Herpes simplex keratitis: A brief clinical overview

World Journal of Virology, Год журнала: 2024, Номер 13(1)

Опубликована: Март 11, 2024

The aim of our minireview is to provide a brief overview the diagnosis, clinical aspects, treatment options, management, and current literature available regarding herpes simplex keratitis (HSK). This type corneal viral infection caused by virus (HSV), which can affect several tissues, including cornea. One significant aspect HSK its potential cause recurrent episodes inflammation damage After initial infection, HSV establish latent in trigeminal ganglion, nerve cluster near eye. may remain dormant for extended periods. Periodic reactivation occur, leading HSK. Factors triggering include stress, illness, immunosuppression, or trauma. Recurrent manifest different patterns, ranging from mild epithelial involvement more severe stromal endothelial disease. severity frequency recurrences vary among individuals. Severe cases HSK, especially those involving stroma scarring, result vision impairment even blindness extreme cases. cornea's clarity crucial good vision, scarring compromise this, potentially visual impairment. management involves not only treating acute but also implementing long-term strategies prevent attempt repairs endings via neurotization. Antiviral medications, such as oral Acyclovir topical Ganciclovir, be prescribed prophylaxis. immune response contribute damage. Inflammation, body's control inadvertently harm tissues. Clinicians should informed about triggers advised on measures minimize risk reactivation. In summary, nature underscores importance both preserve health maintain optimal function.

Язык: Английский

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The immunobiology of corneal HSV-1 infection and herpetic stromal keratitis

Clinical Microbiology Reviews, Год журнала: 2024, Номер 37(3)

Опубликована: Июль 30, 2024

SUMMARY Human alphaherpesvirus 1 (HSV-1) is a highly successful neurotropic pathogen that primarily infects the epithelial cells lining orofacial mucosa. After primary lytic replication in oral, ocular, and nasal mucosal cells, HSV-1 establishes life-long latency neurons within trigeminal ganglion. Patients with compromised immune systems experience frequent reactivation of from latency, leading to virus entry sensory neurons, followed by anterograde transport at innervated surface. Although recurrent infection corneal surface rare, it can result chronic immuno-inflammatory condition called herpetic stromal keratitis (HSK). HSK leads gradual vision loss cause permanent blindness severe untreated cases. Currently, there no cure or vaccine prevent latent infections, posing significant clinical challenge managing preventing loss. The conventional management relies on anti-virals suppress replication, anti-inflammatory drugs (such as corticosteroids) provide symptomatic relief pain inflammation, surgical interventions more cases replace damaged cornea. However, each treatment strategy has limitations, such local systemic drug toxicities emergence anti-viral-resistant strains. In this review, we summarize factors involved pathogenesis highlight alternate therapeutic strategies for HSK. We also discuss potential immunoregulatory cytokines immunometabolism modulators promising therapies against emerging

Язык: Английский

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AAV9-delivery of interleukin-37b gene prevents recurrent herpetic stromal keratitis via the SIGIRR pathway in mice

Journal of Controlled Release, Год журнала: 2025, Номер 381, С. 113600 - 113600

Опубликована: Март 3, 2025

Язык: Английский

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Assessment of IL28 (rs12980275) and (rs8099917) Frequency in Recurrent Ocular Herpes Simplex Virus (HSV) Infection

Life, Год журнала: 2025, Номер 15(3), С. 389 - 389

Опубликована: Март 1, 2025

(1) Introduction: The main way of spreading the herpes simplex virus 1 (HSV-1) is through direct contact, as enters host via mucous membranes. Ocular infection can occur a primary or recurrent one. movement HSV-1 along ophthalmic branch fifth cranial nerve from its latency phase in trigeminal ganglion and activation represent process influenced by various symbiotic factors, such environmental conditions host’s genetic characteristics. aim this study was to assess frequency IL28 (rs12980275) (rs8099917) ocular HSV infections. (2) Materials methods: included 60 patients aged over 18, both sexes, all whom had history labialis (HSL). Patients were tested for HSV-1-specific IgG antibodies, seropositive individuals genotyped single nucleotide polymorphisms (SNPs) rs12980275 rs8099917. A total 57 study. (3) Results: statistically significant association found between keratitis (HSK) heterozygous GT rs8099917 homozygous TT rs8099917, well AG AA (p < 0.01). Interestingly, with GG polymorphism genotypes did not develop keratitis. (4) Conclusion: most frequent SNP variations disease (61.40%) (52.63%). lacked genotypes, suggesting that HSV-seropositive expressing these may have lower predisposition stromal

Язык: Английский

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Cell Intrinsic Determinants of Alpha Herpesvirus Latency and Pathogenesis in the Nervous System

Viruses, Год журнала: 2023, Номер 15(12), С. 2284 - 2284

Опубликована: Ноя. 22, 2023

Alpha herpesvirus infections (α-HVs) are widespread, affecting more than 70% of the adult human population. Typically, start in mucosal epithelia, from which viral particles invade axons peripheral nervous system. In nuclei ganglia, α-HVs establish a lifelong latency and eventually undergo multiple reactivation cycles. Upon reactivation, progeny can move into nerves, back out toward periphery where they entered organism, or central system (CNS). This latency–reactivation cycle is remarkably well controlled by intricate actions intrinsic innate immune responses host, finely counteracted proteins an effort to co-exist If this yin-yang- Nash-equilibrium-like balance state broken due suppression genetic mutations host response factors particularly CNS, presence other pathogenic stimuli, α-HV reactivations might lead life-threatening pathologies. review, we will summarize molecular virus–host interactions starting epithelia leading establishment PNS possible CNS invasion α-HVs, highlighting pathologies associated with uncontrolled virus replication NS.

