Viruses reactivate years to decades later as

Viruses are small particles capable of infecting a cell and potentially causing diseases.

They are microscopic, smaller than bacteria and lack the capacity to thrive and reproduce outside the host body. The infected cell is called the “host cell”. Due to their smallness, most viruses can only be visualized using an electronic microscope.Chickenpox is a highly contagious disease caused by primary infection with Varicella Zoster virus (VZV). Varicella zoster virus (VZV) is an exclusively human virus that belongs to the ?-herpesvirus family. VZV is present worldwide and is highly infectious.

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Primary infection leads to acute varicella or “chickenpox”, usually from exposure either through direct contact with a skin lesion or through airborne spread from respiratory droplets (Sawyer, Chamberlin, Wu, Aintablian and Wallace, 1994), (Gnann and Whitley, 2002). According to Gilden, Kleinschmidt-DeMasters, LaGuardia, Mahalingam and Cohrs, 2000, after initial infection, VZV establishes lifelong latency in cranial nerve and dorsal root ganglia, and can reactivate years to decades later as herpes zoster (HZ) or “shingles”. Shingles is more predominant in adults or in immunocompromised patients and can be more severe. This isn’t really common but can be associated in adults with infections such as pneumonia, hepatitis and encephalitis. More than 90% of adults in the United States acquired the disease in childhood, while the majority of children and young adults have been vaccinated with the live virus vaccine (Gnann et al.

2002)A brief history of varicella infection according to the CDC Primary varicella infection (chickenpox) was not reliably distinguished from smallpox until the end of the 19th century. In 1875, Steiner demonstrated that chickenpox was caused by an infectious agent by inoculating volunteers with the vesicular fluid from a patient with acute varicella. Clinical observations of the relationship between varicella and herpes zoster were made in 1888 by Von Bokay, when children without evidence of varicella immunity acquired varicella after contact with herpes zoster. VZV was isolated from vesicular fluid of both chickenpox and zoster lesions in cell culture by Thomas Weller in 1954. Subsequent laboratory studies of the virus led to the development of a live attenuated varicella vaccine in Japan in the 1970s. The vaccine was licensed for use in the United States in March 1995.

The first vaccine to reduce the risk of herpes zoster was licensed in May 2006.PathogenesisVZV enters the body through the respiratory tract and conjunctiva. The virus is believed to multiply at the site of entry in the nasopharynx and in regional lymph nodes.

A primary viremia occurs 4 to 6 days after infection and disseminates the virus to other organs, such as the liver, spleen, and sensory ganglia. Further replication occurs in the viscera, followed by a secondary viremia, with viral infection of the skin. Virus can be cultured from mononuclear cells of an infected person from 5 days before to 1 or 2 days after the appearance of the rash(CDC,


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