Don't spray aerosol or pump products in enclosed areas. Don't apply aerosol or pump products directly to your face. Spray your hands and then rub them carefully over the face, avoiding your eyes and mouth. Some experts suggest that it's acceptable to apply repellent with low concentrations of DEET to infants older than age 2 months. For children younger than age 2, only one application per day of repellent containing DEET is recommended.
When using repellent on a child, apply it to your own hands and then rub them on your child. Avoid children's eyes and mouth and use the repellent sparingly around their ears. Don't apply repellent to children's hands because children tend to put their hands in their mouths. Don't allow a young child to apply his or her own insect repellent. Keep repellents out of reach of children.
Don't apply repellent to skin under clothing. If repellent is applied to clothing, wash treated clothing before wearing again. Always consult your healthcare provider for more information. When should I call my healthcare provider? However, if any of the following serious symptoms develop, seek medical attention right away: High fever Severe headache Stiff neck Confusion Muscle weakness Vision loss Numbness Paralysis Tremors Seizures Coma Key points Humans get West Nile from the bite of an infected mosquito.
The virus can cause life-threatening illnesses, such as encephalitis, meningitis, or meningoencephalitis.
There is no vaccine available to prevent West Nile virus. So, it is important to avoid mosquito bites. Next steps Tips to help you get the most from a visit to your healthcare provider: Know the reason for your visit and what you want to happen. Before your visit, write down questions you want answered. Bring someone with you to help you ask questions and remember what your provider tells you.
At the visit, write down the name of a new diagnosis, and any new medicines, treatments, or tests. Also write down any new instructions your provider gives you. Know why a new medicine or treatment is prescribed, and how it will help you.
Research is currently being done on interferon therapy for West Nile virus. Interferon therapy is aimed at using substances produced by your immune system to treat encephalitis in people infected by West Nile virus. Your doctor may discuss one or more of these treatments with you if you have encephalitis and your symptoms are severe or life-threatening. West Nile virus is most commonly spread during the summer, especially between June and September. Around 20 percent of infected people will show some fever symptoms, such as headaches, vomiting, and diarrhea.
These symptoms usually pass quickly. Some symptoms, such as fatigue, can continue for up to several months after the initial infection. Fewer than one percent of people who get West Nile virus infections develop severe symptoms or neurological conditions such as meningitis or encephalitis.
Of these cases, fewer than 10 percent are fatal. Every mosquito bite increases your risk of infection. These steps can help you prevent West Nile virus each time you are outdoors:. Mosquito bites are most common in late August to early September. Report any dead birds you see to your local health agency. Dead birds can easily pass the West Nile virus on to mosquitos, which can pass it to humans even with a single bite.
If any signs of the virus are found in the area around the bird, the health agency will likely increase pest control activity or pesticide use. Though a vaccine exists to protect horses against West Nile virus, there is no vaccine for people. Supportive care during a West Nile virus infection, especially a severe one, is important to survival. But immediate and consistent treatment is the best way to make sure that your symptoms remain mild.
This is especially true if you have certain risk factors, such as old age or certain medical conditions. Mosquito bites are round, usually puffy, and severely itchy.
Seek medical attention right away if you have signs or symptoms of serious infection, such as severe headaches, a stiff neck, disorientation or confusion. A serious infection generally needs hospitalization. When a mosquito bites an infected bird, the virus enters the mosquito's bloodstream and eventually moves into its salivary glands. When an infected mosquito bites an animal or a human host , the virus is passed into the host's bloodstream, where it may cause serious illness.
West Nile virus generally spreads to humans and animals from bites of infected mosquitoes. Mosquitoes get infected and carry the virus after biting infected birds. You can't get infected from casual contact with an infected person or animal. Most West Nile virus infections happen during warm weather, when mosquitoes are active.
The incubation period — the period between when you're bitten by an infected mosquito and the appearance of signs and symptoms of the illness — generally ranges from four to 10 days.
It appeared in the United States in the summer of , and since then has been reported in every state — except Hawaii and Alaska — as well as in Canada. In a few cases, West Nile virus might have spread through other routes, including organ transplants and blood transfusions. However, blood donors are screened for the virus, greatly reducing the risk of infection from blood transfusions.
There also have been reports of some transmission of the virus from mother to child during pregnancy or breastfeeding or exposure to the virus in a lab, but these are rare.
These innate pathways are critical not only for immediate antiviral defense pathways such as the upregulation of type I interferons but also for the generation of an effective adaptive T and B cell-mediated sustained immune response 24 , 53a , , , , , Specific human genetic factors that influence the severity of infection with WNV and the antiviral innate immune response have been identified Table 2.
Single nucleotide polymorphism SNP studies have detected SNPs in key regulators of immune function, including interferon pathway elements. A dominant negative splice variant of RNase L, which functions in the antiproliferative roles of interferon, was detected more often in WNV patients than in control patients In addition, a deletion in CCR5, which is known to be protective in infection with HIV, while not associated with susceptibility to WNV, did correspond to severity of infection, presumably due to reduced function of CCR5 pathways in infected hosts 69 , , As more host factors are identified, there are sure to be a number of new determinants of WNV infection.
Current therapeutic options against WNV are mainly supportive; there are no FDA-approved vaccines or treatments available Investigations to identify individual susceptibility markers, recombinant antibodies, peptides, RNA interference, and small molecules with the ability to directly or indirectly neutralize WNV have been reported; however, an effective drug is still lacking 6 , 12 , 70 , 71 , 74 , , There are currently four USDA-licensed vaccines available for equines two are inactivated whole WNV, one is a nonreplicating live canary pox recombinant vector vaccine, and one is an inactivated flavivirus chimeric vaccine.
