The Biology of West Nile Virus

Introduction

The West Nile Virus is a mosquito-borne infectious disease from the genus Flavivirus in the family Flaviviridae. The virus was first identified in 1937 in Uganda and was introduced to the West in 1999 when it was announced as a global public health issue. When introduced to the human body, the Flavivirus replicates in the infected cells’ cytoplasm where it alters the cell environment of the host. The isolates of WNV contain one serotype and are mostly grouped into two lineages: (1) substitutions of signature amino acids and (2) envelope protein sequence deletions (Brinton, 2013). WNV is of importance, as it is presently the most significant mosquito-borne pathogen in the West and particularly Europe (Rudolf et al., 2017).

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Replication Cycle of WNV

The cycle starts with the WNV attaching to the cell surface through receptor-mediated endocytosis. This is through the assistance of WNV’s cell receptors that comprise of several glycosaminoglycans, mannose receptor, and DC-SIGN. This is followed by the maturation of the virus contained in the endosome (characterized by a drop in pH) and as the endosome matures the pH continues to drop to a more acidic environment. A conformational change follows where the viral lipid membrane fuses with the endocytic membrane, releasing the viral RNA genome into the cell cytoplasm. Li et al., (2013) explain that the process uses a well-documented program where there is a replication of the RNA genome and virus assembly, which follows the capsid disassociation.

Capsid disassociation is followed by the translation of viral polyprotein intracellular membranes causing the 10 viral protein’s expression. The cellular and viral proteins replicate the RNA to form replicas that are applied in the formation of new virions. On the endoplasmic reticulum membrane, there is an accumulation of structural proteins where they relate with the nucleocapsid and through the Golgi network, they bud into the cytoplasm.  Finally, the virus matures in an exocytic vesicle through the cleaving of the cellular enzyme in the prM. 

Epidemiology of WNV

Chancey et al., (2015) explains that epidemiology is primarily transmitted through a mosquito bite from the genus Flavivirus in the family Flaviviridae. The flavivirus acquires the virus by feeding on infected birds with transmission intensity depending on the number, the feeding patterns of infected Flavivirus, and the local behavior and the ecology influencing humans to the mosquito’s exposure. Li et al., (2013) explain that there are recorded epidemics in Africa with a high percentage of 55 but there are recent outbreaks in North America and Europe. WNV outbreaks recorded in the Middle East and Europe since 1999 are less than 5% while those recorded in Queens New York since 1999 are approximately 2.6% (Li et al., 2013). However, Mann et al. (2013) argue that the levels of infections are to modulate the intensity of epidemics through protective immunity or to reduce the frequency of epidemics. 

Lan et al. (2012) explain that there lack records of the incidence of the virus in most parts of the world. However, incidences have been recorded in the Caribbean, parts of Central America, North America, Australia, Asia, India, Africa, the Middle East, and in Europe.  Frost et al. (2012) explain that WNV incidences are seasonal in the temperate zones in Mediterranean Basin, Europe, and North America. However, Mann et al (2013) note that the transmission season in the U.S. has increased, as the rate moved South while in the South part of Africa, the incidence increases during the first months of the year following the heavy summer and spring rainfall. 

Pathology of WNV

Swanson and McGavern (2015) explain that the WNV replicates at the inoculation site where it then moves to the lymph nodes, as well as the bloodstream. This is followed by the stimulation of receptors, which are toll-like while the virus penetrates to the central nervous system. In turn, this increases levels of tumor necrosis factor-α, increasing the blood-brain barrier’s permeability. Swanson and McGavern also add that the gray matter and the deep nuclei neurons of the spinal cord, brainstem, and brain are infected by the virus. Paralysis, as Chancey et al. (2015) explain may occur due to collateral destruction of bystander nerve cells

Alternative/new control strategies

Frost et al. (2012) explain that mosquitos are managed following integrated vector management (IVM) or mosquito management (IMM). According to Chancey et al. (2015), the IMM combines the prevention and control measures of mosquitoes by following the biology of the mosquito, the spread of mosquitoes, and their life cycle. The first step is by conducting surveillance, which helps in the identification of the number of mosquitoes and their type. This is followed by eliminating breeding areas through community clean up. Later, measures to control the larvae and pupae through the removal of any stagnant or standing water are initiated. Lastly, insecticides are used to control adult mosquitoes (adulticides). 

Conclusion

West Nile Virus is a mosquito-borne virus that is transmitted by a bite of an infected Flavivirus after sucking blood from infected birds. It affects several areas in the world like North America, Africa, India, and Europe. However, the incidences are seasonal where it occurs after heavy rain falls. The infection process follows a replicating cycle from cell attachment to the maturation in the prM. Fortunately, the virus can be controlled through integrated vector management (IVM) or mosquito management (IMM), which eliminates the virus from its breeding sites, eggs, the pupae, and the adult stage. 

References

Brinton, M. (2013). Replication Cycle and Molecular Biology of the West Nile Virus. Viruses6(1), 13-53. doi: 10.3390/v6010013

Chancey, C., Grinev, A., Volkova, E., & Rios, M. (2015). The Global Ecology and Epidemiology of West Nile Virus. Biomed Research International2015, 1-20. doi: 10.1155/2015/376230

Frost, M., Zhang, J., Edmonds, J., Prow, N., Gu, X., & Davis, R. et al. (2012). Characterization of Virulent West Nile Virus Kunjin Strain, Australia, 2011. Emerging Infectious Diseases18(5). doi: 10.3201/eid1805.111720

Lan, D., Wang, C., Deng, B., Zhou, J., Cui, L., & Tang, C. et al. (2012). Serological investigations on West Nile virus in birds and horses in Shanghai, China. Epidemiology And Infection141(3), 596-600. doi: 10.1017/s0950268812001094

Li, X., Fu, S., Liu, W., Wang, H., Lu, Z., & Tong, S. et al. (2013). West Nile Virus Infection in Xinjiang, China. Vector-Borne And Zoonotic Diseases13(2), 131-133. doi: 10.1089/vbz.2012.0995

Mann, R., Fegan, M., O’Riley, K., Motha, J., & Warner, S. (2013). Molecular characterization and phylogenetic analysis of Murray Valley encephalitis virus and West Nile virus (Kunjin subtype) from an arbovirus disease outbreak in horses in Victoria, Australia, in 2011. Journal Of Veterinary Diagnostic Investigation25(1), 35-44. doi: 10.1177/1040638712467985

Rudolf, I., Betášová, L., Blažejová, H., Venclíková, K., Straková, P., & Šebesta, O. et al. (2017). West Nile virus in overwintering mosquitoes, central Europe. Parasites & Vectors10(1). doi: 10.1186/s13071-017-2399-7Swanson II, P. A., & McGavern, D. B. (2015). Viral diseases of the central nervous system. Current opinion in virology11, 44-54.

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