Herpes is a term that is very loosely used in day-to-day conversation and should actually be spoken of with more specificity. The disease Herpes virus hominis or herpes simplex virus (HSV) (also known as Cold Sore, Night Fever, or Fever Blister) caused by the herpes simplex viruses 1 and herpes simplex virus 2, occurring worldwide is one of the most common agents infecting humans of all ages. The herpes simplex viruses [HSV] are DNA viruses capable of producing a variety of illnesses, including mucocutaneous infections, infections of the CNS, and occasionally infections of the visceral organs.
- Types of Human Herpes Virus
- HHV 1 – Herpes Simplex Virus 1 (HSV 1)
- HHV 2 – Herpes Simplex Virus 2 (HSV 2)
- HHV 3 -Herpes Zoster Virus (VZV)
- HHV 4 – Ebstein Barr Virus (EBV)
- HHV 5 – Cytomegolovirus (CMV)
- HHV 6 – Human B-cell Lymphotrophic
- HHV 7 – Causes Symptoms Similar to the HHV-6
- HHV 8 – It is a Type of Rhadinovirus
Pathology of Herpes Simplex The vesicles [fluid filled eruptions] are inside the epidermis of the skin. Reticular degeneration of the epidermal cells with acantholysis can be seen on histopathological examination. The herpes viruses are known to produce cellular changes that cause infiltration of typical multinucleate giant cells within the lesions.
The Herpes Simplex Virus (HSV) is a virus that manifests itself in two common viral infections, each marked by painful, watery blisters in the skin or mucous membranes (such as the mouth or lips) or on the genitals. The disease is contagious, particularly during an outbreak, and is incurable with present technology. During this time, the asymptomatic person should be extremely careful (washing hands frequently; not touch the blister area, etc.) since transmission is still possible. An infection on the lips is commonly known as a “cold sore” or “fever blister”. These are sometimes confused with canker sores or Apthous ulcers which have a similar appearance; these appear inside the mouth and are not caused by the herpes simplex virus.HSV tend to infect cells of ectodermal origin. After direct exposure to infectious material (i.e. saliva, genital secretions), initial viral replication occurs at the entry site in the skin or mucous membrane.
The Biological Properties of HSV that control the course of infection are neuroinvasiveness (the ability of the virus to invade the brain), its neurotoxicity (its ability to multiply and destroy the brain), and its latency (its ability to remain in a nonreplicating form in the dorsal root ganglia of the CNS). After retrograde axonal flow from neurons at the viral point of entry and local replication, the viral genome becomes latent. No viral particles are produced during latency. In rare cases, the initial replication may lead to disease and life-threatening infection (e.g. encephalitis). After the initial nonspecific inflammatory response to primary infection, specific antibody response occurs in a few days, followed by a cellular immune response in the second or third week. In persons with cellular immune defects, primary HSV infection can result in life-threatening disseminated disease. A stimulus (e.g. physical or emotional stress, fever, ultraviolet light) reactivates the virus in the form of skin vesicles or mucosal ulcers, with symptoms less severe than those of the primary infection. Latent HSV can be reactivated from the trigeminal, sacral, and vagal ganglia.
Symptoms caused by HSV 1 infection (HSV 1 is known to affect the following areas of the body.)
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