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The study is being published September 14 in Science X-Press, an advanced, online edition of the journal Science.
In the study, the scientists suggest that herpes simplex encephalitis may reflect a single gene immunodeficiency that confers susceptibility to herpes simplex virus, an idea that contrasts with the prevailing scientific theory of how genes work to make people vulnerable to infections. In the study, researchers focused on blood cells from two French children with a deficiency for UNC-93B, an endoplasmic reticulum protein involved in the recognition of pathogens. This deficiency resulted in high rates of herpes simplex virus-1 proliferation and cell death. Herpes simplex virus-1 is a common virus that infects about 80 percent of young adults worldwide.
Nonetheless, herpes simplex encephalitis, which was first described in 1941, is the most common type of sporadic viral encephalitis in developed countries, accounting for about 10 to 20 percent of all viral encephalitis cases, as per the University of Maryland Medical Center. Did you know?The study is being published September 14 in Science X-Press, an advanced, online edition of the journal Science. The CSF shows pleocytosis (early neutrophils, late lymphocytes) and elevated protein, depending on the degree of brain necrosis. Some children with HSV encephalitis develop an encephalopathy characterized by choreoathetosis weeks after CSF becomes negative and Acyclovir treatment is discontinued.
Enterovirus (EV) is a small RNA virus transmitted usually from human to human via fecal-oral or respiratory route. Multinucleated giant cells.HIV envelope glycoproteins cause the membranes of HIV-infected macrophages to fuse, forming multinucleated giant cells.
Encephalitis causes mental status changes (depressed or altered level of consciousness, lethargy, personality change) associated with fever, seizures, focal neurological deficits, CSF pleocytosis, EEG abnormalities, and variable neuroimaging findings. The most common autoimmune encephalitis is anti-NMDA receptor encephalitis, which, in some studies, is more frequent than HSV and other viral encephalitides. Anti-NMDA receptor encephalitis is most frequent in young females with ovarian, mediastinal, and other teratomas, but males with testicular and other teratomas and both sexes with other tumors or without evidence of a tumor may be affected. Another probably immunologically-mediated encephalitis is Rasmussen encephalitis, a rare condition that affects mostly children and young adults. This course was produced for the use of students, residents, and staff of NEOMED and affiliated hospitals. Corresponding author: Eun Yeon Joo, Department of Neurology, Samsung, Medical Center, Sungkyunkwan, University School of Medicine, 81 Irwon-ro, Gangnam-gu, Seoul, 135-710, Korea, Tel. Acute retinal necrosis (ARN), a viral retinal disease with poor visual prognosis, following herpes simplex encephalitis (HSE) are uncommonly seen, and there has been no case yet reported of the reverse situation.
A 57-year-old man was referred to Samsung Medical Center with abrupt confusion, fever, and loss of vision in both eyes. His brain magnetic resonance imaging (MRI) showed a hyper-intense lesion in the left medial temporal and bilateral medial occipital areas on T2-weight images, suggestive of HSE (Fig. After administration of intravenous acyclovir for 14 days, his systemic symptoms consistent with encephalitis slowly resolved, but his vision was not restored. Cases with ARN following HSE have been uncommonly reported,5a€“9 and to our knowledge, this is the first report of the reverse situation, HSE following ARN, in even an immune-competent patient.
ARN usually presents as retinal necrosis with discrete borders located in the peripheral retina, rapid progression, circumferential spread, occlusive vasculopathy with arterial involvement, and a prominent inflammatory reaction in the vitreous and anterior chamber.3 Our patient was initially diagnosed with retinal vasculitis and treated with a high-dose systemic corticosteroid, which was not effective. Acute viral encephalitis is an acute inflammation of the nervous system where brain, brain stem or cerebellum is involved due to a virus; It may be primary or post infectious.
A number of viruses can cause clinical picture of acute viral encephalitis and these viruses range from Arboviruses (Japanese, ST Louis, Westren Equine, Kyasanur forest disease (KFD). In most of the cases of acute viral encephalitis there is prodromal period lasting for a few days and symptoms range from headache, myalgia, body aches, malaise and features of upper respiratory tract infection. It is based on clinical picture of acute onset of illness which generally comes in epidemics and involves large number of people. Cases where Herpes simplex virus encephalitis is suspected, antiviral therapy (acyclovir) may be employed with good results. Assuming these findings extend to neurons, they provide a plausible mechanism for herpes simplex encephalitis. Herpes simplex encephalitis, a viral infection of the brain that affects otherwise healthy patients, affects an extremely small percentage of those infected with herpes simplex virus-1: the number of annual cases is two per million people, as per the University of Maryland Medical Center.
