Osteopontin contributes to virus resistance associated with type I IFN expression, activation of downstream ifn-inducible effector genes, and CCR2+CD115+CD206+ macrophage infiltration following ocular HSV-1 infection of mice

Filiberti, Adrian; Gmyrek, Grzegorz B.; Berube, Amanda N.; Carr, Daniel J.J.

doi:10.3389/fimmu.2022.1028341

Cited by 4 publications

(2 citation statements)

References 115 publications

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“…Reactive oxygen species (ROS) release from neutrophils in HSK-infected eyes was hypothesized to be catalyzed by nicotinamide adenine dinucleotide phosphate oxidase 2 enzyme[ 97 ]. The protein Osteopontin may also mitigate the inflammatory process observed in ocular HSV inflammation at the risk of also upregulating viral replication[ 98 ].…”

Section: Understanding the Pathogenesis Of Herpes Simplex Keratitismentioning

confidence: 99%

Herpes simplex keratitis: A brief clinical overview

Musa,

Enaholo,

Aluyi-Osa

et al. 2024

World J Virol

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

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Section: Understanding the Pathogenesis Of Herpes Simplex Keratitismentioning

confidence: 99%

Herpes simplex keratitis: A brief clinical overview

Musa,

Enaholo,

Aluyi-Osa

et al. 2024

World J Virol

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“…SPP1 + TAM subpopulation also often expresses the following genes such as FN1 , IL1RN , and other TAM genes IDO , Mrc1(CD206) , PD-L1 , PD-L2 , CD68 and CD163 . Notably, TAM associated CD68 ( 46 ) and/or CD206 ( 47 ) genes can be found only in the SPP1 + TAM subpopulation of some solid tumors but not in all solid tumors ( 48 ). In addition, SPP1 + CD206 + TAM subpopulation also produces epithelial growth factor (EGF) ( 49 ).…”

Section: Novel Tam Subpopulations In Different Solid Tumorsmentioning

confidence: 99%

Novel tumor-associated macrophage populations and subpopulations by single cell RNA sequencing

Wang,

Zhu,

et al. 2024

Front. Immunol.

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Tumor-associated macrophages (TAMs) are present in almost all solid tumor tissues. 16They play critical roles in immune regulation, tumor angiogenesis, tumor stem cell activation, tumor invasion and metastasis, and resistance to therapy. However, it is unclear how TAMs perform these functions. With the application of single-cell RNA sequencing (scRNA-seq), it has become possible to identify TAM subpopulations associated with distinct functions. In this review, we discuss four novel TAM subpopulations in distinct solid tumors based on core gene signatures by scRNA-seq, including FCN1+, SPP1+, C1Q+ and CCL18+ TAMs. Functional enrichment and gene expression in scRNA-seq data from different solid tumor tissues found that FCN1+ TAMs may induce inflammation; SPP1+ TAMs are potentially involved in metastasis, angiogenesis, and cancer cell stem cell activation, whereas C1Q+ TAMs participate in immune regulation and suppression; And CCL18+ cells are terminal immunosuppressive macrophages that not only have a stronger immunosuppressive function but also enhance tumor metastasis. SPP1+ and C1Q+ TAM subpopulations can be further divided into distinct populations with different functions. Meanwhile, we will also present emerging evidence highlighting the separating macrophage subpopulations associated with distinct functions. However, there exist the potential disconnects between cell types and subpopulations identified by scRNA-seq and their actual function.

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

Antony,

Kinha,

Nowińska

et al. 2024

Clin Microbiol Rev

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

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Osteopontin contributes to virus resistance associated with type I IFN expression, activation of downstream ifn-inducible effector genes, and CCR2+CD115+CD206+ macrophage infiltration following ocular HSV-1 infection of mice

Cited by 4 publications

References 115 publications

Herpes simplex keratitis: A brief clinical overview

Herpes simplex keratitis: A brief clinical overview

Novel tumor-associated macrophage populations and subpopulations by single cell RNA sequencing

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

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