Infectious Disorders
Genital herpes: neurologic complications
May. 05, 2026
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Epstein-Barr virus infections of the nervous system …
- Updated 04.29.2025
- Released 01.27.1999
- Expires For CME 04.29.2028
Epstein-Barr virus infections of the nervous system
Introduction
Overview
Epstein-Barr virus is a ubiquitous herpes virus that causes infectious mononucleosis. It is a very common viral infection affecting up to 95% of the adult global population (50). Neurologic complications due to acute Epstein-Barr virus infection include acute encephalitis, cerebellar ataxia, cranial nerve palsies, and Guillain-Barré syndrome. Studies also show a high prevalence of Epstein-Barr virus seropositivity among patients with multiple sclerosis.
Key points
|
• Epstein-Barr virus is a herpes virus that causes infectious mononucleosis. | |
|
• Neurologic symptoms can be seen with infectious and postinfectious complications of Epstein-Barr virus infection. | |
|
• Epstein-Barr virus infection is closely associated with multiple sclerosis, and although an area of extensive research, the causal relationship has not been definitively demonstrated. |
Historical note and terminology
Discovered in 1964 from lymphoma cells of the jaw, Epstein-Barr virus has since been implicated in a variety of disease processes, both benign and malignant (16). The virus was discovered by Anthony Epstein, Yvonne Barr, and colleagues by studying lymphomas from the jaws of central African children, which was found by surgeon Denis Burkitt (08). Epstein-Barr virus was the first virus discovered that was associated with cancer (13), and years later, it was identified as the cause of infectious mononucleosis, also known as glandular fever (20). The virus belongs to the gamma 1 or lymphocryptovirus herpesvirus family and is one of the most common viruses among humans. It is also known as human herpesvirus 4 and is implicated in a variety of diseases such as nasopharyngeal carcinoma, hairy cell leukoplakia, Burkitt lymphoma, and lymphomas in the immunocompromised (50). The following discussion will concentrate on neurologic manifestations of Epstein-Barr virus infection.
Clinical manifestations
Presentation and course
Young children and young adults have a predilection for symptomatic infections, with severity ranging from mild to fulminant, life-threatening complications. Infectious mononucleosis due to Epstein-Barr virus is one of the most common causes of prolonged illness in adolescents and young adults in Western societies. Infection is often spread by saliva in teens and young adults, designating infectious mononucleosis as the “kissing disease”. After an incubation period of 4 to 7 weeks, a typical triad of fever, pharyngitis, and lymphadenopathy (especially of the occipital and cervical nodes) begins. Other clinical features may include splenomegaly, mononuclear leukocytosis, and hepatocellular dysfunction, rarely presenting with jaundice (33).
Epstein-Barr virus has been associated with multiple neurologic complications, including acute encephalitis, meningitis, acute cerebellar ataxia, myelitis, Guillain-Barré syndrome, cranial nerve palsies, neuropsychiatric syndromes, mononeuropathies, and acute disseminated encephalomyelitis (03; 52). Meningitis and encephalitis are the most common complications of acute Epstein-Barr virus infection, with encephalitis being less frequent than meningitis. The initial symptoms of meningitis are severe headache and neck stiffness. Encephalitis may present with coma, seizures, delirium, or focal neurologic deficits before infectious mononucleosis is apparent. Epstein-Barr virus encephalitis may also present with ataxia due to cerebellitis (24) and is also associated with Alice in Wonderland syndrome, which is an encephalopathy characterized by visual hallucinations and perceptual distortions of objects and body parts, also known as metamorphopsia (27). It remains the commonest infectious cause of Alice in Wonderland syndrome, and although the pathophysiology remains controversial, local cerebral edema and ischemia similar to that shown in migraine-associated Alice in Wonderland syndrome have been postulated (37).
Acute disseminated encephalomyelitis is a post-infectious immune-mediated syndrome presenting with encephalopathy and focal neurologic deficits, with lesions often seen in both the brain and spinal cord. Epstein-Barr virus may be the antecedent infection, and diagnosis is based on a reactive Epstein-Barr virus IgM serology (34). Epstein-Barr virus may cause an acute myelitis, but this is more common in immunocompromised patients through local reactivation of the virus (52). It is an inflammatory myelopathy, with lymphocytic pleocytosis and elevated protein concentration in the CSF as well as T2 hyperintensities on MRI of cervical and thoracic spinal cord segments (42). Symptoms may include paresthesias, extremity weakness, and loss of sphincter control (31).
