Dormant No More: The Neurogical Impact of Herpes Simplex Virus Reactivation Following Traumatic Brain Injury
Herpes simplex viruses (HSV), including HSV-1 and HSV-2, are neurotropic viruses capable of establishing lifelong latency in sensory ganglia and reactivating under various triggers, including traumatic brain injury (TBI). TBI induces secondary injury cascades such as neuroinflammation, excitotoxicit...
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| Format: | Article |
| Language: | Indonesian |
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Indonesian Society of Neuroanesthesia & Critical Care (INA-SNACC)
2025-02-01
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| Series: | Jurnal Neuroanestesi Indonesia |
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| Online Access: | https://inasnacc.org/ojs2/index.php/jni/article/view/659 |
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| author | Theodorus Kevin Putra Johansyah Cindy Thiovany Soetomo Tiffany Tiffany Sri Maliawan |
| author_facet | Theodorus Kevin Putra Johansyah Cindy Thiovany Soetomo Tiffany Tiffany Sri Maliawan |
| author_sort | Theodorus Kevin Putra Johansyah |
| collection | DOAJ |
| description | Herpes simplex viruses (HSV), including HSV-1 and HSV-2, are neurotropic viruses capable of establishing lifelong latency in sensory ganglia and reactivating under various triggers, including traumatic brain injury (TBI). TBI induces secondary injury cascades such as neuroinflammation, excitotoxicity, and blood-brain barrier disruption, which create a conducive environment for HSV reactivation. The reactivation of HSV after TBI, particularly HSV-1 and HSV-2, can lead to significant neurological consequences, including encephalitis, cognitive decline, and the development of neurodegenerative diseases like Alzheimer’s disease and Chronic Traumatic Encephalopathy. Current therapeutic approaches focus on antiviral agents like acyclovir and valacyclovir, which manage acute HSV infection but are less effective in preventing long-term neurological damage. Emerging research highlights the potential of anti-inflammatory and neuroprotective strategies to complement antiviral therapies, aiming to reduce the neuronal damage caused by viral reactivation and inflammation. However, gaps remain in understanding the precise mechanisms linking TBI-induced neuroinflammation to HSV reactivation and its long-term impact on neurological health. This review synthesizes the current literature on the pathophysiology of HSV reactivation following TBI, and their contributions to acute and chronic neurological outcomes |
| format | Article |
| id | doaj-art-3ee29d43b65840d8beddb44911285d15 |
| institution | OA Journals |
| issn | 2088-9674 2460-2302 |
| language | Indonesian |
| publishDate | 2025-02-01 |
| publisher | Indonesian Society of Neuroanesthesia & Critical Care (INA-SNACC) |
| record_format | Article |
| series | Jurnal Neuroanestesi Indonesia |
| spelling | doaj-art-3ee29d43b65840d8beddb44911285d152025-08-20T02:11:09ZindIndonesian Society of Neuroanesthesia & Critical Care (INA-SNACC)Jurnal Neuroanestesi Indonesia2088-96742460-23022025-02-011414752https://doi.org/10.24244/jni.v14i1.659Dormant No More: The Neurogical Impact of Herpes Simplex Virus Reactivation Following Traumatic Brain InjuryTheodorus Kevin Putra Johansyah0 Cindy Thiovany Soetomo1Tiffany Tiffany2Sri Maliawan3Neurosurgery Division, Department of Surgery, Faculty of Medicine, Universitas Udayana, Prof. Dr. I.G.N.G. Ngoerah General Hospital, Denpasar, Bali Faculty of Medicine, Universitas Udayana, Denpasar, BaliFaculty of Medicine, Universitas Udayana, Denpasar, BaliNeurosurgery Division, Department of Surgery, Faculty of Medicine, Universitas Udayana, Prof. Dr. I.G.N.G. Ngoerah General Hospital, Denpasar, Bali Herpes simplex viruses (HSV), including HSV-1 and HSV-2, are neurotropic viruses capable of establishing lifelong latency in sensory ganglia and reactivating under various triggers, including traumatic brain injury (TBI). TBI induces secondary injury cascades such as neuroinflammation, excitotoxicity, and blood-brain barrier disruption, which create a conducive environment for HSV reactivation. The reactivation of HSV after TBI, particularly HSV-1 and HSV-2, can lead to significant neurological consequences, including encephalitis, cognitive decline, and the development of neurodegenerative diseases like Alzheimer’s disease and Chronic Traumatic Encephalopathy. Current therapeutic approaches focus on antiviral agents like acyclovir and valacyclovir, which manage acute HSV infection but are less effective in preventing long-term neurological damage. Emerging research highlights the potential of anti-inflammatory and neuroprotective strategies to complement antiviral therapies, aiming to reduce the neuronal damage caused by viral reactivation and inflammation. However, gaps remain in understanding the precise mechanisms linking TBI-induced neuroinflammation to HSV reactivation and its long-term impact on neurological health. This review synthesizes the current literature on the pathophysiology of HSV reactivation following TBI, and their contributions to acute and chronic neurological outcomeshttps://inasnacc.org/ojs2/index.php/jni/article/view/659herpes simplex virustraumatic brain injuryneuroinflammationhsv reactivation |
| spellingShingle | Theodorus Kevin Putra Johansyah Cindy Thiovany Soetomo Tiffany Tiffany Sri Maliawan Dormant No More: The Neurogical Impact of Herpes Simplex Virus Reactivation Following Traumatic Brain Injury Jurnal Neuroanestesi Indonesia herpes simplex virus traumatic brain injury neuroinflammation hsv reactivation |
| title | Dormant No More: The Neurogical Impact of Herpes Simplex Virus Reactivation Following Traumatic Brain Injury |
| title_full | Dormant No More: The Neurogical Impact of Herpes Simplex Virus Reactivation Following Traumatic Brain Injury |
| title_fullStr | Dormant No More: The Neurogical Impact of Herpes Simplex Virus Reactivation Following Traumatic Brain Injury |
| title_full_unstemmed | Dormant No More: The Neurogical Impact of Herpes Simplex Virus Reactivation Following Traumatic Brain Injury |
| title_short | Dormant No More: The Neurogical Impact of Herpes Simplex Virus Reactivation Following Traumatic Brain Injury |
| title_sort | dormant no more the neurogical impact of herpes simplex virus reactivation following traumatic brain injury |
| topic | herpes simplex virus traumatic brain injury neuroinflammation hsv reactivation |
| url | https://inasnacc.org/ojs2/index.php/jni/article/view/659 |
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