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The Secret Behind Cold Sores: Do You Know How the Herpes Simplex Virus Lurks in the Nerves?
The herpes simplex virus (HSV) is the culprit for cold sores, which not only cause superficial itching but may also lead to more serious diseases such as herpes simplex encephalitis (HSE). HSE is an encephalitis caused by the herpes simplex virus. Although its incidence is relatively rare, affecting approximately one in 500,000 individuals each year, its potential threat cannot be ignored.
Overview of HSE
It is estimated that about 90% of HSE cases are caused by HSV-1, the same virus that causes cold sores. Surveys show that about 57% of adults in the United States are infected with HSV-1, although most infected people do not experience symptoms of cold sores. Most cases of HSE occur in patients who already have HSV-1 antibodies, and only a few have a history of recurrent oral herpes. This suggests that most infections do not result in obvious symptoms, but when the virus becomes active again, it may result in HSE.
Symptoms and Diagnosis
Most people with HSE have a reduced level of consciousness and altered mental status, including confusion and personality changes.
As the disease progresses, people may have fever and seizures, and gradual changes in the electrical activity in their brain. Once symptoms appear, patients may even lose their sense of smell and have difficulty reading, writing and understanding language. A definitive diagnosis requires a lumbar puncture to test the cerebrospinal fluid for the virus, a process that takes several days, so doctors usually start giving the antiviral drug Cyclopidogrel immediately while waiting for test results.
HSE-related conditions
HSE is not just an individual disease; it may also trigger other related immune responses, such as anti-NMDA receptor encephalitis, which can affect neurocognitive recovery, and occurs in about 30% of HSE patients.
Epidemiology and Pathophysiology
According to studies, the annual incidence of HSE is approximately 2 to 4 cases per million population. The main cause of the disease is that the herpes simplex virus is introduced from the periphery of the face and enters the brain along the nerve axons. Although the virus usually lies dormant in the ganglion of the trigeminal nerve, why it reactivates remains unclear, and recent studies suggest that stress may play an important role in animal models.
Treatment and Prognosis
Without treatment, HSE causes rapid death in about 70% of patients, and survivors may face severe neurological damage.
HSE is often treated with high-dose intravenous acid loops, but despite this, one-third of cases are fatal, more than half of survivors suffer long-term neurological damage, and only about 20% survive. % of treated patients return to normal life with minimal impairment. Early treatment (within 48 hours of symptom onset) usually improves the chances of recovery.
ConclusionThe complex mechanisms of latency and reactivation of herpes simplex virus make HSE a public health issue worthy of in-depth study. Until we understand the underlying mechanisms better, how can we protect ourselves from such potential threats?
