Bilateral herpes simplex-2 acute retinal necrosis with encephalitis in premature twins

Gupta, Amit; Rani, Padmaja Kumari; Bagga, Bhupesh; Dore, P; Mittal, Ashok; Jalali, Subhadra

doi:10.1016/j.jaapos.2010.08.011

Cited by 13 publications

(12 citation statements)

References 7 publications

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“…Among infants with perinatally acquired HSV-2 infection, ARN can be part of the presentation during the first month of life 11 . Also, ARN can be a component of congenital herpes infection 12 , a relatively rare fetal manifestation of maternal herpes infection.…”

Section: Discussionmentioning

confidence: 99%

Acute Retinal Necrosis Caused by Herpes Simplex Virus Type 2 in Children: Reactivation of an Undiagnosed Latent Neonatal Herpes Infection

Grose

2012

Seminars in Pediatric Neurology

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Herpes simplex virus type 2 (HSV-2) is known to cause acute retinal necrosis (ARN). The availability of HSV-2 specific PCR tests for diagnostic analysis has greatly increased our ability to discriminate ARN caused by HSV-2 from ARN caused by either HSV-1 or VZV. Of great interest, HSV-2 appears to be the most common cause of viral ARN in children and adolescents. Although a few children with ARN are known to have had neonatally acquired herpes infection, most children lack a history of known herpes disease. Thus, the origin of the HSV-2 infection is a mystery. The hypothesis of this review is that HSV-2 ARN in children and adolescents may be the first sign of a previously undiagnosed and asymptomatic neonatal HSV-2 infection, which has reactivated several years later from latency in a cranial nerve and entered the retina. The review brings together 7 previously published ARN cases, plus one new case is added. Thus this review also expands the spectrum of complications from neonatal HSV-2 infection.

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Section: Discussionmentioning

confidence: 99%

Acute Retinal Necrosis Caused by Herpes Simplex Virus Type 2 in Children: Reactivation of an Undiagnosed Latent Neonatal Herpes Infection

Grose

2012

Seminars in Pediatric Neurology

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“…HSV-2 mainly infects epithelial cells and causes genital herpes. It also infects neuronal cells and leu-kocytes including dendritic cells (34)(35)(36), leading to encephalitis and disseminated diseases that affect other organ systems (37,38). HSV-2 can establish a lifelong latent infection in sacral ganglia (39), resulting in up to 40% human adults living with HSV-2 latency (40).…”

mentioning

confidence: 99%

HSV-2 Immediate-Early Protein US1 Inhibits IFN-β Production by Suppressing Association of IRF-3 with IFN-β Promoter

Zhang

Liu

Wang

et al. 2015

The Journal of Immunology

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HSV-2 is the major cause of genital herpes, and its infection increases the risk of HIV-1 acquisition and transmission. After initial infection, HSV-2 can establish latency within the nervous system and thus maintains lifelong infection in humans. It has been suggested that HSV-2 can inhibit type I IFN signaling, but the underlying mechanism has yet to be determined. In this study, we demonstrate that productive HSV-2 infection suppresses Sendai virus (SeV) or polyinosinic-polycytidylic acid-induced IFN-β production. We further reveal that US1, an immediate-early protein of HSV-2, contributes to such suppression, showing that US1 inhibits IFN-β promoter activity and IFN-β production at both mRNA and protein levels, whereas US1 knockout significantly impairs such capability in the context of HSV-2 infection. US1 directly interacts with DNA binding domain of IRF-3, and such interaction suppresses the association of nuclear IRF-3 with the IRF-3 responsive domain of IFN-β promoter, resulting in the suppression of IFN-β promoter activation. Additional studies demonstrate that the 217–414 aa domain of US1 is critical for the suppression of IFN-β production. Our results indicate that HSV-2 US1 downmodulates IFN-β production by suppressing the association of IRF-3 with the IRF-3 responsive domain of IFN-β promoter. Our findings highlight the significance of HSV-2 US1 in inhibiting IFN-β production and provide insights into the molecular mechanism by which HSV-2 evades the host innate immunity, representing an unconventional strategy exploited by a dsDNA virus to interrupt type I IFN signaling pathway.

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“…Neither infant had concurrent ROP. 9 Our first case is significant for the development of ARN in the absence of encephalitic or systemic HSV symptoms.…”

mentioning

confidence: 81%

Bilateral Acute Retinal Necrosis with Concurrent Retinopathy of Prematurity in Two Neonates

LaMattina

Wirostko

Costakos

2014

Ocular Immunology and Inflammation

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Bilateral herpes simplex-2 acute retinal necrosis with encephalitis in premature twins

Cited by 13 publications

References 7 publications

Acute Retinal Necrosis Caused by Herpes Simplex Virus Type 2 in Children: Reactivation of an Undiagnosed Latent Neonatal Herpes Infection

Acute Retinal Necrosis Caused by Herpes Simplex Virus Type 2 in Children: Reactivation of an Undiagnosed Latent Neonatal Herpes Infection

HSV-2 Immediate-Early Protein US1 Inhibits IFN-β Production by Suppressing Association of IRF-3 with IFN-β Promoter

Bilateral Acute Retinal Necrosis with Concurrent Retinopathy of Prematurity in Two Neonates

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