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Arbovirus is an informal name for any virus that is transmitted by arthropod vectors. The term arbovirus is a portmanteau word ( arthropod- borne virus). Tibovirus ( tick- borne virus) is sometimes used to more specifically describe viruses transmitted by , a superorder within the arthropods. Arboviruses can affect both animals (including humans) and plants. In humans, symptoms of arbovirus infection usually occur 3–15 days after exposure to the virus and last three or four days. The most common clinical features of infection are fever, headache, and malaise, but other features of viral hemorrhagic fever syndrome and encephalitis may also occur.
| Dengue virus | Dengue fever | 3–14 days | Asymptomatic in most cases; fever, headache, rash, muscle, and joint pains | 7–10 days | Shock, internal bleeding, and organ damage | <1% with treatment, 1–5% without; about 25% in severe cases | Aedes mosquitoes, especially Aedes aegypti | Humans | Near the equator globally | VariesInfection provides lifelong immunity to the specific serotype causing illness, but temporary immunity to other serotypes. |
| Japanese encephalitis virus | Japanese encephalitis | 5–15 days | Asymptomatic in most cases; fever, headache, fatigue, nausea, and vomiting | Encephalitis, seizures, paralysis, coma, and long-term brain damage | 20–30% in encephalitis cases | Culex mosquitoes, especially Culex tritaeniorhynchus | and Wader | Southeast and East Asia | Yes | |
| Rift Valley fever virus | Rift Valley fever | 2–6 days | Fever, headache, myalgia and liver abnormalities | 4–7 days | Hemorrhagic fever, meningoencephalitis | 1% in humans; in pregnant livestock, 100% fatality rate for fetuses | Culex tritaeniorhynchus and Aedes vexans | Micropteropus pusillus and Hipposideros abae | Eastern, Southern, and Western Africa | Yes |
| Tick-borne encephalitis virus | Tick-borne encephalitis | 7–14 days | Fever, headache, muscle pain, nausea, vomiting, meningitis, and encephalitis | Paralysis and long-term brain damage | 1–2% | Ixodes scapularis, Ixodes ricinus, and Ixodes persulcatus | Small rodents | Eastern Europe and Southern Russia | Yes | |
| West Nile virus | West Nile fever, encephalitis | 2–15 days | Asymptomatic in most cases; fever, headache, fatigue, nausea, vomiting, rash | 3–6 days | Swollen lymph nodes, meningitis, encephalitis, acute flaccid paralysis | 3–15% in severe cases | Culex mosquitoes | Passerine birds | North America, Europe, West and Central Asia, Oceania, and Africa | Yes |
| Yellow fever virus | Yellow fever | 3–6 days | Fever, headache, back pain, loss of appetite, nausea, and vomiting | 3–4 days | Jaundice, liver damage, gastrointestinal bleeding, recurring fever | 3% in general; 20% in cases with severe complications | Aedes mosquitoes, especially Aedes aegypti | Tropical and subtropical regions of South America and Africa | Yes |
Transmission between the vector and the host occurs when the vector feeds on the blood of the vertebrate, wherein the virus that has established an infection in the salivary glands of the vector comes into contact with the host's blood. While the virus is inside the host, it undergoes a process called amplification, where the virus replicates at sufficient levels to induce viremia, a condition in which there are large numbers of present in the blood. (2025). 9783211243343 ISBN 9783211243343 The abundance of virions in the host's blood allows the host to transmit the virus to other organisms if its blood is consumed by them. When uninfected vectors become infected from feeding, they are then capable of transmitting the virus to uninfected hosts, resuming amplification of virus populations. If viremia is not achieved in a vertebrate, the species can be called a "dead-end host", as the virus cannot be transmitted back to the vector.
An example of this vector-host relationship can be observed in the transmission of the West Nile virus. Female mosquitoes of the genus Culex prefer to consume the blood of passerine birds, making them the hosts of the virus. When these birds are infected, the virus amplifies, potentially infecting multiple mosquitoes that feed on its blood. These infected mosquitoes may go on to further transmit the virus to more birds. If the mosquito is unable to find its preferred food source, it will choose another. Human blood is sometimes consumed, but since the West Nile virus does not replicate that well in , humans are considered a dead-end host.
