Molecular Aspects of Herpes Simplex Virus I Latency, Reactivation, and Recurrence

Miller, Craig S.; Danaher, Robert J.; Jacob, Robert J. K.

doi:10.1177/10454411980090040901

Cited by 68 publications

(41 citation statements)

References 323 publications

(170 reference statements)

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“…Infectious virus particles are transported to the peripheral nerve terminals by anterograde axonal transport pathway, released, and infect cells at or near the site of initial infection. 34 Reactivation is not completely understood, but external stimuli, such as UV light, stress and fever, are known for decades to induce HSV-1 reactivation. Depending on several factors, including the host immune status, the reactivation may be asymptomatic or lead to a recurrent lesion, which may vary considerably in severity from punctuate lesions that are invisible to naked eyes to severe, debilitating lesions in immunocompromised individuals.…”

Section: Lytic Infection Vs Latencymentioning

confidence: 99%

Herpes simplex virus 1 (HSV-1) for cancer treatment

2006

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Cancer remains a serious threat to human health, causing over 500 000 deaths each year in US alone, exceeded only by heart diseases. Many new technologies are being developed to fight cancer, among which are gene therapies and oncolytic virotherapies. Herpes simplex virus type 1 (HSV-1) is a neurotropic DNA virus with many favorable properties both as a delivery vector for cancer therapeutic genes and as a backbone for oncolytic viruses. Herpes simplex virus type 1 is highly infectious, so HSV-1 vectors are efficient vehicles for the delivery of exogenous genetic materials to cells. The inherent cytotoxicity of this virus, if harnessed and made to be selective by genetic manipulations, makes this virus a good candidate for developing viral oncolytic approach. Furthermore, its large genome size, ability to infect cells with a high degree of efficiency, and the presence of an inherent replication controlling mechanism, the thymidine kinase gene, add to its potential capabilities. This review briefly summarizes the biology of HSV-1, examines various strategies that have been used to genetically modify the virus, and discusses preclinical as well as clinical results of the HSV-1-derived vectors in cancer treatment.

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Section: Lytic Infection Vs Latencymentioning

confidence: 99%

Herpes simplex virus 1 (HSV-1) for cancer treatment

2006

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“…5,9,10 Shortly after replicating at the initial site of infection, HSV-1 uses retrograde axonal transport to gain access to the sensory neurons in the trigeminal ganglia, where it establishes latency. 11 Repeated cycles of reactivation can lead to herpes stromal keratitis, an extensively studied immunopathological process.…”

mentioning

confidence: 99%

IL-6 Contributes to Corneal Nerve Degeneration after Herpes Simplex Virus Type I Infection

Chucair-Elliott

Jinkins

Carr

et al. 2016

The American Journal of Pathology

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Herpes simplex virus type 1 (HSV-1) is a leading cause of neurotrophic keratitis characterized by decreased corneal sensation because of damage to the corneal sensory fibers. We and others have reported regression of corneal nerves during acute HSV-1 infection. To determine whether denervation is caused directly by the virus or indirectly by the elicited immune response, mice were infected with HSV-1 and topically treated with dexamethasone (DEX) or control eye drops. Corneal sensitivity was measured using a Cochet-Bonnet esthesiometer and nerve network structure via immunohistochemistry. Corneas were assessed for viral content by plaque assay, leukocyte influx by flow cytometry, and content of chemokines and inflammatory cytokines by suspension array. DEX significantly preserved corneal nerve structure and sensitivity on infection. DEX reduced myeloid and T-cell populations in the cornea and did not affect viral contents at 4 and 8 days post infection. The elevated protein contents of chemokines and inflammatory cytokines on infection were greatly suppressed by DEX. Subconjunctival delivery of neutralizing antibody against IL-6 to infected mice resulted in partial preservation of corneal nerve structure and sensitivity. Our study supports a role for the immune response, but not local virus replication in the development of HSV-1einduced neurotrophic keratitis. IL-6 is one of the factors produced by the elicited inflammatory response to HSV-1 infection contributing to nerve regression.

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“…Almost all adults show evidence of having been infected by HSV-1, its genome residing latently in the trigeminal ganglia and in the CNS of both healthy individuals and those suffering from neurological disease (14). The trigeminal ganglion is the primary site of HSV-1 latency, although other sites including the sensory neurons (33) and other sensory ganglia such as the nodose ganglion of the vagus nerve (18), the dorsal root ganglia (20), the sympathetic ganglia (51), and the brain may be involved (3,47). The persistence of HSV-1 in nonneuronal tissue has also been suggested but remains controversial (33).…”

mentioning

confidence: 99%

Effect of Apolipoprotein E on the Cerebral Load of Latent Herpes Simplex Virus Type 1 DNA

Burgos

Ramı́rez

Sastre

et al. 2006

J Virol

115

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Herpes simplex virus type 1 (HSV-1) is neurotropic and enters a latent state lasting the lifetime of the host. This pathogen has recently been proposed as a risk factor for Alzheimer's disease (AD) in conjunction with apolipoprotein E4 (ApoE4). In a murine acute infection model, we showed that viral neuroinvasiveness depends directly on the overall ApoE dosage and especially on the presence of isoform ApoE4. If an interaction between ApoE and HSV-1 is involved in AD, it may occur during latency rather than during acute infection. Certainly, ApoE plays an important role in late-onset AD, i.e., at a time in life when the majority of people harbor HSV-1 in their nervous system. In the present work, wild-type, APOE knockout, APOE3, and APOE4 transgenic mice were used to analyze the influence of the ApoE profile on the levels of latent virus DNA. The knockout mice had significantly lower concentrations of the virus in the nervous system than the wild-type mice, while the APOE4 mice had very high levels in the brain compared to the APOE3 animals. ApoE4 seems to facilitate HSV-1 latency in the brain much more so than ApoE3. The APOE dosage correlated directly with the HSV-1 DNA concentration in the brain, strengthening the hypothesis that HSV-1, together with ApoE, might be involved in AD.

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Molecular Aspects of Herpes Simplex Virus I Latency, Reactivation, and Recurrence

Cited by 68 publications

References 323 publications

Herpes simplex virus 1 (HSV-1) for cancer treatment

Herpes simplex virus 1 (HSV-1) for cancer treatment

IL-6 Contributes to Corneal Nerve Degeneration after Herpes Simplex Virus Type I Infection

Effect of Apolipoprotein E on the Cerebral Load of Latent Herpes Simplex Virus Type 1 DNA

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