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  • 19.05.2018
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Herpes virus in facial nerves

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Pathophysiology of facial nerve paralysis induced by herpes simplex virus type 1 infection.

Herpes virus in facial nerves
Herpes virus in facial nerves
Herpes virus in facial nerves
Herpes virus in facial nerves
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Facial nerve palsy after reactivation of herpes simplex virus type 1 in diabetic mice.

Herpes zoster oticus is herpes zoster virus infection of the clusters of nerve cells ganglia that control the nerves responsible for hearing and balance 8th cranial nerve and for facial movement 7th cranial nerve. Herpes zoster shingles is infection that results from a reactivation of the varicella-zoster virus, the virus that causes chickenpox. After an episode of chickenpox, this virus lies dormant in nerve roots and can be reactivated, travelling down the nerve fibers to the skin, where it causes painful sores. Most often the cause of reactivation is unknown but sometimes it occurs when the immune system is weakened, for example, by cancer, AIDS, or certain drugs.
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Facial nerve palsy after reactivation of herpes simplex virus type 1 in diabetic mice.

The frequency of antibodies to herpes zoster virus did not differ in patients and controls. A rise in antibody titer, indicating primary herpes simplex virus infection, was not found in these patients. That Bell palsy may be caused by reactivation of herpes simplex virus is suggested by 1 clinical, neurologic, laboratory, and immunologic similarities between idiopathic facial paralysis and known manifestations of reactivated herpes simplex virus infection, and 2 the known neurotropism of herpes simplex virus, including its presence in latent form in the trigeminal ganglia, and parallels with known facial paralysis due to varicella zoster virus, a closely related agent. The presence of antibodies to herpes simplex virus is the only common factor among the patients tested in this study.
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Daigrel | 22.05.2018
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