Herpes virus brain damage

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PubMed is a searchable database of medical literature and lists journal articles that discuss Herpes simplex encephalitis. Click on the link to view a sample search on this topic. Have a question? References References. Anderson WE. Herpes Simplex Encephalitis. Medscape Reference. Klein RS. Herpes simplex virus type 1 encephalitis. Some researchers even say that the Herpes virus may lead to early dementia.

Others sources claim that the connection is more prominent in women and older people. In other words, a younger person who has this virus may not notice the effects until much later in life. Seizures In the most severe cases, herpes can cause a person to have seizures. This is mainly due to the fact that the herpes virus attacks certain cells in the brain. Unfortunately, some of this damage can lead to serious brain malfunction, also known as a seizure.

Such pathogens are, however, subject to reactivation and capable of invading the central nervous system, where they may exert direct damage to brain. Simanek said reactivation of herpes viruses triggers the release of pro-inflammatory cytokines, which have been linked to cognitive impairment. Cytokines are hormones involved in cell signaling and regulation; pro-inflammatory cytokines play an important role in the immunological response to infection and tissue injury.

Excessive inflammation, however, has been linked to various chronic disease outcomes. Herpes simplex virus type 2—associated neurological disease may result from primary infection or reactivation of latent HSV Neurological disease after primary HSV-2 infection is seen most often in neonates.

After the neonatal period, HSV-2 infection is principally, but not exclusively, acquired through sexual activity. Primary HSV-2 infection is delayed in most individuals until adolescence and early adulthood with the advent of sexual activity.

Primary HSV-2 infection in immunocompetent adolescents and adults is usually asymptomatic, with most patients being unaware of their HSV-2 exposure. Neurons in the sacral ganglia traditionally have been considered to be the site of HSV-2 latency. Examination of HSV-2 latency using polymerase chain reaction PCR techniques have demonstrated HSV-2 latency in ganglia throughout the central nervous system CNS axis, albeit at significantly lower frequencies than in the sacral ganglia.

Latency of HSV-2 has also been demonstrated to occur in trigeminal ganglia. The widespread latency of HSV-2 suggests that the virus may reach ganglia far removed from the site of primary infection. The molecular mechanisms underlying HSV latency are incompletely understood. Latent HSV infection is reactivated by local and systemic stimuli. Current evidence suggests that the most plausible mechanism for HSV reactivation is stimulation of latently infected cells through pathways yet to be determined.

The fate of neurons supporting replication of reactivated HSV remains undecided. Many patients with HSV-2 infection shed low levels of virus continuously without demonstrated reactivation. Humans are the only known reservoir of HSV The frequency of HSV-2 seropositivity varies by population. An estimated 45 million persons in the United States have genital herpes infection, 1 with new infections occurring at an estimated rate of approximately 1 million per year.

Seropositivity for HSV-2 correlates with the number of sexual partners, the age of sexual debut, increasing age, black or Hispanic race, female sex, and the presence of other sexually transmitted diseases, including human immunodeficiency virus HIV infection.

Although HSV-1 has a predilection for the development of encephalitis after intracerebral injection in the mouse model, HSV-2 generally causes meningitis. Virtually any part of the neuraxis may be affected by this virus, including the retina, brain, brainstem, cranial nerves, spinal cord, and nerve roots. When HSV-2 infection is mentioned, neonatal herpes simplex encephalitis HSE , a devastating disorder, is the disease most commonly considered.

Seventy percent of affected neonates are born to mothers without symptoms or signs of genital herpes. Risk factors for neonatal HSV disease include first-episode maternal infection in the third trimester, invasive monitoring, delivery before a gestational age of 38 weeks, and maternal age of less than 21 years.

Laboratory test results often show abnormal liver function and disseminated intravascular coagulation. The cranial magnetic resonance images MRIs and computed tomograms initially show diffuse edema and later cerebral atrophy, calcifications, and cystic encephalomalacia. Electroencephalography shows slow background and paroxysmal discharges. During the prodrome of genital herpes and concomitant with the herpetic eruption, affected patients experience headache, neck stiffness, and low-grade fever.

Back, buttock, perineal, and lower extremity pain may be associated with urinary retention and constipation. Analysis of CSF reveals a lymphocytic pleocytosis.

Recurrent aseptic meningitis due to HSV-2 may occur with or without symptomatic herpetic mucocutaneous disorder. The manifestations of this disorder are identical to that observed with primary genital herpes.

Many of these cases were previously diagnosed as Mollaret meningitis, before the recognition that HSV-2 may be causative. Analysis of CSF often reveals a large mononuclear cell with an indistinct cytoplasm referred to as the Mollaret cell. Herpes simplex virus type 2 is not the only virus responsible for Mollaret meningitis, and some authorities have suggested that the term be restricted to recurrent aseptic meningitis without an identifiable cause.

A woman aged 33 years presented with a 4-day history of intractable headache, photophobia, nausea, and neck and back discomfort. She had 3 previous hospital admissions for a similar disorder, the first and most severe of which occurred concomitantly with her initial outbreak of genital herpes.

Results of her examination were remarkable for a low-grade fever and stiff neck.