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| Arbovirus infection | |
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| Tissue infected with theRift Valley fever virus | |
| Specialty | Infectious disease |
Arbovirus is an informal name for anyvirus that istransmitted byarthropodvectors. The termarbovirus is aportmanteau word (arthropod-bornevirus).[1]Tibovirus (tick-bornevirus) is sometimes used to more specifically describe viruses transmitted byticks, asuperorder within the arthropods.[2] Arboviruses can affect both animals (including humans) and plants.[3] 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 arefever,headache, andmalaise, but other features ofviral hemorrhagic fever syndrome andencephalitis may also occur.[4]
The incubation period – the time between when infection occurs and when symptoms appear – varies from virus to virus, but is usually limited between 2 and 15 days for arboviruses.[5] The majority of infections, however, are asymptomatic.[6] Among cases in which symptoms do appear, symptoms tend to be non-specific, resembling aflu-like illness, and are not indicative of a specific causative agent. These symptoms include fever, headache, malaise, rash and fatigue. Rarely, vomiting and hemorrhagic fever may occur. Thecentral nervous system can also be affected by infection, as encephalitis andmeningitis are sometimes observed.[7] Prognosis is good for most people, but is poor in those who develop severe symptoms, with up to a 20% mortality rate in this population depending on the virus. The very young, elderly, pregnant women, and people with immune deficiencies are more likely to develop severe symptoms.[citation needed]
| Arbovirus | Disease(s) | Incubation period | Symptoms | Duration of symptoms | Complications | Case fatality rate | Vector(s) | Primaryhost(s) | Geographic distribution | Does infection provide lifelong immunity? |
|---|---|---|---|---|---|---|---|---|---|---|
| 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, especiallyAedes aegypti | Humans | Near the equator globally | Varies[note 1] |
| 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, especiallyCulex tritaeniorhynchus | Domestic pigs andwading birds | 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 andAedes vexans | Micropteropus pusillus andHipposideros 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, andIxodes 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, especiallyAedes aegypti | Primates | Tropical and subtropical regions of South America and Africa | Yes |
| Zika virus[8] | Zika fever | 3–14 days | Fever, rash, joint pain, nausea and vomiting | 2–7 days | Neurological complications (meningoencephalitis, microcephaly, Gullain-Barré Syndrome) | <1%[9] | Aedes mosquitoes | Primates | Africa, the Americas, Asia and the Pacific[10] | Yes[11] |
Arboviruses maintain themselves in nature by going through a cycle between ahost, an organism that carries the virus, and avector, an organism that carries and transmits the virus to other organisms.[13] For arboviruses, vectors are commonly mosquitoes, ticks,sandflies[14] and other arthropods that consume the blood ofvertebrates for nutritious or developmental purposes.[15] Vertebrates which have their blood consumed act as the hosts, with each vector generally having an affinity for the blood of specific species, making those species the hosts.[16]
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.[17][18] While the virus is inside the host, it undergoes a process called amplification, where the virus replicates at sufficient levels to induceviremia, a condition in which there are large numbers ofvirions present in the blood.[19] 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.[20]
An example of this vector-host relationship can be observed in the transmission of the West Nile virus. Female mosquitoes of the genusCulex prefer to consume the blood ofpasserine birds, making them the hosts of the virus.[21] When these birds are infected, the virus amplifies, potentially infecting multiple mosquitoes that feed on its blood.[19] 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 inmammals, humans are considered a dead-end host.[20][22]
Person-to-person transmission of arboviruses is not common, but can occur.Blood transfusions,organ transplantation, and the use ofblood products can transmit arboviruses if the virus is present in the donor's blood or organs.[23][24][25] Because of this, blood and organs are often screened for viruses before being administered.[25][26] Rarely,vertical transmission, or mother-to-child transmission, has been observed in infected pregnant[27] and breastfeeding women.[28] Exposure to used needles may also transmit arboviruses if they have been used by an infected person or animal.[29] This puts intravenous drug users and healthcare workers at risk for infection in regions where the arbovirus may be spreading in human populations.[25][27]
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Arboviruses are apolyphyletic group, belonging to various viral genera and therefore exhibiting different virologic characteristics.
