Viruses are one of the most infectious agents known to man. They have a wide host range because they can cause infection in plants, animals, humans, bacteria and even archaea. As diverse as their host range is, they are limited in that they can only replicate inside of a host cell. Once they find a host cell and are able to replicate, they either become dormant for a period of time, living in the host without causing infection, or they cause infection, and in some cases death, and are then transmitted to a new host. Viruses can be transmitted from any host but is most often transmitted from human to human, animal to human, or insects such as mosquitoes. Mosquitoes are unique viral hosts called carriers, meaning that they can transmit the disease although it does not cause infection within the host. West Nile virus is one example of several viruses transmitted by mosquitoes that infect and kill humans, animals or both. The origin of the name West Nile virus comes from the virus first being isolated from a woman located in the West Nile District of Uganda in 19375. West Nile virus, which primarily causes infection in birds, horses and humans, causes fever and rash. In severe cases, it causes encephalitis, or inflammation of the brain, that can lead to death. Since its discovery, West Nile virus has caused hundreds of human deaths and thousands of animal deaths, primarily of birds and horses. To date, there are no vaccines or other treatments for West Nile virus. To understand why there is no viable vaccine or treatment for West Nile virus, it is necessary to study the genome, structure, life cycle, and the pathogenicity of the virus.
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West Nile Virus is a class IV, positive-sense, single-stranded RNA virus of approximately 10,000-11,000 bases belonging to the family Flaviviridae. Flaviviruses are commonly 40-60nm, enveloped, and have an icosahedral-shaped nucleocapsid2. Flaviviruses package their positive-strand RNA genome into particles consisting of a rigid outer protein shell and an underlying lipid membrane. The major envelope glycoprotein, E, and a small membrane protein, M, form the outer shell. C-terminal-helical hairpins anchor E and M in the lipid membrane. The most important step in the viral life cycle is attachment to a host cell. The virus must attach to a host cell by binding to a receptor on the cell surface. If the virus cannot bind to a receptor, it cannot enter into the cell and replicate and will be detected and destroyed by the host's immune system. For West Nile virus, the major envelope glycoprotein, E, is responsible for receptor binding. Receptor binding directs the virus to the endocytic pathway. Once flaviviruses reach an endosome, they must fuse their lipid membrane with the host cell membrane in order to deliver the viral genome into the cytoplasm for replication. When the pH of an endosome decreases, a conformational rearrangement occurs in E, which delivers the energy required for membrane fusion by bending the two membranes towards each other, inducing them to fuse 3. After uncoating, translation of the genomic RNA occurs in the cytoplasm. The translation product is a polyprotein precursor that is later cleaved to produce mature proteins. Replicase proteins use plus strand genomic RNA as a template to make complementary minus-strands. The complementary strand is then used to make more plus-strand genomic RNA. After replication, viral proteins assemble capsids around the newly synthesized genomic RNA. Before egress can occur, viruses must undergo a maturation step. In this maturation step, proteases cleave pre-membrane protein, which results in the reorganization of E protein into a pseudo-icosahedral arrangement that is characteristic of mature viruses. Once the newly synthesized viruses are mature, they lyse the host cell and travel to infect new host cells8.
West Nile virus is typically asymptomatic but as the infection progresses, the infected person or animal will experience fever, rash, and encephalitis, or inflammation of the brain. West Nile encephalitis has an incubation period of 3 - 12 days and can lead to severe brain damage or death5. Antigen-presenting cells (APC) such as macrophages and dendritic cells are the most peripheral components of a host immune response, facilitating both the destruction of invaders and initiation of pathogen recognition. This is significant because they are also the primary sites of infection. West Nile virus can also infect cells in the brain and surrounding cerebrospinal fluid, causing the onset of encephalitis. During transmission, West Nile virus is intimately associated with mosquito saliva. Mosquito saliva dysregulates antigen-presenting cells (APC) antiviral signaling, and reveal a possible mechanism for the observed enhancement of viral pathogenicity. Results of in vivo studies indicate that the predominant effect of mosquito feeding is to significantly reduce the recruitment of CD4+ T cells, increasing mortality and decreasing division rates4. Follow-up studies of patients that were infected with West Nile virus showed that they suffer from memory problems, loss of balance and tremors, all of which can span the rest of the patient's lifetime. Some of the patients have also exhibited a persistence of the symptoms of the virus, such as fever. Researchers hypothesize that if an infected person does not recover within the first two years after initial infection, they may never recover. Studies have shown that up to 40% of infected patients still exhibit symptoms for up to five years after initial infection7. The persistence of symptoms and nervous system damage in infected patients shows that West Nile virus is a highly virulent pathogen.