Before the advent of anti-viral drugs vidarabine in 1973 and acyclovir in 1981, mortality rates reached up to 70 percent. These are eosinophilic masses consisting of packed viral particles and products of their replication.


Viruses that cause inclusions are herpes simplex, cytomegalovirus, varicella-zoster, papovaviruses, and measles.
A few adolescents and adults develop also psychiatric and other manifestations which appear either as a relapse or a continuation of the initial encephalitis. About seventy percent of neonatal HSV infections are caused by HSV-2 (herpes genitalis) and thirty percent by HSV-2. Some patients with this clinical profile have viral encephalitis and a few have infections by other agents, including Bartonella, Chlamydia, Mycoplasma pneumonia, and other.
It is characterized clinically by psychiatric features, memory disturbance, speech disorder, seizures, dyskinesias, decreased level of consciousness, autonomic instability, and hypoventilation. These tumors contain neural elements not previously encountered by the immune system and exposed to it because there is no blood-brain barrier. Rasmussen encephalitis is characterized clinically by progressive, drug-resistant focal epilepsy, hemiplegia, and cognitive decline and pathologically by cortical inflammation, neuronal loss, and gliosis confined to one cerebral hemisphere. The Pathology of Rasmussen Syndrome: Stages of Cortical Involvement and Neuropathological Studies in 45 Hemispherectomies. We herein present the reverse situation, an immune-competent patient with HSE following ARN. The prevalence of the disease is equal in both genders, and it occurs in the 5tha€“7th decade of life.4 Though the diagnosis of ARN is made clinically in most patients, polymerase chain reaction (PCR) analysis of the aqueous humor or vitreous is known as a confirmative method to detect the causative virus. The patient was in his usual state of health until two weeks prior, when he began to develop sudden loss of vision in his right eye.
Fundus examination showed retinal hemorrhage, confluent retinal necrosis affecting almost the whole retina, vascular sheathing involving both arterioles and venules, optic disc swelling, and exudative retinal detachment in both eyes (Fig. On follow-up examination, retinal necrosis did not progress, but he still suffered from severe bilateral ocular pain with partial improvement of the exudative retinal detachment (Fig. ARN associated with HSE is known to be caused by axonal transmission of a reactivated latent virus from the brain to the retina, and retinitis occasionally occurs after the encephalitis. Fluid-attenuated inversion recovery magnetic image revealed hyperintensity in the left medial temporal (arrow) and bilateral occipital cortices (arrow heads). Primary form occurs when there is direct invasion or replication of virus in the nervous system while post infectious follows either other viral infections or after administration of certain vaccines. Signs of meningeal irritation appear followed by convulsions, confusion, disorientation, stupor and even coma. Serological tests may help in identifying the causative organism if there is four fold increase in antibody titers.
Course of the disease is variable that is it may have a short lived benign course or a severe fulminating course leaving behind a number of sequlae. While the introduction of anti-viral therapy has been a boon to patients, brain damage still poses a substantial risk. These patients have auto-antibodies against the NMDR receptor and other surface antigens, suggesting an auto-immune basis for this illness. However, even when PCR, bacterial and viral cultures, serology, and other tests are done, no viral or other pathogen is identified in a significant proportion of patients. The MRI may show cortical and subcortical signal abnormalities in about 50% of cases and the CSF shows lymphocytic pleocytosis, elevated protein, and oligoclonal bands. Antibodies generated as a result of this sensitization cross the blood-brain barrier and attach to the NMDA receptor on the neuronal membrane. The inflammation consists exclusively of T-lymphocytes and microgial activation with neuronophagia and microgial nodules.
