Epidemiology of Varicella Zoster Virus

Varicella-zoster virus

Varicella-zoster virus is a virus that belongs to the herpesviruses group. It is a DNA virus which is single and double-stranded with a linear duplex DNA molecule which is centrally located. Its genome consists of two isomers containing the prototype, segment, and the inverted segment. The predominance of the isomers is influenced by the orientation of the prototype, segment, and the inverted segment. The virions of the virus are spherical with an approximate diameter of 190nm (Zerboni et al., 2014). It has capsomeres in its nucleoplasid which are icosahedral in shape. The capsid has tegument proteins surrounding it which are responsible for reproduction process of the virus in cells which it infects.

Virulence Factors

The most essential mechanism of virulence of this virus is its ability to form a latent infection in the host within the dorsal root ganglia. The latency gives the virus the ability to infect the host after it re-emerges through reactivation of its viral pathogenesis (Kennedy et al., 2015). The varicella-zoster virus must be able to evade the host immunity during its replication process to form a re-infection. The immunity of the host also plays a role in the virulence of the virus for reactivation more especially from its latent state (Kennedy et al., 2015). Antiviral immunity of the T cells is very crucial in fighting against the reactivation of the virus from the dorsal root ganglia. Individuals who have a low immunity with a low cell count of T cells are at risk of infection because the virus is able to evade the antiviral immunity by the T cells.

Immunity

The innate immunity is responsible for the protection of the host from the initial infection of the virus which is a naturally acquired infection. The innate immunity system works through the activation of Natural Killer cells and antiviral cytokines which work to curb the infection at the sites of inoculation as well as initiate another immune response by the adaptive immune system. The NK cells control the spread of the infection by lysing the cells infected (Gershon, et al., 2015). The innate immunity is also activated by T cells that are specific to Varicella zoster virus and prevents the spread of the infection utilizing the MHC I and MHC II cells (Kennedy et al., 2015). However, the evasion mechanisms of the virus, delay the response from acquired immunity. The adaptive immune system also responses to the infection by making IgM and IgG antibodies from B cells that are specific to the virus. CD4 and CD8 cells are also formed from IgA antibodies to create a memory response to the virus. If the virus evades these mechanisms, it then forms a latent state in the dorsal root ganglia. T cells are essential at this stage in preventing reactivation of the virus from latency.

Infectious Disease Infection

Varicella-Zoster virus is the causative agent for chickenpox also known as varicella. The disease commonly affects young children but can also affect adults in form of shingles also called herpes zoster. It mostly affects the skin with a rash appearing on the head and progresses to the trunk and extremities. If the disease is left untreated, it complicates to cause infections like pneumonia, bleeding tendencies, encephalitis, and Group A streptococcal skin infections in children. The complications are more likely to occur in individuals with a low immunity. The virus is also reactivated from latency in the dorsal root ganglia during states of immune-suppression to cause shingles in adults.

Epidemiology

Varicella-zoster virus is a contagious transmitted through inhalation when infected people cough or sneeze. It can also be obtained through direct contact with infected individual’s saliva, mucus or blisters. Indirect contact with contaminated objects and items like clothing of infected people can also spread the disease. The reservoir of the virus is human.

Presentations

A patient who is infected with Varicella zoster virus will present with a generalized body rash that is itching for two to four days. The patient reports of the rash appearing on the head and progresses to the trunk and eventually to the extremities (Gershon, et al., 2015). The rash forms vesicles that form pus and then rapture and become dry with more concentration on the trunk. The patient may also present with macular lesions alongside the skin vesicles. Children will present with fevers up to 102F accompanied with malaise and itching. Adults will present with rashes that form painful blisters on the skin for a period of two to three weeks. They may also complain of a headache and have a fever.

Prevention

Varicella is preventable using the varicella vaccine which enables the body to produce antibodies against the virus. The vaccine is administered to an individual who has attained 12 months or older and has not been infected with chickenpox (Baird et al., 2015). Older adults beyond the age of 50 years receive Zostervax vaccine to immunize against herpes zoster.

Treatment

The drug of choice for treatment of chickenpox is Acyclovir (CDC, 2018). It is an antiviral drug that acts as an analog to deoxyguanosine triphosphate (dGTP) which inhibits varicella-zoster virus DNA polymerase. Other antivirals recommended are famiclovyr and valacrovyr. However, antivirals are used in individuals at risk of developing complications. Acetaminophen is also used to relieve fever and pain. Home remedies used include; applying lotions, over-the-counter antihistamines, warm baths and keeping nails short while avoiding scratching the blisters (CDC, 2018).

Clinical Relevance

There are no Multi-drug Resistance strains of the organism. Laboratory technicians are at risk of getting contaminated with the virus more especially during specimen collection and handling. Nurses are also at risk of direct and indirect contact of the virus when giving health care in hospital for patients infected with chicken pox.

References

Baird, N. L., Bowlin, J. L., Nagel, M. A., Gilden, D., Arvin, A. M., & Newland, J. G. (2015). Varicella zoster virus. Antimicrobial Therapy and Vaccines, Antimicrobial Agents, 3rd Edition,(VL Yu, ed.), Oxford University Press, Pittsburgh, PA.

Chickenpox | CDC. (2018). Retrieved from https://www.cdc.gov/chickenpox/index.html

Gershon, A. A., Breuer, J., Cohen, J. I., Cohrs, R. J., Gershon, M. D., Gilden, D., ... & Seward, J. F. (2015). Varicella zoster virus infection. Nature reviews Disease primers, 1, 15016.

Gilden, D., Nagel, M., Cohrs, R., Mahalingam, R., & Baird, N. (2015). Varicella zoster virus in the nervous system. F1000Research, 4.

Kennedy, P. G., Rovnak, J., Badani, H., & Cohrs, R. J. (2015). A comparison of herpes simplex virus type 1 and varicella-zoster virus latency and reactivation. Journal of General Virology, 96(7), 1581-1602.

Zerboni, L., Sen, N., Oliver, S. L., & Arvin, A. M. (2014). Molecular mechanisms of varicella zoster virus pathogenesis. Nature reviews microbiology, 12(3), 197.