Host Molecules That Promote Pathophysiology of Ocular Herpes

Shukla, Sajal Deea; Vályi-Nagy, Tibor

doi:10.3389/fmicb.2022.818658

Cited by 7 publications

(4 citation statements)

References 78 publications

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“…HEK: HSV-1 predominantly replicates in the corneal epithelial cells but can also infect underlying stromal fibroblast cells. The HSV-1 replication and shedding in the cornea can be symptomatic or asymptomatic depending on the activation of innate antiviral responses and the immune control of virus replication [ 35 , 290 ]. The lytic HSV-1 replication in the corneal epithelium occurs within 12–24 h, and this leads to the development of punctate epithelial keratopathy characterized by granular spots [ 1 , 11 , 291 ].…”

Section: Pathogenesis Of Corneal Hsv-1 Infectionmentioning

confidence: 99%

Role of Innate Interferon Responses at the Ocular Surface in Herpes Simplex Virus-1-Induced Herpetic Stromal Keratitis

et al. 2023

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Herpes simplex virus type 1 (HSV-1) is a highly successful pathogen that primarily infects epithelial cells of the orofacial mucosa. After initial lytic replication, HSV-1 enters sensory neurons and undergoes lifelong latency in the trigeminal ganglion (TG). Reactivation from latency occurs throughout the host’s life and is more common in people with a compromised immune system. HSV-1 causes various diseases depending on the site of lytic HSV-1 replication. These include herpes labialis, herpetic stromal keratitis (HSK), meningitis, and herpes simplex encephalitis (HSE). HSK is an immunopathological condition and is usually the consequence of HSV-1 reactivation, anterograde transport to the corneal surface, lytic replication in the epithelial cells, and activation of the host’s innate and adaptive immune responses in the cornea. HSV-1 is recognized by cell surface, endosomal, and cytoplasmic pattern recognition receptors (PRRs) and activates innate immune responses that include interferons (IFNs), chemokine and cytokine production, as well as the recruitment of inflammatory cells to the site of replication. In the cornea, HSV-1 replication promotes type I (IFN-α/β) and type III (IFN-λ) IFN production. This review summarizes our current understanding of HSV-1 recognition by PRRs and innate IFN-mediated antiviral immunity during HSV-1 infection of the cornea. We also discuss the immunopathogenesis of HSK, current HSK therapeutics and challenges, proposed experimental approaches, and benefits of promoting local IFN-λ responses.

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Section: Pathogenesis Of Corneal Hsv-1 Infectionmentioning

confidence: 99%

Role of Innate Interferon Responses at the Ocular Surface in Herpes Simplex Virus-1-Induced Herpetic Stromal Keratitis

et al. 2023

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“…At the same time, current treatment has not yet been able to completely eliminate latent HSV infection from the body, resulting in recurrence of the disease, which has a significant impact on the physical and mental health of patients and their quality of life. HSV-1 mainly causes cold sores on the lips, occasionally causes corneal lesions, and can also spread to the central nervous system causing serious diseases ( Shukla and Valyi-Nagy, 2022 ). Antiviral drugs that target HSV viral DNA polymerase neither eradicate latent virus nor decrease the risk, frequency or severity of relapse.…”

Section: Antiviral Activity Of Emodinmentioning

confidence: 99%

Promising Role of Emodin as Therapeutics to Against Viral Infections

et al. 2022

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Emodin is an anthraquinone derivative that is widely present in natural plants and has a wide spectrum of pharmacological effects, such as antibacterial, anti-inflammatory, anti-fibrotic and anticancer and so on. Through reviewing studies on antiviral effect of emodin in the past decades, we found that emodin exhibits ability of inhibiting the infection and replication of more than 10 viruses in vitro and in vivo, including herpes simplex virus type 1 (HSV-1) and type 2 (HSV-2), human cytomegalovirus (HCMV), Epstein-Barr virus (EBV), coxsackievirus B (CVB), hepatitis B virus (HBV), influenza A virus (IAV), SARS-CoV, viral haemorrhagic septicaemia rhabdovirus (VHSV), enterovirus 71 (EV71), dengue virus serotype 2 (DENV-2) and Zika virus (ZIKV). Therefore, this review aims to summarize the antiviral effect of emodin, in order to provide reference and hopes to support the further investigations.

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“…This binding not only activates intracellular signaling pathways involved in innate immune responses but also activates a couple of host enzymes facilitate viral egress. 13 Heparanase (HPSE) is one such host enzyme that is considered a hallmark of progression of viral infection within the host cell. It is an endo-β- d -glycosidase that acts upon the glycosidic bonds of heparan sulfate (HS), cleaving it and bringing about structural modifications at the extracellular matrix.…”

mentioning

confidence: 99%

Exploring Heparanase Levels in Tears: Insights From Herpes Simplex Virus-1 Keratitis Patients and Animal Studies

Gagan,

Khapuinamai,

Kapoor

et al. 2024

Invest. Ophthalmol. Vis. Sci.

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Purpose Heparanase (HPSE) cleaves heparan sulfate proteoglycans during herpes simplex virus-1 (HSV-1) infection, aiding in viral egress and disease progression. Its action has been well established in in vitro and in vivo models, but its relevance in human patients remains unclear. This study aimed to specifically evaluate tear HPSE levels of patients with herpes simplex keratitis (HSK) and to correlate these findings with a commonly used murine model. Methods Tear samples from patient and mice samples were collected at LV Prasad Eye Institute, Hyderabad, India, and at the University of Illinois, Chicago, IL, respectively. Tears were collected from HSV-1 patients, bacterial/fungal keratitis cases, and healthy individuals. For in vivo study, C57BL/6 mice were infected with HSV-1 (McKrae strain) followed by tear fluid collection at various time points (0–10 days). Results The HSV-1, bacterial keratitis, fungal keratitis, and healthy control groups each had 30 patients. There was a significant difference in HPSE expression in the HSV-1 infected eyes (1.55 ± 0.19 units/mL) compared to HSV-1 contralateral eyes (1.23 ± 0.13 units/mL; P = 0.82), bacterial keratitis eyes (0.87 ± 0.15 units/mL; P = 0.0078), fungal keratitis eyes (0.64 ± 0.09 units/mL; P < 0.00001), and normal controls (0.53 ± 0.06 units/mL; P < 0.00001). C57BL/6 mice tear HPSE expression in infected eyes was 0.66 to 5.57 ng heparan sulfate (HS) removed per minute when compared to non-infected eye (range, 0.70–3.67 ng HS removed per minute). Conclusions To the best of our knowledge, this study is the first to report elevated HPSE levels in the tears of patients with different forms of HSV-1 keratitis, and it confirms similar findings in a murine model, providing a valuable basis for future in vivo and clinical research on HSV-1 ocular infection.

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Host Molecules That Promote Pathophysiology of Ocular Herpes

Cited by 7 publications

References 78 publications

Role of Innate Interferon Responses at the Ocular Surface in Herpes Simplex Virus-1-Induced Herpetic Stromal Keratitis

Role of Innate Interferon Responses at the Ocular Surface in Herpes Simplex Virus-1-Induced Herpetic Stromal Keratitis

Promising Role of Emodin as Therapeutics to Against Viral Infections

Exploring Heparanase Levels in Tears: Insights From Herpes Simplex Virus-1 Keratitis Patients and Animal Studies

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