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Currently, there is no West Nile virus vaccine available for humans. There is a vaccine for horses but the effectiveness of this vaccine in preventing West Nile virus infections has yet to be fully evaluated2. There are no antibiotics or antiviral medications that can be used in the treatment of West Nile virus, therefore all care is supportive. The best ways to prevent West Nile virus infection is to use personal protection while outdoors when mosquitoes are present, identify disease activity in birds and mosquitoes in time to warn the public, eliminate places for mosquitoes to breed, treat standing water sources that cannot be eliminated in order to kill the immature mosquito, and spray for adult mosquitoes when deemed necessary6. In order to prevent future epidemics, mosquito populations are being monitored for density, species, and presence of West Nile Virus5. The prognoses of disease with and without treatment are dependent upon the extent of the infection. Patients that have fever and do not undergo treatment are likely to experience fever for a few years past initial infection. Patients that have encephalitis and do not undergo treatment suffer from permanent impairment or death. There are no vaccines or treatments for humans, therefore the prognoses for treated patients are unknown.
Culex tarsalis is currently the main vector of West Nile virus in the United States. This virus is spread via mosquitoes that have fed upon birds that harboring the virus. The mosquitoes then acquire the virus from the birds and transmit the disease via biting humans or animals. Over 200 species of birds, several mammals, and even a few reptiles have been found positive for West Nile virus in surveillance efforts. Human and horses are "dead-end hosts" that cannot transmit the virus to further species5. West Nile virus has been endemic in several locations including North America, Africa, the Indian subcontinent, the Middle East, the former Soviet Union, and Europe. The emergence and/or reemergence of West Nile virus is attributed to human travel and migration, and ecological factors such as a drought. In 2002, West Nile virus was reported as being transmitted by blood transfusion, organ transplantation, transplacental transfer and breastfeeding5. While everyone exposed to a mosquito that carries the virus is susceptible, people older than 50, or more specifically, those who are immune-compromised, are at greatest risk6. In 2005, an outbreak of West Nile virus disease occurred in Sacramento County, California in which 163 human cases were reported. In response to surveillance indicating increased West Nile virus activity, the Sacramento-Yolo Mosquito and Vector Control District conducted an emergency aerial spray. The economic impact of the outbreak, including the vector control event and the medical cost to treat West Nile virus infections, was determined to be approximately $2.28 million for medical treatment and loss of patients' productivity for patients affected by both fever and encephalitis. Vector control costs were approximately $701,790, including spray procedures and overtime hours of the workers. The total economic impact of West Nile virus in this outbreak was approximately $2.98 million1. This example of economical impact of West Nile virus in Sacramento County is representative of how West Nile epidemics have affected communities worldwide.
West Nile virus is constantly undergoing changes in its structural proteins, allowing it to be evasive and continue causing infections and deaths. Like several other viruses without a vaccine or treatment, West Nile virus is very detrimental in endemic populations, and until an effective vaccine is developed, there is always a risk for a new strain of the virus to evolve and cause an outbreak. Even if a human vaccine and viable animal vaccine existed, it is impossible to capture all mosquitoes that may be carriers for the disease; therefore, it is impossible to eradicate the virus. Until a vaccine is developed, the best way to protect against West Nile virus is to take precaution when in areas endemic to the virus, monitor mosquito populations and always be aware of developments with not only West Nile virus, but other flaviviruses and viruses alike.
1. Barber, Loren M., et al. "Economic Cost Analysis of West Nile Virus Outbreak, Sacramento
County, California, USA, 2005." Emerging Infectious Diseases 16 (March 2010): 480-486.
2. Center for Disease Control. "Virology: Classification of West Nile Virus." www.cdc.gov.
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CDC, Web (Last modified): 2 July 2003.
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