Язык: Английский

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Cytosolic DNA sensors activation of human astrocytes inhibits herpes simplex virus through IRF1 induction

Frontiers in Cellular and Infection Microbiology, Год журнала: 2024, Номер 14

Опубликована: Май 14, 2024

While astrocytes participate in the CNS innate immunity against herpes simplex virus type 1 (HSV-1) infection, they are major target for virus. Therefore, it is of importance to understand interplay between astrocyte-mediated and HSV-1 infection.

Язык: Английский

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Harmol used for the treatment of herpes simplex virus induced keratitis

Virology Journal, Год журнала: 2024, Номер 21(1)

Опубликована: Май 27, 2024

Abstract Herpes simplex virus type 1 (HSV-1) infection of the eyes results in herpes keratitis (HSK), which has led to vision loss and even blindness patients. However, rate drug resistance HSV is on rise; therefore, new antiviral agents with sufficient safety profiles must be developed. At present, we assessed anti-HSV-1 activity 502 natural compounds their ability reduce HSV-1-induced cytopathic effect. We chose harmol for further studies because it exhibited highest activity. found that inhibited both HSV-1 F HSV-1/153 (a clinical drug-resistant strain) replication, an EC 50 9.34 µM 5.84 µM, respectively. Moreover, reduced replication corneal tissues viral progeny production tears, also alleviated early surface lesions related HSK. For example, treatment preserved thickness nerve density HSK mice. Interestingly, showed a promising effect induced mouse model. Furthermore, combined acyclovir (ACV) greater than either one alone vitro. Therefore, may therapeutic agent managing

Язык: Английский

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Role of IL-27 in HSV-1–Induced Herpetic Stromal Keratitis

The Journal of Immunology, Год журнала: 2023, Номер 211(3), С. 474 - 485

Опубликована: Июнь 16, 2023

Abstract Herpetic stromal keratitis (HSK) is a painful and vision-impairing disease caused by recurrent HSV-1 infection of the cornea. The virus replication in corneal epithelium associated inflammation play dominant role HSK progression. Current treatments targeting or are partially effective promote latency, long-term use can cause side effects. Thus, understanding molecular cellular events that control crucial for developing novel therapies. In this study, we report ocular induces expression IL-27, pleiotropic immunoregulatory cytokine. Our data indicate stimulates IL-27 production macrophages. Using primary mouse model receptor knockout mice, show plays critical controlling shedding from cornea, optimum induction effector CD4+ T cell responses, limiting vitro bone marrow–derived macrophages, an antiviral regulating macrophage-mediated killing, IFN-β production, IFN-stimulated gene after infection. Furthermore, macrophage survival, Ag uptake, costimulatory molecules involved responses. results promotes endogenous anti-inflammatory responses represents promising target suppressing

Язык: Английский

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Adenovirus protein VII binds the A-box of HMGB1 to repress interferon responses

PLoS Pathogens, Год журнала: 2023, Номер 19(9), С. e1011633 - e1011633

Опубликована: Сен. 13, 2023

Viruses hijack host proteins to promote infection and dampen defenses. Adenovirus encodes the multifunctional protein VII that serves both compact viral genomes inside virion disrupt chromatin. Protein binds abundant nuclear high mobility group box 1 (HMGB1) sequesters HMGB1 in is an can also be released from infected cells as alarmin amplify inflammatory responses. By sequestering HMGB1, prevents its release, thus inhibiting downstream signaling. However, consequences of this chromatin sequestration on transcription are unknown. Here, we employ bacterial two-hybrid interaction assays human cell culture interrogate mechanism VII-HMGB1 interaction. contains two DNA binding domains, A- B-boxes, bend factor while C-terminal tail regulates We demonstrate interacts directly with A-box inhibited by tail. cellular fractionation, show renders containing constructs insoluble, thereby acting prevent their release cells. This not dependent HMGB1’s ability bind but does require post-translational modifications VII. Importantly, inhibits expression interferon β, HMGB1-dependent manner, affect interferon-stimulated genes. Together, our results specifically harnesses through domain depress innate immune response infection.

Язык: Английский

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Adenovirus protein VII binds the A-box of HMGB1 to repress interferon responses

bioRxiv (Cold Spring Harbor Laboratory), Год журнала: 2023, Номер unknown

Опубликована: Апрель 18, 2023

ABSTRACT Viruses hijack host proteins to promote infection and dampen defenses. Adenovirus encodes the multifunctional protein VII that serves both compact viral genomes inside virion disrupt chromatin. Protein binds abundant nuclear high mobility group box 1 (HMGB1) sequesters HMGB1 in is an can also be released from infected cells as alarmin amplify inflammatory responses. By sequestering HMGB1, prevents its release, thus inhibiting downstream signaling. However, consequences of this chromatin sequestration on transcription are unknown. Here, we employ bacterial two-hybrid interaction assays human cell biological systems interrogate mechanism VII-HMGB1 interaction. contains two DNA binding domains, A- B-boxes, bend factor while C-terminal tail regulates We demonstrate interacts directly with A-box inhibited by tail. cellular fractionation, show renders containing constructs insoluble, thereby acting prevent their release cells. This not dependent HMGB1’s ability bind but does require post-translational modifications VII. Importantly, inhibits expression interferon β, HMGB1- manner, affect interferon- stimulated genes. Together, our results specifically harnesses through domain depress innate immune response infection.

Язык: Английский

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