Though passive immunization has been used in a few cases, it has serious limitations, such as inadvertent transfer of blood-borne pathogens, inconsistent quality of the donor antisera, cost, and allergic reactions A case study of two WNV encephalitis patients treated with alpha interferon, the standard of care for infection with the related flavivirus hepatitis C virus, showed substantial improvement and an improved convalescence course Several approaches are being pursued for the development of a vaccine in humans that may prove valuable for use by targeted populations.
Investigations include live attenuated vaccines, recombinant subunit vaccines, vectorized vaccines, DNA vaccines with constructs that express the WNV E protein, live recombinant vaccines, and an attenuated strain based on nonglycosylated E and mutant NS1 proteins 15 , It was shown to be safe and immunogenic in phase II clinical trials, with high seroconversion rates, but it is no longer available WNV has now persisted and become established in North America.
Of particular significance is the expansion of the mosquito vectors harboring WNV to include Aedes albopictus , a common mammal-biting mosquito 2 , 73 , It is hoped that the increase in our knowledge of the interactions of WNV with the mosquito vector will lead to new avenues for therapeutics and preventative measures. Mosquito responses at the levels of protein and gene expression as well as a more complete understanding of viral pathogenesis in the vector, especially with regard to the immune response, may point to novel targets to focus our efforts to inhibit or block WNV infection in both mosquitoes and mammals.
For example, a single-chain human monoclonal antibody developed through phage display directed against the fusion loop of the envelope protein showed both pan-flaviviral protection and therapeutic efficacy when tested in the murine model 71 , Recent advances in nanoparticle technology have also been employed in vaccination studies of murine WNV infection and show promising efficacy of TLR9-targeted biodegradable nanoparticles, which produce a high number of circulating effector T cells and antigen-specific lymphocytes Potential relevant viral susceptibility mechanisms, including host antagonism of chemokine responses as has been noted in infection with the related flavivirus hepatitis C virus 35 , may reveal infectious mechanisms used by WNV and other mosquito-borne flaviviruses.
The pace of discovery of vector, virus, and host components of pathogenesis continues to provide critical insights for the successful development of controls and treatments for WNV. We are grateful to our long-standing colleague John F.
C is supported by grant 5T32AI Tonya M. Colpitts received a B. Her research focuses on the exploration of the interactions between mosquitoes and flaviviruses, the identification of human host factors that bind flaviviral proteins, and the examination of how flavivirus infection affects proteins and pathways of human cells.
She is also researching the interactions of flavivirus capsid protein with nuclear and cytoplasmic proteins as well as the role of capsid in the nucleus of the cell during infection.
Michael J. Conway received a B. His current research interests involve vector-virus-host interactions that occur as disease vectors deposit salivary components and pathogens into the host. Ruth R. Montgomery received a B. After postdoctoral work on macrophage endocytosis with Ira Mellman, she remained at Yale, where she is now Associate Professor of Medicine. The focus of her lab is human innate immunity, specifically the interaction of macrophages, neutrophils, and dendritic cells with pathogens such as West Nile virus and the agent of Lyme disease, Borrelia burgdorferi , including elucidating effects of vector saliva on phagocyte function.
In studies of the pathogenesis of West Nile virus, the Montgomery lab has described inhibition of macrophage function, an unexpected biphasic role for PMNs in infection, and effects of aging on innate immunity, including dysregulation of TLR3 responses in macrophages and reduced responses of dendritic cells to infection with West Nile virus.
Erol Fikrig received a B. Fikrig did a residency in internal medicine at Vanderbilt University School of Medicine and was a fellow in infectious diseases and immunobiology at Yale University School of Medicine. He currently leads a research group studying the immunopathogenesis of arthropod-borne diseases. Lyme disease, human granulocytic anaplasmosis, and West Nile encephalitis are areas of particular interest.
Studies are directed at understanding the interactions between pathogen, host, and vector that result in virulence and transmission and the molecular basis of disease in animal models and patient populations. National Center for Biotechnology Information , U. Journal List Clin Microbiol Rev v. Clin Microbiol Rev.
Author information Copyright and License information Disclaimer. Corresponding author. Address correspondence to Erol Fikrig, ude. All Rights Reserved.
This article has been cited by other articles in PMC. Abstract Summary: West Nile Virus was introduced into the Western Hemisphere during the late summer of and has been causing significant and sometimes severe human diseases since that time.
Life Cycle Entry of WNV is through receptor-mediated endocytosis after virus attachment to the cell surface. Open in a separate window. Fig 1. Vector Response to Infection There have been many recent studies aimed at elucidating the transcriptomic and proteomic response to flavivirus infection in the mosquito vector. Transmission to Vertebrate Host WNV is transmitted to its vertebrate hosts by an infected mosquito vector during the probing process of blood feeding.
Mosquito Saliva Factors Saliva from hematophagous insects has been shown to alter the transmissibility of many pathogens 1 , 50 , , , , , , Diagnostics The diagnosis of WNV infection is based largely on clinical criteria and testing for antibody responses Immune Response Control of WNV infection by the human and murine hosts has been investigated for both innate and adaptive immune responses.
Table 1 In vivo function of murine genes in WNV infection. Genetic Determinants of Disease Specific human genetic factors that influence the severity of infection with WNV and the antiviral innate immune response have been identified Table 2.
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