Epstein-Barr virus infection has also been associated with peripheral nervous system syndromes, including cranial neuropathies and polyradiculopathies (11). Hottenrott described a case of Epstein-Barr virus causing a lumbosacral radiculitis with radicular pain in an immunocompetent patient (23). Brachial plexus neuropathy associated with infectious mononucleosis has also been reported (47).
Guillain-Barré syndrome is associated with multiple antecedent infections, the most common being Campylobacter jejuni, cytomegalovirus, Epstein-Barr virus, and Mycoplasma pneumoniae. All four of these infections associated with Guillain-Barré syndrome cause the formation of antibodies that cross-react with glycoconjugate proteins on peripheral nerves. Epstein-Barr virus, cytomegalovirus, and Mycoplasma pneumoniae can also form cold agglutinins that bind to carbohydrate antigens on glycoconjugate proteins, which is a similar mechanism to how antibodies are produced to gangliosides (26). Miller Fisher syndrome, a variant of Guillain-Barré syndrome, can be precipitated by Epstein-Barr virus infection as shown in a case report of a 14-year-old boy with bilateral cranial nerve dysfunction, limb hyporeflexia, and positive anti-GQ1b antibodies (10). The pathophysiological mechanism of Epstein-Barr virus-induced Miller Fisher syndrome is likely similar to that of the cross-reactivity theory with Epstein-Barr virus and Guillain-Barré syndrome (04).
A considerable amount of research has been conducted to investigate the association between Epstein-Barr virus and multiple sclerosis; however, a causal relationship has not been definitively demonstrated. Seropositivity for Epstein-Barr virus is as high as 100% in some study cohorts of patients with multiple sclerosis, with lower rates being found in patients without multiple sclerosis of the same age range (01). Risk of multiple sclerosis following Epstein-Barr virus infection is suggested in a longitudinal analysis of a cohort of adults with multiple sclerosis (05; 44). It is also suggested that Epstein-Barr virus-related infectious mononucleosis is a greater risk for multiple sclerosis than asymptomatic Epstein-Barr virus infection (30).
There are multiple hypotheses on the mechanism of the pathogenesis of Epstein-Barr virus leading to multiple sclerosis. The first posits that Epstein-Barr virus antigens trigger cross-reactivity to CNS self-antigens by T-cells previously exposed to Epstein-Barr virus. This is further promoted by poor clearing of Epstein-Barr virus-infected B cells, prolonging CD8+ T-cell exposure to Epstein-Barr virus antigens (36). Another hypothesis states that multipel sclerosis is not primarily an autoimmune disease, but rather a disease that has secondary autoimmune reactions that cause bystander injury when the CNS is exposed to Epstein-Barr virus antigens--both latent antigens during latency and lytic antigens during viral replication--leading to the relapse symptoms (attacks) observed in multiple sclerosis. This is suggested by the presence of gadolinium-enhancing lesions on brain MRI scans in relapsing-remitting multiple sclerosis (02; 32). In this hypothesis, therefore, it is the clinical attacks in relapsing-remitting multiple sclerosis that are immune-driven when Epstein-Barr virus antigen-induced autoimmunity causes bystander injury in the CNS. A third hypothesis describes a “two-hit” scenario that allows inflammatory cells to migrate into the CNS in the presence of Epstein-Barr virus infection (19).
Despite the strong association between Epstein-Barr virus and multiple sclerosis occurrence, the etiology and pathogenesis of multiple sclerosis are complex and heterogenous and have yet to be fully understood; thus, the role of Epstein-Barr virus in its pathogenesis remains unclear (06). Little evidence yet exists to definitively prove any of the hypotheses above.
Although subacute sclerosing panencephalitis is classically known as a consequence of measles infection, there have been a few cases reported that include Epstein-Barr virus as a factor. Hochberg and colleagues described a case of a 13-year-old girl who died of subacute sclerosing panencephalitis during an acute mononucleosis infection (22). Brain tissue staining showed both measles and Epstein-Barr virus antigenic material. One hypothesis is that decreased cellular immunity from acute mononucleosis may be responsible for activation of latent measles virus. Epstein-Barr virus has also been implicated in nasopharyngeal cancer (51) as well as primary CNS lymphomas in immunocompetent and immunocompromised patients (29; 18).
