Herpes Simplex Virus in Solid Organ Transplantation

Wilck, Marissa B.; Zuckerman, Richard A.

doi:10.1111/ajt.12105

Cited by 70 publications

(30 citation statements)

References 63 publications

(78 reference statements)

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“…The best test for diagnosis in these suspected cases is a lumbar puncture and examination of CSF for the presence of anti-VZV antibodies and VZV DNA as noted above. Patients with VZV vasculopathy are treated with 10–15 mg/kg intravenous acyclovir for 14 days based upon Level 2 class of evidence (systemic review of cohort studies or individual cohort studies) extrapolated from treatment studies of herpes simplex virus central nervous system disease (reviewed in Wilck et al, 2013), as well as expert opinions and case series without controls of VZV vasculopathy (Nagel et al, 2008). For recurrent disease, a second course may be required, particularly in immunocompromised patients, followed by oral antivirals for several months.…”

Section: Clinical Features Laboratory Abnormalities Diagnosis Anmentioning

confidence: 99%

Varicella zoster virus vasculopathy: The expanding clinical spectrum and pathogenesis

Nagel

Jones

Wyborny

2017

Journal of Neuroimmunology

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Varicella zoster virus (VZV) is a ubiquitous, human alphaherpesvirus that produces varicella on primary infection then becomes latent in ganglionic neurons along the entire neuraxis. In elderly and immunocompromised individuals, VZV reactivates and travels along nerve fibers peripherally resulting in zoster. However, VZV can also spread centrally and infect cerebral and extracranial arteries (VZV vasculopathy) to produce transient ischemic attacks, stroke, aneurysm, sinus thrombosis and giant cell arteritis, as well as granulomatous aortitis. The mechanisms of virus-induced pathological vascular remodeling are not fully elucidated; however, recent studies suggest that inflammation and dysregulation of programmed death ligand-1 play a significant role.

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Section: Clinical Features Laboratory Abnormalities Diagnosis Anmentioning

confidence: 99%

Varicella zoster virus vasculopathy: The expanding clinical spectrum and pathogenesis

Nagel

Jones

Wyborny

2017

Journal of Neuroimmunology

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“…Herpes simplex virus infections (painful, grouped ulcerating vesicles in the perioral, genital regions) may occur frequently in KTRs either due to high net immunosuppressed state or during episodes of febrile illnesses [65]. Diagnosis is often by Tzanck smear and rarely requires blood PCR of HSV.…”

Section: Herpes Simplex Virus Infectionmentioning

confidence: 99%

“…Patients with recurrent pre transplant HSV should receive Valacyclovir prophylaxis, especially if not on Valganiclvir prophylaxis and if it is a CMV D-/R-donor recipient pair. Disseminated disease or HSV meningitis is usually treated with IV acyclovir [65].…”

Section: Herpes Simplex Virus Infectionmentioning

confidence: 99%

Infections After Kidney Transplantation: The Bug Bear Of Kidney Transplantation In Tropics

Basu¹

2015

TOUNJ

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Abstract:Infections are the bugbear of kidney transplantation in the tropics, being responsible for majority of the deaths. Despite the several challenges posed by infections in kidney transplant recipient in the tropics, various developments have resulted in a decline in the rate of infections as well as their consequences. This review aims to be a basic overview of the common infections in KTR with an attempt to provide a unique tropical country perspective.

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“…Another concern is that asTORi treatment can reactivate latent HSV1 infections, the sequelae of which could complicate patient outcomes. This has been observed in a latently infected neuron culture model [50] as well as in organ transplant patients treated with immunosuppressive agents including mTOR inhibitors [51]. Despite these concerns, augmenting the initial phase of viral replication specifically within tumour tissues, either through transient systemic or localized intra-tumoural mTOR inhibitor therapy, could provide the added benefit of reducing cancer cell proliferation and inducing a subsequent increase in viral replication, which upon drug removal could elicit a more potent therapeutic immune response [52].…”

Section: Discussionmentioning

confidence: 89%

Active-site mTOR inhibitors augment HSV1-dICP0 infection in cancer cells via dysregulated eIF4E/4E-BP axis

et al. 2018

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Herpes Simplex Virus 1 (HSV1) is amongst the most clinically advanced oncolytic virus platforms. However, efficient and sustained viral replication within tumours is limiting. Rapamycin can stimulate HSV1 replication in cancer cells, but active-site dual mTORC1 and mTORC2 (mammalian target of rapamycin complex 1 and 2) inhibitors (asTORi) were shown to suppress the virus in normal cells. Surprisingly, using the infected cell protein 0 (ICP0)-deleted HSV1 (HSV1-dICP0), we found that asTORi markedly augment infection in cancer cells and a mouse mammary cancer xenograft. Mechanistically, asTORi repressed mRNA translation in normal cells, resulting in defective antiviral response but also inhibition of HSV1-dICP0 replication. asTORi also reduced antiviral response in cancer cells, however in contrast to normal cells, transformed cells and cells transduced to elevate the expression of eukaryotic initiation factor 4E (eIF4E) or to silence the repressors eIF4E binding proteins (4E-BPs), selectively maintained HSV1-dICP0 protein synthesis during asTORi treatment, ultimately supporting increased viral replication. Our data show that altered eIF4E/4E-BPs expression can act to promote HSV1-dICP0 infection under prolonged mTOR inhibition. Thus, pharmacoviral combination of asTORi and HSV1 can target cancer cells displaying dysregulated eIF4E/4E-BPs axis.

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Herpes Simplex Virus in Solid Organ Transplantation

Cited by 70 publications

References 63 publications

Varicella zoster virus vasculopathy: The expanding clinical spectrum and pathogenesis

Varicella zoster virus vasculopathy: The expanding clinical spectrum and pathogenesis

Infections After Kidney Transplantation: The Bug Bear Of Kidney Transplantation In Tropics

Active-site mTOR inhibitors augment HSV1-dICP0 infection in cancer cells via dysregulated eIF4E/4E-BP axis

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