Loss of Transfected Human Brain Micro-Vascular Endothelial Cell Integrity during Herpes Simplex Virus Infection

Lee, Sau Har; Atiya, Nadia; Wang, Seok Mui; Manikam, Rishya; Raju, Chandramathi Samudi; Sekaran, Shamala Devi

doi:10.1159/000495180

Cited by 5 publications

(3 citation statements)

References 23 publications

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“…The pathophysiology of anti-NMDAR encephalitis after HSV encephalitis is still unclear. In vitro model of the blood-brain barrier, HSV can reduce the cell-cell barrier resistance lead to a viability loss of the infected endothelial cells [26]. Blood-brain barrier disruption provides a convenient for entry of complement and other pro-in ammatory molecules.…”

Section: Discussionmentioning

confidence: 99%

Pediatric Anti-NMDAR Encephalitis in Southern China: Analysis of 107 Cases

Hou

et al. 2020

Preprint

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Background: Research on pediatric anti-N-methyl-D-aspartate receptor (NMDAR) encephalitis is limited. We studied clinical features of children with anti-NMDAR encephalitis in southern China.Methods: Pediatric anti-NMDAR encephalitis between 2014 and 2019 from one tertiary medical center was analyzed. The Modified Rankin Scale (mRS) score was adopted to evaluate outcomes.Results: 107 children (M/F=50/57; mean onset age=6.3 y) with anti-NMDAR encephalitis were involved. Boys significantly showed earlier onset age, higher ratio of fever, longer hospital day, more courses of steroid treatment, higher mRS score after treatment. 48.6% of patients had prodromal events with infectious events most common. The most common symptom at onset and during whole course was seizures and psychiatric symptoms respectively. Initial median white cell count of cerebral spinal fluid (CSF) was 22.0x106/L. 12.1% of patients had positive herpes simplex virus DNA of CSF. All patients had CSF positive NMDAR antibodies, although 86.9% of patients had serologically positive. 9.3% of patients had overlapped other neuronal antibodies. Electroencephalograph showed abnormalities with slow wave (95.3%) and epileptic activity (41.5%). Delta brush was revealed in 3.8% of patients. 36.4% of patients had lesions in brain MRI, with local lesions most common. No tumor was found in all. 84.9% of patients responded well to the first line therapy (steroid plus immunoglobulin), while 12 patients accepted second-line therapy (Rituximab) with 91.7% of effective rate. 12.1% of patients relapsed. 2 male patients died. The median length of hospital stay was 28 days. The mRS score was significantly improved after treatment. 51.0% of patients had a full recovery. 76.6% of patients had mild neurological disability (mRS≤2). Male, speech disorder, initial score of mRS and administration of second-line therapy were independent risk factors associated with the outcome.Conclusions: Of pediatric anti-NMDAR encephalitis in southern China: the mean onset age was about 6-year-old, earlier in boys; boys remained slower to recover and with a worse prognosis; the most common respective symptom at onset and during whole course was seizures and psychiatric symptoms; combination with tumor was rare; most patients respond well to the immunotherapy; relapse and fatality rate were relatively low; most patients had a good prognosis.

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Section: Discussionmentioning

confidence: 99%

Pediatric Anti-NMDAR Encephalitis in Southern China: Analysis of 107 Cases

Hou

et al. 2020

Preprint

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“…These weaken the BBB by cleaving tight-junction proteins [40][41][42], thereby facilitating the migration of both proinflammatory cytokines and the viral agent from the sera to the brain parenchyma [37,43]. Evidence from human cell culture models indicates that HSV also damages the BBB by reducing the viability of microvascular endothelial cells of the infected brain [44]. However, while there is clear evidence that HSV can disrupt the BBB, there appear to be no studies that have investigated the effects of HSV on the hippocampus directly or that compared the effects of HSV on the hippocampus with its effects on other brain areas.…”

Section: Herpes Simplex Virus (Hsv)mentioning

confidence: 99%

Vulnerability of the Hippocampus to Insults: Links to Blood–Brain Barrier Dysfunction

Davidson,

Stevenson

2024

IJMS

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The hippocampus is a critical brain substrate for learning and memory; events that harm the hippocampus can seriously impair mental and behavioral functioning. Hippocampal pathophysiologies have been identified as potential causes and effects of a remarkably diverse array of medical diseases, psychological disorders, and environmental sources of damage. It may be that the hippocampus is more vulnerable than other brain areas to insults that are related to these conditions. One purpose of this review is to assess the vulnerability of the hippocampus to the most prevalent types of insults in multiple biomedical domains (i.e., neuroactive pathogens, neurotoxins, neurological conditions, trauma, aging, neurodegenerative disease, acquired brain injury, mental health conditions, endocrine disorders, developmental disabilities, nutrition) and to evaluate whether these insults affect the hippocampus first and more prominently compared to other brain loci. A second purpose is to consider the role of hippocampal blood–brain barrier (BBB) breakdown in either causing or worsening the harmful effects of each insult. Recent research suggests that the hippocampal BBB is more fragile compared to other brain areas and may also be more prone to the disruption of the transport mechanisms that act to maintain the internal milieu. Moreover, a compromised BBB could be a factor that is common to many different types of insults. Our analysis indicates that the hippocampus is more vulnerable to insults compared to other parts of the brain, and that developing interventions that protect the hippocampal BBB may help to prevent or ameliorate the harmful effects of many insults on memory and cognition.

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“…Moreover, the obliteration of human brain microvascular endothelial cells emerged as an alternative mechanism for invasion during HSV infection 94 . HSV‐1 infection can potentially disrupt the integrity of the BBB, permitting the virus to infiltrate the brain and give rise to encephalitis.…”

Section: Neuroinflammation and Its Role In Hsv Infectionmentioning

confidence: 99%

Immunopathology of herpes simplex virus‐associated neuroinflammation: Unveiling the mysteries

Hussain,

Gupta,

Samuel

et al. 2023

Reviews in Medical Virology

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The immunopathology of herpes simplex virus (HSV)‐associated neuroinflammation is a captivating and intricate field of study within the scientific community. HSV, renowned for its latent infection capability, gives rise to a spectrum of neurological expressions, ranging from mild symptoms to severe encephalitis. The enigmatic interplay between the virus and the host's immune responses profoundly shapes the outcome of these infections. This review delves into the multifaceted immune reactions triggered by HSV within neural tissues, intricately encompassing the interplay between innate and adaptive immunity. Furthermore, this analysis delves into the delicate equilibrium between immune defence and the potential for immunopathology‐induced neural damage. It meticulously dissects the roles of diverse immune cells, cytokines, and chemokines, unravelling the intricacies of neuroinflammation modulation and its subsequent effects. By exploring HSV's immune manipulation and exploitation mechanisms, this review endeavours to unveil the enigmas surrounding the immunopathology of HSV‐associated neuroinflammation. This comprehensive understanding enhances our grasp of viral pathogenesis and holds promise for pioneering therapeutic strategies designed to mitigate the neurological ramifications of HSV infections.

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Loss of Transfected Human Brain Micro-Vascular Endothelial Cell Integrity during Herpes Simplex Virus Infection

Cited by 5 publications

References 23 publications

Pediatric Anti-NMDAR Encephalitis in Southern China: Analysis of 107 Cases

Pediatric Anti-NMDAR Encephalitis in Southern China: Analysis of 107 Cases

Vulnerability of the Hippocampus to Insults: Links to Blood–Brain Barrier Dysfunction

Immunopathology of herpes simplex virus‐associated neuroinflammation: Unveiling the mysteries

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