| African swine fever virus | dsDNA | 170-190 kilobases | ~200 Nanometre | Icosahedral | Yes | Endocytosis | Nucleus | Budding | and red and white blood cells | 22 |
| CHIKV | +ssRNA | 11.6 kilobases | 60 - 70 nm | Icosahedral | Yes | Membrane fusion | Cell cytoplasm | Budding | Epithelial cells, endothelial cells, primary and | Three genotypes |
| Dengue virus | +ssRNA | ~11,000 | ~50 nm | Icosahedral | Yes | Membrane fusion | Cell cytoplasm | Budding | Langerhans cell and white blood cells | Four |
| Japanese encephalitis virus | +ssRNA | ~11,000 nucleobases | ~50 nm | Icosahedral | Yes | Membrane fusion | Cell cytoplasm | Budding | Five genotypes | |
| Rift Valley fever virus | -ssRNA | Spherical | Yes | Cell cytoplasm | Budding | NoneNo significant distinct genetic populations exist due to the species having recent common ancestry. | ||||
| Tick-borne encephalitis virus | +ssRNA | ~11,000 nucleobases | 40-50 nm | Icosahedral | Yes | Membrane fusion | Cell cytoplasm | Budding | Neuron | Five genotypes |
| West Nile virus | +ssRNA | ~11,000 nucleobases (11-12 kilo bases) | 45-50 nm | Icosahedral | Yes | Membrane fusion | Cell cytoplasm | Budding | ||
| Yellow fever virus | +ssRNA | ~11,000 nucleobases | 40-60 nm | Icosahedral | Yes | Membrane fusion | Cell cytoplasm | Budding | and white blood cells | |
| Zika virus | +ssRNA | 10794 nucleobases | 40 nm | Icosahedral | Yes | Membrane fusion | Cell cytoplasm | Budding |
Vaccines are in development for the following arboviral diseases:
The WHO caution against the use of aspirin and ibuprofen as they can increase the risk of bleeding.
Mapping methods such as GIS and GPS have allowed for spatial and temporal analyses of arboviruses. Tagging cases or breeding sites geographically has allowed for deeper examination of vector transmission.
To see the epidemiology of specific arboviruses, the following resources hold maps, fact sheets, and reports on arboviruses and arboviral epidemics.
| World Health Organization | The WHO compiles studies and maps of the distribution, risk factors, and prevention of specific viruses. The WHO also hosts DengueNet, a database which can be queried about Dengue cases. | http://www.who.int/en/ [1] |
| CDC ArboNet Dynamic Map | This interactive map is created by USGS using data from the CDC ArboNET. It provides distribution maps of cases in humans and vectors in the United States. | https://web.archive.org/web/20161215234534/http://diseasemaps.usgs.gov/mapviewer/ |
| Center for Disease Control ArboCatalog | The ArboCatalog documents probable arboviruses recorded by the Center for Disease Control, and provides detailed information about the viruses. | https://wwwn.cdc.gov/Arbocat/Default.aspx |
| Dengue fever occur globally |
| First large scale effort to prevent arbovirus infection takes place in Florida, Havana, and the Panama Canal Zone |
| First arbovirus, the yellow fever virus, is discovered |
| Dengue fever transmission is discovered |
| Tick-borne encephalitis virus is discovered |
| Yellow fever vaccine is invented |
| West Nile virus is discovered |
| Japanese encephalitis are invented |
| Insecticide treated are developed |
| West Nile virus reaches the Western Hemisphere |
| Dengue fever spreads globally |
Thomas Milton Rivers published the first clear description of a virus as distinct from a bacterium in 1927. (2025). 9780615827735, Rockpile Press. ISBN 9780615827735 The discovery of the West Nile virus came in 1937, and has since been found in Culex populations causing epidemics throughout Africa, the Middle East, and Europe. The virus was introduced into the Western Hemisphere in 1999, sparking a series of epidemics. During the latter half of the 20th century, Dengue fever reemerged as a global disease, with the virus spreading geographically due to urbanization, population growth, increased international travel, and global warming, and continues to cause at least 50 million infections per year, making Dengue fever the most common and clinically important arboviral disease.
Yellow fever, alongside malaria, was a major obstacle in the construction of the Panama Canal. France supervision of the project in the 1880s was unsuccessful because of these diseases, forcing the abandonment of the project in 1889. During the United States effort to construct the canal in the early 1900s, William C. Gorgas, the Chief Sanitary Officer of Havana, was tasked with overseeing the health of the workers. He had past success in eradicating the disease in Florida and Havana by reducing mosquito populations through draining nearby pools of water, cutting grass, applying oil to the edges of ponds and swamps to kill larvae, and capturing adult mosquitoes that remained indoors during the daytime. Joseph Augustin LePrince, the Chief Sanitary Inspector of the Canal Zone, invented the first commercial larvicide, a mixture of carbolic acid, resin, and caustic soda, to be used throughout the Canal Zone. The combined implementation of these sanitation measures led to a dramatic decline in the number of workers dying and the eventual eradication of yellow fever in the Canal Zone as well as the containment of malaria during the 10-year construction period. Because of the success of these methods at preventing disease, they were adopted and improved upon in other regions of the world.
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