Relationship Between Herpes And Neuronal Disorders

In a mouse model, a type of facial paralysis called Bell's palsy has been linked to the presence and reactivation of latent HSV-1 inside the sensory nerves of the face (geniculate ganglia). 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.
Scientists discovered a link between HSV-1 and Alzheimer's disease in 1979. In the presence of a certain gene variation, 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 HSV-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.
Herpes simplex is most easily transmitted by direct contact with a lesion or the body fluid of an infected individual. Transmission may also occur through skin-to-skin contact during periods of asymptomatic shedding. Barrier protection methods are the most reliable method of preventing transmission of herpes, but they merely reduce rather than eliminate risk.
Herpes viruses cycle between periods of active disease, followed by a remission period during which the sores disappear. After initial infection, the viruses move to sensory nerves, where they reside as life-long, latent viruses. Causes of recurrence are uncertain, though some potential triggers have been identified. Over time, episodes of active disease reduce in frequency and severity.
Herpes simplex should not be confused with conditions caused by other viruses in the herpesviridae family such as herpes zoster, which is a viral disease caused by varicella zoster virus. Oral herpes is easily diagnosed if the patient presents with visible sores or ulcers. Early stages of orofacial herpes and genital herpes are harder to diagnose; laboratory testing is usually required.
The painful clusters of blisters reappear, usually in the same area, with agonizing regularity. Once the disease has been contracted, the patient is infected for life. However, after several years, some people will become perpetually asymptomatic and will no longer experience outbreaks, though they may still be contagious to others.
HSV remains dormant in the lower spinal column, ready to migrate down the sensory nerves to the skin during lower immunity, and any herpes treatment must address this as well. Vaccines are in clinical trials but have not demonstrated effectiveness. Treatments can reduce viral reproduction and shedding, prevent the virus from entering the skin, and alleviate the severity of symptomatic episodes.
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