HSV infection causes several distinct medical disorders. Common infection of the skin or mucosa may affect the face and mouth (orofacial herpes), genitalia (genital herpes), or hands (herpes whitlow). More serious disorders occur when the virus infects and damages the eye (herpes keratitis), or invades the central nervous system, damaging the brain (herpes encephalitis). Patients with immature or suppressed immune systems, such as newborns, transplant recipients, or AIDS patients are prone to severe complications from HSV infections. HSV infection has also been associated with cognitive deficits of bipolar disorder, and Alzheimer's disease, although this is often dependent on the genetics of the infected person.
There is a single report of a systemic infection with HSV-2, where a healthy 28-year old woman with a healthy immune system died 12 days after contracting the virus.
In all cases HSV is never removed from the body by the immune system. Following a primary infection, the virus enters the nerves at the site of primary infection, migrates to the cell body of the neuron, and becomes latent in the ganglion. As a result of primary infection, the body produces antibodies to the particular type of HSV involved, preventing a subsequent infection of that type at a different site. In HSV-1 infected individuals, seroconversion after an oral infection will prevent additional HSV-1 infections such as whitlow, genital herpes, and keratitis. Prior HSV-1 seroconversion seems to reduce the symptoms of a later HSV-2 infection, although HSV-2 can still be contracted. Most indications are that an HSV-2 infection contracted prior to HSV-1 seroconversion will also immunize that person against HSV-1 infection.
| Condition | Description | Illustration |
|---|
| Herpes labialis | Infection occurs when the virus comes into contact with oral mucosa or abraded skin. | |
| Herpes genitalis | When symptomatic, the typical manifestation of a primary HSV-1 or HSV-2 genital infection is clusters of inflamed papules and vesicles on the outer surface of the genitals resembling cold sores. | |
| Herpetic whitlow | Herpes whitlow is a painful infection that typically affects the fingers or thumbs. Occasionally infection occurs on the toes or on the nail cuticle. | |
| Herpes gladiatorum | Individuals that participate in contact sports such as wrestling, rugby, and soccer sometimes acquire a condition caused by HSV-1 known as herpes gladiatorum, ''scrumpox'', ''wrestler’s herpes'', or ''mat herpes'', which presents as skin ulceration on the face, ears, and neck. Symptoms include fever, headache, sore throat and swollen glands. It occasionally affects the eyes or eyelids. | |
| Herpetic keratoconjunctivitis | Primary infection typically presents as swelling of the conjunctiva and eye-lids (blepharoconjunctivitis), accompanied by small white itchy lesions on the surface of the cornea. | |
| Herpesviral encephalitis | A herpetic infection of the brain that is thought to be caused by the retrograde transmission of virus from a peripheral site on the face following HSV-1 reactivation, along the trigeminal nerve axon, to the brain. HSV is the most common cause of viral encephalitis. When infecting the brain, the virus shows a preference for the temporal lobe.. | |
| Herpesviral meningitis | HSV-2 is the most common cause of Mollaret's meningitis, a type of recurrent viral meningitis. | |
| Neonatal herpes simplex | Neonatal HSV infection is a rare but serious condition, usually caused by vertical transmission of HSV (type 1 or 2) from mother to newborn. | |
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| During immunodeficiency | In patients with a weakened immune system, herpes simplex can cause unusual lesions in the skin. One of the most striking is the appearance of clean linear erosions in skin creases, with the appearance of a knife cut. |
| Herpetic sycosis | Herpetic sycosis is a recurrent or initial herpes simplex infection affecting primarily the hair follicle. |
| Eczema herpeticum | Infection with herpesvirus in patients with chronic atopic dermatitis may result in spread of herpes simples throughout the eczematous areas. This is supported by findings that show the presence of HSV-1 DNA in saliva at a higher frequency in patients with Bell's palsy relative to those without the condition. However, since HSV can also be detected in these ganglia in large numbers of individuals that have never experienced facial paralysis, and high titers of antibodies for HSV are not found in HSV-infected individuals with Bell's palsy relative to those without, this theory has been contested. In other studies, HSV-1 DNA was not detected in the cerebrospinal fluid of Bell's palsy sufferers, raising questions whether HSV-1 is the causative agent in this type of facial paralysis. The potential effect of HSV-1 in the etiology of Bell's palsy has prompted the use of antiviral medication to treat the condition. The benefits of acyclovir and valacyclovir have been studied. But the effect appears small, if at all detectable. Alzheimer's diseaseScientists discovered a link between HSV-1 and Alzheimer's disease in 1979. In the presence of a certain gene variation (APOE-epsilon4 allele carriers), HSV-1 appears to be particularly damaging to the nervous system and increases one’s risk of developing Alzheimer’s disease. The virus interacts with the components and receptors of lipoproteins, which may lead to the development of Alzheimer's disease. Without the presence of the gene allele, HSV type 1 does not appear to cause any neurological damage and thus increase the risk of Alzheimer’s. A study published in The Journal of Pathology, has shown a striking localization of herpes simplex virus type 1 DNA within the beta-amyloid plaques that characterize Alzheimer's disease, and suggests that this virus is a major cause of the plaques and hence probably a significant aetiological factor in Alzheimer's disease. |
Further Reading
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