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Hidden danger in the brain: Why does herpes simplex virus cause encephalitis?
Herpes Simplex Encephalitis (HSE) is an encephalitis caused by the herpes simplex virus. Although this disease is relatively rare, it is potentially fatal. It is estimated that approximately 1 in 500,000 people are affected each year, with some studies suggesting that approximately 5.9 out of every 100,000 births will develop HSE.
Ninety percent of HSE cases are caused by oral herpes simplex virus type 1 (HSV-1), the same virus that causes cold sores.
According to 2006 estimates, approximately 57% of adults in the United States are infected with HSV-1, yet most of these infected people never develop symptoms of cold sores. The remaining cases are caused by genital herpes simplex virus type 2 (HSV-2), which is usually transmitted through sexual contact. Approximately two-thirds of HSE cases occur in individuals who are already seropositive for HSV-1, only 10% of whom have a history of recurrent oral herpes, and approximately one-third of cases result from a primary infection with HSV-1. It mainly occurs among young people under the age of 18.
About half of people over the age of 50 develop HSE. Although HSV-1 is the main cause of encephalitis in adults and children, HSV-2 is the main cause in neonates and immunocompromised individuals.
Symptoms and signs
Most HSE patients experience a decline in consciousness and mental state, manifesting as confusion and personality changes. An increase in the number of white blood cells is found in the patient's cerebrospinal fluid, but no pathogenic bacteria or fungi are present. At the same time, patients usually have a fever and sometimes have seizures.
As the disease progresses, changes in electrical activity initially appear in one temporal lobe and then spread to the other temporal lobe after 7 to 10 days.
Imaging tests such as CT or MRI will show characteristic changes in the temporal lobes. After the first symptoms appear, people may lose their sense of smell and may have difficulty reading, writing, or communicating verbally. Confirmation requires testing of cerebrospinal fluid via a lumbar puncture to detect the presence of the virus.
Related Diseases
Herpes simplex virus encephalitis may also trigger a secondary immune response of anti-NMDA receptor encephalitis, which occurs in about 30% of HSE patients and has a significant impact on neurocognitive repair.
EpidemiologyThe annual incidence of HSV-1 encephalitis is approximately 2 to 4 cases per million population, indicating that, despite its rarity, widespread awareness and research is needed to understand its impact.
PathophysiologyHSE is thought to be caused by the virus entering the brain from a peripheral site on the face through nerve axons in the salivary glands. The virus lies dormant in the ganglia of the trigeminal nerve, and why it reactivates and how it enters the brain remains unclear, although there is evidence that changes in the immune system may be related to stress.
Diagnosis
The diagnosis of HSE usually requires a brain CT scan (with or without contrast) to exclude significantly increased intracranial pressure, obstructive cerebral edema, or tumor effects. Brain MRI may reveal increased T2 signal intensity in the frontotemporal regions, indicative of viral (HSV) encephalitis.
TreatmentHSV encephalitis is treated primarily with high-dose intravenous acyclovir, 10 mg/kg (for adults) given over 1 hour to avoid renal damage. Untreated HSE rapidly kills people in about 70% of cases; survivors often suffer severe neurological damage. Even with treatment, HSE is fatal in one-third of cases, and more than half of survivors suffer long-term neurological damage.
Twenty percent of treated patients recover mild damage, while only 2.5 percent of untreated survivors recover fully normal brain function.
Many cases of amnesia involving HSE have been documented in the scientific literature. Treatment as early as 48 hours after symptoms begin increases the chances of a good recovery, but it is uncommon to experience a relapse within weeks to months after treatment. Early evidence suggests that abnormal inflammation caused by the herpes simplex virus may lead to granulomatous inflammation in the brain, which can be treated with steroids.
Conclusion Although herpes simplex virus encephalitis is non-contagious, its potential danger should not be underestimated because there are many other viruses that can cause similar encephalitis symptoms, which are usually relatively mild. This situation makes people wonder, why can this virus hide in the human body for so long and yet may cause serious consequences at any time?