Varicella Zoster Virus: Epidemiology, Impact and Prevention

The Varicella-Zoster Virus (VZV) is part of the alphaherpesvirus subfamily consisting of HSV-1 and HSV-2, it has a nucleocapsid that covers the inner core. The core has the linear DNA genome that is double-stranded with the protein tegument separating the capsid from the lipid envelope.

After the initial exposure to the virus, it undergoes a latency period in the body and may be reactivated later in life when encouraging conditions prevail to cause zoster.

The route and the source of transmission of VZV are not well understood. The lesions in the skin contain infectious virus particles and in contrast, it is difficult in isolating the virus from the upper respiratory tract.

The spread of the virus in the body has no ill effects on a healthy person but in immunocompromised people and the neonates may cause fatal infections of the brain or the lungs.

Recurrency of infection occurs after many years in 10-20% of individuals especially in individuals whose immunity status is compromised by diseases such as AIDS. Uncomplicated varicella patients have a fever which is less than 38.6°C but occasionally may be as high as 41°C. After the appearance of each lesion and within 1-2 days, the crusting phase of the lesions begins with the clouding of the vesicular fluid.

The number of lesions associated with varicella varies in the different patients infected. They may range from very few like 10 to greater than 1500 in children who are healthy. The normal range in healthy children is 100-300 lesions. The lesions associated with varicella usually heal due to the formation of new epithelial cells at the base of each lesion. However, scarring may occur if the primary lesions appeared along a hairline or on the eyebrows.

After an initial attack by VZV, the virus never clears from the body but undergoes a latency period in the nervous system. It is only reactivated to cause shingles under conditions such as immune deficiency as a result of AIDS or chemotherapy, cancer and emotional stress. Therefore, any person who has ever had chickenpox is at risk of shingles.

The rashes associated with shingles start as tiny blisters with a red base. The new blister then continues forming for 3-5 days. Due to the occurrence of lesions on the skin, it is left bare leading to invasion by several bacterias. It is by far the most common complication of varicella. The rashes appearing after chickenpox attack are often hemorrhagic which may be at times severe as to cause death in the exposed individuals. Viral pneumonia and encephalitis are exhibited in immunocompromised individuals and are life-threatening.

Postherpetic neuralgia is a significant complication of herpes zoster. Many patients report severe pain at the lesion’s locality for the period between 2-3 weeks. Within twelve months most patients have reported improvements but some experience unending pain which may lead to suicidal contemplations. In the United States, the incident rate is 5 people in a population of 1000. This rate tends to increase with immunosuppression and to decrease as the number of children who are immunized against this disease becomes adults.

The pain associated results in loss of productive hours for the patients. The children cannot attend school while adults lose plenty of work time hours. There is a need to enhance ventilation and avoid close contact with the people who are exhibiting symptoms characteristic of varicella. This will enhance a healthy nation and reduce the morbidity of the virus in the population.

Many factors affect the host and these include; personal traits and behaviors, the genetic predisposition and the immunologic factors in the host. All these factors serve to increase the chances of the disease or the severity of its symptoms.

The agent may include biological, physical or chemical. For Varicella, it is a biological agent and is necessary for chickenpox or zoster to occur. The environment is affected by such factors as the physical, social or biological elements and they contribute to the disease process.

Primary prevention occurs before the onset of a disease and is meant to prevent the healthy but at risk from acquiring a disease. Its main purpose is to reduce incidence rates of diseases by proving prophylaxis for the diseases. Secondary prevention occurs when the disease has affected a person and care is given to reduce the effects of the disease and the disease burden. Tertiary prevention offers rehabilitative care to those recovering from ailments that may be lifelong. It is meant to enable them to live a normal life as their healthy counterparts.

Reference List

Arvin, A. (1996). Varicella Zoster Virus. Clinical Microbiology Reviews, 9 (3): 361-381

Huch, J. et al. (2010). Impact of Varicella-Zoster Virus on Dendritic Cell Subsets in Human Skin During Natural Infection. Journal of Virology. Web.

National Centre for Immunization and Respiratory Diseases-CDC (2007). Varicella and Varicella Vaccines. Epidemiology and Prevention of Vaccine-Preventable Diseases. Web.

Wong, D. (2003). Varicella Zoster Virus. Welcome to Wong’s Virology. Web.

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StudyCorgi. "Varicella Zoster Virus: Epidemiology, Impact and Prevention." February 18, 2022. https://studycorgi.com/varicella-zoster-virus-epidemiology-impact-and-prevention/.

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StudyCorgi. 2022. "Varicella Zoster Virus: Epidemiology, Impact and Prevention." February 18, 2022. https://studycorgi.com/varicella-zoster-virus-epidemiology-impact-and-prevention/.

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