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Encephalitis ll: Pathophysiology01:26

Encephalitis ll: Pathophysiology

Encephalitis is inflammation of the brain parenchyma caused by direct viral invasion or immune-mediated mechanisms triggered by infections or tumors. Both processes lead to neuronal injury, disrupted neurotransmission, and diverse neurological symptoms, often with overlapping clinical and pathological features.Autoimmune EncephalitisIn autoimmune encephalitis, antibodies target neuronal antigens on cell surfaces, synapses, or within neurons. A key example is anti-NMDAR encephalitis, which can...
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Encephalitis is inflammation of the brain parenchyma, most often due to infections or autoimmune processes. It presents with neuropsychiatric features such as fever, altered mental status, behavioral changes, cognitive dysfunction, seizures, focal deficits, and sometimes autonomic instability. In some cases, the meninges are also involved, resulting in meningoencephalitis.Infectious CausesInfectious encephalitis is most commonly viral but can also result from bacterial, fungal, or parasitic...
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Herpes simplex type 1 (HSV‑1) is a widespread pathogen responsible for orolabial lesions. It is an enveloped, double-stranded DNA (dsDNA) virus belonging to the family Herpesviridae. Once the virus infects a host cell, its double‑stranded DNA genome is delivered into the nucleus, where a coordinated cascade of immediate‑early, early, and late gene expression directs viral DNA replication, structural protein synthesis, and virion assembly. After primary infection of epithelial cells, HSV-1...
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Arboviral encephalitis refers to brain inflammation caused by arthropod-borne viruses, particularly those transmitted through mosquito vectors. Among these, West Nile virus (WNV), a member of the Flaviviridae family, is a significant public health concern. WNV is an enveloped, positive-sense, single-stranded RNA virus. Human infection typically begins when an infected mosquito introduces the virus into the dermis during feeding. The primary transmission cycle involves birds as amplifying hosts...
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Differentiation of the SH-SY5Y Human Neuroblastoma Cell Line
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Neuronal apoptosis in herpes simplex virus - 1 encephalitis (HSE).

S Athmanathan1, B V Vydehi, C Sundaram

  • 1Jhaveri Microbiology Centre, L. V. Prasad Eye Institute, Nizam's Institute of Medical Sciences, Hyderabad, India.

Indian Journal of Medical Microbiology
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PubMed
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Herpes simplex virus encephalitis (HSE) may involve apoptosis, a programmed cell death. This study found evidence of virus-induced apoptosis in brain tissue and cell lines, suggesting its role in HSE pathogenesis.

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Area of Science:

  • Neuroscience
  • Virology
  • Cell Biology

Background:

  • Herpes simplex virus (HSV) infections are common and can affect the central nervous system, leading to life-threatening encephalitis.
  • The precise cellular mechanisms driving Herpes simplex virus encephalitis (HSE) pathogenesis remain largely unknown.
  • Virus-induced apoptosis (programmed cell death) is a potential contributor to the molecular pathology of encephalitis.

Purpose of the Study:

  • To investigate the presence and role of apoptosis in Herpes simplex virus type 1 encephalitis (HSE).
  • To examine apoptosis in post-mortem brain tissue from an HSE patient.
  • To assess HSV-1-induced apoptosis in a human glioblastoma cell line (SNB 19) in vitro.

Main Methods:

  • Histopathological analysis of brain tissue using hematoxylin and eosin staining.
  • Detection of HSV-1 antigen via indirect immunoperoxidase assay.
  • Apoptosis detection using TUNEL assay in brain tissue and membrane blebbing/Hoechst 33258 staining in cell lines.

Main Results:

  • Brain tissue showed classical signs of viral encephalitis, including intranuclear inclusions and neuronal loss.
  • Abundant HSV-1 viral antigen was detected in neurons, microglial, and satellite cells.
  • Both post-mortem brain tissue and in vitro cell line assays demonstrated significant apoptosis, indicating HSV-1 induction.

Conclusions:

  • Virus-induced apoptosis is implicated in the molecular pathogenesis of Herpes simplex virus encephalitis (HSE).
  • These findings highlight apoptosis as a key cellular event in HSE.
  • Further research using neuronal cell lines is recommended to fully elucidate HSV-1's role in apoptosis.