A 57-year-old man who had been under steroid therapy for retinal vasculitis the prior two weeks, presented with abrupt confusion and high fever. As shown by our patient, opposite direct transmission from the retina to the brain seems to be possible. Intraocular or systemic corticosteroids may induce retinal necrosis in patients with viral infection. Systemic steroid therapy may have exacerbated herpes viral infection in the retina, with subsequent spread to the contralateral eye and brain. Herpes simplex virus type 2 as a cause of acute retinal necrosis syndrome in young patients.
Herpes simplex encephalitis and bilateral acute retinal necrosis syndrome after craniotomy. Three consecutive episodes of acute retinal necrosis due to herpes simplex-1 over twelve years following herpetic encephalitis.


The involvement of meninges and other parts of nervous system when inflammation spreads to spinal cord is termed encephalomyelitis. The above symptoms lasting for a few days are followed by neurologic symptoms which come acutely and abruptly. EEG shows a slow wave activity with disruption of normal rhythm with high amplitude bursts and spike and wave complexes.
If a patient is having convulsion then anti-convulsants (Phenytoin 100mg three times a day) are given. The degree of brain destruction (especially in the frontal and temporal lobes) and the inflammatory and reactive changes are more severe than any other viral encephalitis and can be detected by imaging. In the past, the diagnosis of HSV encephalitis required brain biopsy with fluorescent antibody staining using anti-HSV antibodies, microscopic study (to detect inclusions and viral particles) and viral culture.
A necrotizing encephalitis that caused a diffuse melt down of the brain, without predilection for the frontal and temporal lobes. Neonatal EV infection, usually transmitted from the mother, can cause fatal disseminated disease involving the brain, heart, liver, lungs, and other organs.
Brain biopsies, done in a few cases, show mild nonspecific changes including perivascular lymphocytes and microglial activation. This leads to decrease of the NMDA receptor in GABAergic and glutamatergic synapses and increase of extracellular glutamate which causes the symptoms. Thus, it is recommended that corticosteroids should be used in combination with antiviral agents or after beginning antiviral therapy.12 In this patient, the contralateral eye became infected, and HSE occurred during initial corticosteroid therapy without antiviral medication. Cerebral edema is relieved by marmitol (20% solution in 20 minutes every 6 hly), Furesmide and steroids. Atypical cases may have asymmetric pathology, mass-like necrotic and hemorrhagic fronto-temporal lesions, and a wider anatomical distribution, including myelitis and brainstem encephalitis.
Most cases of autoimmune encephalitis are caused by antibodies against neural antigens located on the cell membrane. The pathology involves primarily the cerebral cortex and may be focal such that areas of severe cortical damage are bordered by normal brain. Ophthalmic examination and polymerase chain reaction of the vitreous specimen revealed ARN by herpes simplex virus type 2. Two days after initiation of intravenous methylprednisolone, he complained of decreased vision in his left eye. In cases with an unusual clinical course, especially in retinal vasculitis with arterial involvement, viral uveitis including HSV infection should be suspected.
After intravenous acyclovir therapy, retinal necrosis with hemorrhage was decreased, but vascular sheathing (black arrows) and exudative retinal detachment persisted. Hemispherectomy, which is the only cure for the seizures, has provided abundant material for pathological analysis. One week after initiation of intravenous methylprednisolone, he became drowsy and high fever occurred, and he was then referred to Samsung Medical Center.
On the night of admission, the patient experienced a generalized tonic-clonic seizure during sleep. Bilateral rhegmatogenous retinal detachment with optic atrophy was found six weeks later, thus vitrectomy with silicone oil tamponade was done in the right eye.
When a patient presents with fever, obtundation, seizures, and abnormal CSF, it is preferable to treat with antiviral agents (and antibiotics) rather than defer treatment until the diagnosis is established. Neuronal damage in Rasmussen encephalitis is thought to be mediated by T-cell cytotoxicity and microglial activation. This case implies that ARN may be a risk factor for HSE and the virus may reach the brain from the eye. Infectious retinitis including acute retinal necrosis was suspected, but in terms of the location of necrosis, his clinical features were not typical of ARN Diagnostic vitrectomy confirmed the presence of HSV-1. Inappropriate administration of a systemic steroid may exacerbate herpes viral infection in the retina, with subsequent spread to the brain. However, in patients with HSV encephalitis, prompt treatment saves lives and prevents permanent neurologic deficits. Polio has been eradicated in most of the world but still persists in some developing countries.



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