| Arbovirus | Genome type | Genome length | Diameter | Capsid shape | Enveloped? | Viral entry | Replication site | Viral shedding | Infected cell(s) | Genetic variability |
|---|---|---|---|---|---|---|---|---|---|---|
| African swine fever virus | dsDNA | 170-190 kilobases | ~200nm | Icosahedral | Yes | Endocytosis | Nucleus | Budding | Endothelial cells andred andwhite blood cells | 22genotypes |
| Chikungunya virus (CHIKV) | +ssRNA | 11.6 kilobases | 60 - 70 nm | Icosahedral | Yes | Membrane fusion | Cell cytoplasm | Budding | Epithelial cells,endothelial cells, primaryfibroblasts andmacrophages | Three genotypes |
| Dengue virus | +ssRNA | ~11,000nucleobases | ~50 nm | Icosahedral | Yes | Membrane fusion | Cell cytoplasm | Budding | Langerhans and white blood cells | Fourserotypes |
| 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 | None[note 1] | ||||
| Tick-borne encephalitis virus | +ssRNA | ~11,000 nucleobases | 40-50 nm | Icosahedral | Yes | Membrane fusion | Cell cytoplasm | Budding | Neural cells | 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 | Hepatocytes and white blood cells | |
| Zika virus | +ssRNA | 10794 nucleobases | 40 nm | Icosahedral | Yes | Membrane fusion | Cell cytoplasm | Budding |
Preliminary diagnosis of arbovirus infection is usually based on clinical presentations of symptoms, places and dates of travel, activities, and epidemiological history of the location where infection occurred.[30] Definitivediagnosis is typically made in alaboratory by employing some combination ofblood tests, particularlyimmunologic,serologic and/orvirologic techniques such asELISA,[30][31]complement fixation,[31]polymerase chain reaction,[31][32]neutralization test,[33] andhemagglutination-inhibition test.[34]
In the past, arboviruses were organized into one of four groups: A, B, C, and D. Group A denoted members of the genusAlphavirus,[35][36] Group B were members of the genusFlavivirus,[37] and Group C remains as the Group C serogroup of the genusOrthobunyavirus.[38] Group D was renamed in the mid-1950s to the Guama group and is currently the Guama serogroup in the genusOrthobunyavirus.[39] Currently, viruses are jointly classified according toBaltimore classification anda virus-specific system based on standardbiological classification. With the exception of theAfrican swine fever virus, which belongs to theAsfarviridae family of viruses, all major clinically important arboviruses belong to one of the following four groups:[citation needed]
Vector control measures, especiallymosquito control, are essential to reducing the transmission of disease by arboviruses. Habitat control involves drainingswamps and removal of other pools ofstagnant water (such as old tires, large outdoor potted plants, empty cans, etc.) that often serve as breeding grounds for mosquitoes.Insecticides can be applied inrural andurban areas, inside houses and other buildings, or in outdoor environments. They are often quite effective for controlling arthropod populations, though use of some of these chemicals is controversial, and someorganophosphates andorganochlorides (such asDDT) have been banned in many countries.Infertile male mosquitoes have been introduced in some areas in order to reduce the breeding rate of relevant mosquito species.Larvicides are also used worldwide in mosquito abatement programs.Temefos is a common mosquito larvicide.[40]
People can also reduce the risk of getting bitten by arthropods by employing personal protective measures such as sleeping undermosquito nets, wearingprotective clothing, applyinginsect repellents such aspermethrin andDEET to clothing and exposed skin, and (where possible) avoiding areas known to harbor high arthropod populations. Arboviral encephalitis can be prevented in two major ways: personal protective measures and public health measures to reduce the population of infected mosquitoes. Personal measures include reducing time outdoors particularly in early evening hours, wearing long pants and long sleeved shirts and applying mosquito repellent to exposed skin areas. Public health measures often require spraying of insecticides to kill juvenile (larvae) and adult mosquitoes.[41]
