Herpoxin, herpes virus inhibitor consists of two proteins isolated from snake venom of Naja n. kaouthia, which separately and together inhibit the replication of herpes simplex viruses type 1 and type 2 in cell cultures. Herpoxin is characterized as a purified component of snake venom, of the phospholipase A2 (PhA2) enzyme family, which inhibits production of the typical cytopathogenic effects (CPE) produced by herpes viruses type 1 and type 2. Herpoxin consists of two peptides Herp-A and Herp-B having molecular weights 14,000 and 15,000 daltons, respectively, as revealed by gel electrophoresis. The partial sequence for the first fifteen N-terminal amino acids of both Herp-A and Herp-B is: Asn-Leu-Tyr-Gln-Phe-Lys-Asn-Met-Ile-Gln-Cys-Thr-Val-Pro-Asn, which will be referred to as SEQ ID No: 1. The known partial sequences for Herp-A and Herp-B proteins are identical and are typical of phospholipases. However, Herp-A and Herp-B are antigenicaily distinct. Herpoxin is claimed for its method of purification and as a treatment for herpes virus type 1 and type 2 induced oral and genital lesions and other infections. Herpoxin is further claimed as a therapeutic agent for non invasive topical application to treat other viral infections such as: herpes zoster, Kaposi sarcoma in AIDS patents, eczema, etc. It is also an object of this invention to provide Herpoxin as a composition for the treatment of skin infections induced by other microbial agents.
Herpes simplex is a viral disease caused by both Herpes simplex virus type 1 (HSV-1) and type 2 (HSV-2). Infection with the herpes virus is categorized into one of several distinct disorders based on the site of infection. Oral herpes, the visible symptoms of which are colloquially called cold sores or fever blisters, is an infection of the face or mouth. Oral herpes is the most common form of infection. Genital herpes, known simply as herpes, is the second most common form of herpes. Other disorders such as herpetic whitlow, herpes gladiatorum, ocular herpes (keratitis), cerebral herpes infection encephalitis, Mollaret's meningitis, neonatal herpes, and possibly Bell's palsy are all caused by herpes simplex viruses.
Herpes viruses cycle between periods of active disease—presenting as blisters containing infectious virus particles—that last 2–21 days, followed by a remission period. Genital herpes, however, is often asymptomatic, though viral shedding may still occur. After initial infection, the viruses are transported along sensory nerves to the sensory nerve cell bodies, where they become latent and reside life-long. Causes of recurrence are uncertain, though some potential triggers have been identified, including immunosuppressant drugs. The previously latent virus then multiplies new virus particles in the nerve cell and these are transported along the axon of each neuron to the nerve terminals in the skin, where they are released. Over time, episodes of active disease reduce in frequency and severity.
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