Prognosis and complications
Epstein-Barr virus encephalitis is often self-limiting and is relatively benign compared to other herpes encephalitides (03). Rarely, the clinical course is complicated by cerebral edema, which can cause raised intracranial pressure and death. In children, it can be associated with subsequent developmental delay, and some adults show persistence of neuropsychiatric disorders after resolution of the acute illness (03). Similarly, Epstein-Barr virus myelitis is often complicated by permanent sequelae, with limited resolution of limb paresis. The prognosis of primary CNS lymphoma associated with Epstein-Barr virus among people living with HIV improves with the use of effective antiretroviral therapy. The prognosis in immunocompetent patients depends on many factors, and predictive scores such as the International Extranodal Lymphoma Study Group (IELSG) score and Memorial Sloan Kettering Cancer Center (MSKCC) prognostic score can be used to stratify patients’ prognoses (18). Prognostic factors generally include the age of the patient (with older age being associated with poorer outcomes) and the occurrence of adverse events associated with mass effect from the tumor itself.
Compared to other viruses, such as hepatitis E virus, cytomegalovirus and Epstein-Barr virus cause milder forms of Guillain-Barré syndrome with better neurologic outcomes, and full recovery is usually around 6 months post-onset (14).
Biological basis
Etiology and pathogenesis
Epstein-Barr virus is a human herpes virus, also known as human herpesvirus 4. The virus is unique in that it infects B lymphocytes and epithelial cells through binding to CD21 and cellular integrins, respectively. The virus can exist in a latent phase or a lytic phase, with neurologic complications occurring in both phases. In the latent phase, the virus remains dormant within the host B cells, expressing a limited set of genes, a variety of Epstein-Barr virus nuclear antigens (EBNA), namely EBNA-1, 2, 3A, 3B, 3C, and EBNA-LP. The lytic phase involves Epstein-Barr virus reactivation, with active viral replication triggering the expression of many different antigens, such as the early lytic antigen EBV-EA and the late lytic antigen gp350 (15). The pathophysiology of neurologic complications may involve Epstein-Barr virus entering nerve tissue through infected B lymphocytes. Pathologic studies show perivascular lymphocytic infiltrates, parenchymal edema, microglial proliferation, and demyelination in the central nervous system (12). Other studies show that altered gene expression of Epstein-Barr virus-infected B lymphocytes leads to increased trafficking of these cells into the central nervous system (45). Overcoming barriers to central nervous system entry in this manner has been implicated in pathological changes that lead to diseases such as primary central nervous system lymphoma and multiple sclerosis (45; 38). Evidence of active Epstein-Barr virus infection in the CNS is shown by the presence of Epstein-Barr virus DNA and virus-specific IgM and IgG antibodies in cerebrospinal fluid (46).
Epidemiology
Epstein-Barr virus is a ubiquitous virus, with an estimate of 95% of adults globally being seropositive (50). The ability of the virus to establish latency and reactivate after initial infection, along with mild clinical symptoms in most infected individuals, allows for the ubiquity of the virus. In developing countries, children often seroconvert by the age of 3 or 4 years (40). Primary infection occurs at younger ages in lower socioeconomic settings, whereas primary infection occurs at older ages in regions with higher socioeconomic settings (21).
The incidence of Epstein-Barr virus-related disorders of the nervous system remains unclear and varies widely from study to study. However, it is clear that although Epstein-Barr virus is highly prevalent in all world populations, the occurrence of neurologic complications is likely much lower, with estimates from studies ranging between 0.5% to 18% of Epstein-Barr virus-infected individuals (46; 17).
Prevention
Two types of Epstein-Barr virus vaccines are being developed: prophylactic vaccines to prevent Epstein-Barr virus infection and therapeutic vaccines to treat malignancies associated with Epstein-Barr virus. A prophylactic vaccine targeting the viral glycoprotein gp350 showed a reduction of infectious mononucleosis by nearly 80% in an early phase 2 study (30). Despite these vaccines not showing potential for preventing Epstein-Barr virus infection, the observed reduction in the risk of infectious mononucleosis has promise for prevention of multiple sclerosis as Epstein-Barr virus-associated infectious mononucleosis is a greater risk factor for multiple sclerosis than asymptomatic Epstein-Barr virus infection (30).
Differential diagnosis
Confusing conditions
The differential diagnosis for a mononucleosis-like illness other than Epstein-Barr virus includes cytomegalovirus, acute HIV, human herpesvirus 6, toxoplasmosis, and anicteric hepatitis. As for other neurologic complications, encephalitis can be caused by Epstein-Barr virus, herpes simplex virus, a number of arboviruses, and numerous other bacteria, viruses, fungi, and parasites. Cerebellar ataxia in children is often caused by a post-infectious process, including Epstein-Barr virus, Mycoplasma pneumoniae, varicella zoster virus, as well as other organisms (24).
