflammation increases, latency is reduced, but reactivation is not affected. Altogether, our study suggests that reduced latency correlated with reduced levels of inflammatory molecules and blocking or reducing expression of CD80 could be used to mitigate the immune responses, therefore controlling HSV-induced infection. Full article
(This article belongs to the Special Issue Viruses and Eye Diseases)
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Review

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11 pages, 1634 KiB  
Review
A Journey through the Minefield of the Discovery and Characterization of Latency-Related RNA/Latency-Associated Transcript
by Homayon Ghiasi
Viruses 2024, 16(10), 1562; https://doi.org/10.3390/v16101562 - 30 Sep 2024
Viewed by 1105
Abstract
Scientific knowledge evolves in small steps, with occasional backsteps to correct inaccuracies, all occurring within a competitive environment. This perspective for the first time looks at the history of latency-related RNA (LR-RNA) that was later renamed latency-associated transcript (LAT). At the 1986 International [...] Read more.
Scientific knowledge evolves in small steps, with occasional backsteps to correct inaccuracies, all occurring within a competitive environment. This perspective for the first time looks at the history of latency-related RNA (LR-RNA) that was later renamed latency-associated transcript (LAT). At the 1986 International Herpesvirus Workshop (IHW) meeting in Leeds, England, Daniel L Rock and Anthony B Nesburn first reported the discovery of human herpes virus 1 (HSV-1) latency-related (LR) RNA that is antisense to ICP0. Less than a month after the IHW meeting, a paper was submitted to Science magazine and 8 months later appeared in print thanking “D. Rock for suggesting RNA complementary to the ICP0 message may be present in latently infected cells”. This perspective is not a review of the LAT literature but intends to clarify the timeline of LAT discovery and subsequent breakthroughs such as reactivation, apoptosis, CD8+ T cell exhaustion, and LAT expression in different cell types detected during latency. While many review articles have been written about LAT since 1987, the most comprehensive and balanced review about LAT was written by Dr. David Bloom’s group. In this overview, I will discuss our original collaboration with Dr. Dan Rock and subsequent work that our group performed, which is still ongoing. Finally, I will discuss the controversies associated with LAT from its inception to current times. Full article
(This article belongs to the Special Issue Viruses and Eye Diseases)
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