Antiviral treatment and other therapeutic interventions for herpes simplex virus epithelial keratitis

Wilhelmus, Kirk R.

doi:10.1002/14651858.cd002898.pub5

Cited by 107 publications

(100 citation statements)

References 281 publications

(463 reference statements)

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“…Primary infection results after HSV spread via direct contact with mucous membrane of the host 5,11. In the case of ocular infections, the virus is transported following primary retrograde infection via sensory neurons to establish latency in trigeminal ganglia; here, it remains asymptomatic until reactivation of the virus leads to secondary or recurrent infections 4,8,12,13. The host cell’s DNA polymerase, located in the nucleus of the cell, is required for HSV to transcribe and replicate 8,14…”

Section: Pathophysiologymentioning

confidence: 99%

Herpes simplex keratitis: challenges in diagnosis and clinical management

Azher¹,

Yin²,

Tajfirouz³

et al. 2017

OPTH

123

119

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Herpes simplex virus is responsible for numerous ocular diseases, the most common of which is herpetic stromal keratitis. This is a recurrent infection of the cornea that typically begins with a subclinical infection of the cornea that establishes a latent infection of sensory ganglia, most often the trigeminal ganglia. Recurring infections occur when the virus is reactivated from latency and travels back to the cornea, where it restimulates an inflammatory response. This inflammatory response can lead to decreased corneal sensation, scarring, and blindness. The diagnosis of these lesions as the result of a recurrent herpes simplex virus infection can at times be problematic. Currently, herpetic stromal keratitis is diagnosed by its clinical presentation on the slit-lamp examination, but the literature does not always support the accuracy of these clinical findings. Other diagnostic tests such as polymerase chain reaction assay, enzyme-linked immunosorbent assay, immunofluorescent antibody, and viral cultures have provided more definitive diagnosis, but also have some limitations. That said, accurate diagnosis is necessary for proper treatment, in order to prevent serious consequences. Current treatment reduces the severity of lesions and controls further viral spread, but does not provide a cure.

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Section: Pathophysiologymentioning

confidence: 99%

Herpes simplex keratitis: challenges in diagnosis and clinical management

Azher¹,

Yin²,

Tajfirouz³

et al. 2017

OPTH

123

119

View full text Add to dashboard Cite

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“…Type I interferons (type I IFNs) are mainly known for their antiviral activity, and IFN therapy is currently used to treat several viral infections, including hepatitis B and C and herpes virus (21)(22)(23). The role of type I IFNs in bacterial and parasitic infection is less clear, as they are known to protect mice from Plasmodium falciparum infection, but on the other hand, can promote infection pathology with Listeria monocytogenes, Toxoplasma, and Trypanosoma (24)(25)(26)(27).…”

mentioning

confidence: 99%

Type I interferons induced by endogenous or exogenous viral infections promote metastasis and relapse of leishmaniasis

Rossi

Castiglioni

Hartley

et al. 2017

Proc. Natl. Acad. Sci. U.S.A.

103

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The presence of the endogenous Leishmania RNA virus 1 (LRV1) replicating stably within some parasite species has been associated with the development of more severe forms of leishmaniasis and relapses after drug treatment in humans. Here, we show that the disease-exacerbatory role of LRV1 relies on type I IFN (type I IFNs) production by macrophages and signaling in vivo. Moreover, infecting mice with the LRV1-cured Leishmania guyanensis (LgyLRV1 − ) strain of parasites followed by type I IFN treatment increased lesion size and parasite burden, quantitatively reproducing the LRV1-bearing (LgyLRV1 + ) infection phenotype. This finding suggested the possibility that exogenous viral infections could likewise increase pathogenicity, which was tested by coinfecting mice with L. guyanensis and lymphocytic choriomeningitis virus (LCMV), or the sand fly-transmitted arbovirus Toscana virus (TOSV). The type I IFN antiviral response increased the pathology of L. guyanensis infection, accompanied by down-regulation of the IFN-γ receptor normally required for antileishmanial control. Further, LCMV coinfection of IFN-γ-deficient mice promoted parasite dissemination to secondary sites, reproducing the LgyLRV1 + metastatic phenotype. Remarkably, LCMV coinfection of mice that had healed from L. guyanensis infection induced reactivation of disease pathology, overriding the protective adaptive immune response. Our findings establish that type I IFN-dependent responses, arising from endogenous viral elements (dsRNA/LRV1), or exogenous coinfection with IFN-inducing viruses, are able to synergize with New World Leishmania parasites in both primary and relapse infections. Thus, viral infections likely represent a significant risk factor along with parasite and host factors, thereby contributing to the pathological spectrum of human leishmaniasis.Leishmania RNA virus 1 | Totiviridae | arboviruses | trypanosomatid protozoan parasite | Leishmania subgenus Viannia

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“…Furthermore, neurons derived from induced pluripotent stem cells isolated from patients with such genetic deficits are more permissive to HSV-1, suggesting the neuronal antiviral response is important in preventing HSE [37]. While clinical trial outcomes utilizing recombinant IFN for HSE pathology are varied [38], this therapy proved promising in treatment of HSV lesions [39]. Preclinical demonstration of effective neuronal IFN signaling in combating HSV infection, discussed below, warrants further clinical investigation into the use of recombinant IFN in conjunction with antivirals.…”

Section: Clinical Presentation and Epidemiologymentioning

confidence: 99%

Neurons Versus Herpes Simplex Virus: The Innate Immune Interactions that Contribute to a Host–Pathogen Standoff

Rosato

Leib

2015

Future Virol.

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Herpes simplex virus (HSV) is a prevalent neurotropic virus, which establishes lifelong latent infections in the neurons of sensory ganglia. Despite our long-standing knowledge that HSV predominately infects sensory neurons during its life cycle, little is known about the neuronal antiviral response to HSV infection. Recent studies show that while sensory neurons have impaired intrinsic immunity to HSV infection, paracrine IFN signaling can potentiate a potent antiviral response. Additionally, antiviral autophagy plays an important role in neuronal control of HSV infection. Here we review the literature of antiviral signaling and autophagy in neurons, the mechanisms by which HSV can counteract these responses, and postulate how these two pathways may synergize to mediate neuronal control of HSV infection and yet result in lifelong persistence of the virus.

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Antiviral treatment and other therapeutic interventions for herpes simplex virus epithelial keratitis

Cited by 107 publications

References 281 publications

Herpes simplex keratitis: challenges in diagnosis and clinical management

Herpes simplex keratitis: challenges in diagnosis and clinical management

Type I interferons induced by endogenous or exogenous viral infections promote metastasis and relapse of leishmaniasis

Neurons Versus Herpes Simplex Virus: The Innate Immune Interactions that Contribute to a Host–Pathogen Standoff

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