Associated or underlying disorders
Epstein-Barr virus may be involved in the progressive neuronal degeneration observed in people living with HIV. One theory suggests that the presence of ongoing Epstein-Barr viral replication in the central nervous system leads to aberrant immune activity that promotes HIV-associated neuronal injury (28). This hypothesis is supported by the observation that 18% of a cohort of people living with HIV had Epstein-Barr virus DNA in cerebrospinal fluid. In addition, those with detectable Epstein-Barr virus DNA in the CSF had higher levels of HIV RNA in the cerebrospinal fluid and a rate of pleocytosis up to three times higher (28).
Diagnostic workup
Epstein-Barr virus causes a peripheral lymphocytosis with greater than 10% atypical lymphocytes. Heterophile antibodies are IgM antibodies that agglutinate sheep or horse erythrocytes; they were used diagnostically more frequently in the past as they are less specific than the current Epstein-Barr virus-specific antibody assays used today. Viral serologies help determine acute versus latent Epstein-Barr virus infection. The presence of viral capsid antigen IgM and IgG antibodies in the absence of antibodies to virus-associated nuclear antigen is evidence of a current or recent Epstein-Barr virus infection. A reactive viral capsid antigen IgG and Epstein-Barr virus-associated nuclear antigen IgG, with a nonreactive viral capsid antigen IgM, is indicative of a previous infection.
In meningitis and encephalitis caused by Epstein-Barr virus, there is a CSF lymphocytic pleocytosis with the protein concentration being normal or elevated, and glucose levels are normal. Diagnosis is made through detection of antibodies or detection of Epstein-Barr virus DNA in CSF by polymerase chain reaction, or both findings (52). Quantitative CSF polymerase chain reaction in Epstein-Barr virus infections has shown a lower viral load in patients with postinfectious complications and a higher viral load in patients with primary encephalitis (49).
Detection of CSF Epstein-Barr virus DNA by polymerase chain reaction can also be seen in patients with primary CNS lymphoma (25). However, establishing this is not always possible, and negative polymerase chain reaction does not exclude primary CNS lymphoma (25). Nevertheless, the predictive value of the CSF Epstein-Barr virus PCR in the correct clinical settings can be very high (41).
Given the high seroprevalence of Epstein-Barr virus, particularly in adults older than 40 years of age (40), Epstein-Barr virus can sometimes be detected a false positive or “bystander” identified during the infectious workup of certain pathologies and may not actually be the causative organism of the pathology being investigated (39; 09). Latent infection can be reactivated in the setting of immune system activation, and, as such, its detection has to be interpreted carefully (35).
Management
Management of Epstein-Barr viral infections includes supportive care and symptomatic treatment. There is no effective antiviral therapy reported against the Epstein-Barr virus. Neurologic complications of acute viral infection can often be managed supportively, and further specialized treatment may be required depending on the disorder. In people living with HIV, primary central nervous system lymphoma may respond to antiretroviral therapy, which may be combined with methotrexate or whole-brain radiotherapy where appropriate (07).
More recent studies have investigated treatment of Epstein-Barr virus infection and Epstein-Barr virus-related tumors by targeting gp350 and other viral antigens with promising results (43; 48).
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Contributors
All contributors' financial relationships have been reviewed and mitigated to ensure that this and every other article is free from commercial bias.
Authors
-
Deanna Saylor MD MHS
Dr. Saylor of John Hopkins Hospital has no relevant financial relationships to disclose.
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Mashina Chomba MBChB MMed
Dr. Chomba of University Teaching Hospital in Lusaka, Zambia received an honorarium from Roche as a keynote speaker.
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Editor
-
Christina M Marra MD
Dr. Marra of the University of Washington School of Medicine has no relevant financial relationships to disclose.
See Profile
Former Authors
- Burk Jubelt MD
- Catherine Amlie-Lefond MD
- Jennifer Siriwardane MD
- Karen L Roos MD FAAN
Patient Profile
- Age range of presentation
-
- 2 to 65+ years
- Sex preponderance
-
- male=female
- Heredity
-
- none
- Population groups selectively affected
-
- none selectively affected
- Occupation groups selectively affected
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- none selectively affected
ICD & OMIM codes
- ICD-10
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- Mononucleosis due to Epstein-Barr virus: B27.0
- Malaise and fatigue: R53
- Sequelae of other specified infectious and parasitic diseases: B94.8
- ICD-11
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- Epstein-Barr virus: XN0R2
- Mononucleosis due to Epstein-Barr virus: 1D81.0
- Congenital Epstein-Barr virus infection: KA62.1
- Viral encephalitis, not elsewhere classified: 1C80
- Other specified combined immunodeficiencies: 4A01.1Y
- Viral myelitis: 1D02.1
- Other specified infectious liver disease: DB90.Y
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