Vaccines are available for the following arboviral diseases:
Vaccines are in development for the following arboviral diseases:
Because the arboviral encephalitides are viral diseases,antibiotics are not an effective form of treatment and no effectiveantiviral drugs have yet been discovered. Treatment is supportive, attempting to deal with problems such as swelling of the brain, loss of the automatic breathing activity of the brain and other treatable complications likebacterial pneumonia.[1]
The WHO caution against the use of aspirin andibuprofen as they can increase the risk of bleeding.[51][52]
Most arboviruses are located in tropical areas, however as a group they have a global distribution. The warm climate conditions found intropical areas allows for year-round transmission by the arthropod vectors. Other important factors determining geographic distribution of arthropod vectors include rainfall, humidity, and vegetation.[53]
Mapping methods such asGIS andGPS have allowed for spatial and temporal analyses of arboviruses. Tagging cases or breeding sites geographically has allowed for deeper examination of vector transmission.[54]
To see the epidemiology of specific arboviruses, the following resources hold maps, fact sheets, and reports on arboviruses and arboviral epidemics.
| Resource | Description | Link |
|---|---|---|
| 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/ |
| 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 |
| Year | Event |
|---|---|
| 1800s | Dengue feverepidemics occur globally |
| 1898–1914 | First large scale effort to prevent arbovirus infection takes place inFlorida,Havana, and thePanama Canal Zone |
| 1901 | First arbovirus, theyellow fever virus, is discovered |
| 1906 | Dengue fever transmission is discovered |
| 1936 | Tick-borne encephalitis virus is discovered |
| 1937 | Yellow fevervaccine is invented |
| 1937 | West Nile virus is discovered |
| 1950s | Japanese encephalitisvaccines are invented |
| 1980s | Insecticide treatedmosquito nets are developed |
| 1999 | West Nile virus reaches theWestern Hemisphere |
| Late 1900s | Dengue fever spreads globally |
Arboviruses were not known to exist until therise of modern medicine, with thegerm theory and an understanding thatviruses were distinct from othermicroorganisms. The connection betweenarthropods anddisease was not postulated until 1881 whenCuban doctor and scientistCarlos Finlay proposed thatyellow fever may be transmitted bymosquitoes instead of human contact,[55] a reality that was verified by MajorWalter Reed in 1901.[56] The primary vector,Aedes aegypti, had spread globally from the 15th to the 19th centuries as a result ofglobalization and theslave trade.[57] This geographic spreading causeddengue feverepidemics throughout the 18th and 19th centuries,[58] and later, in 1906, transmission by theAedes mosquitoes was confirmed, making yellow fever and dengue fever the first two diseases known to be caused by viruses.[59]
Thomas Milton Rivers published the first clear description of a virus as distinct from a bacterium in 1927.[60][61] The discovery of theWest Nile virus came in 1937,[62] and has since been found inCulex populations[63] causing epidemics throughoutAfrica, theMiddle East, andEurope. The virus was introduced into theWestern Hemisphere in 1999, sparking a series of epidemics.[64] During the latter half of the 20th century, Dengue fever reemerged as a global disease, with the virus spreading geographically due tourbanization,population growth, increased international travel, andglobal warming,[65] and continues to cause at least 50 million infections per year, making Dengue fever the most common and clinically important arboviral disease.[66][67]
Yellow fever, alongsidemalaria, was a major obstacle in the construction of thePanama Canal.French supervision of the project in the 1880s was unsuccessful because of these diseases, forcing the abandonment of the project in 1889.[68] During theAmerican effort to construct the canal in the early 1900s,William C. Gorgas, the Chief Sanitary Officer ofHavana, was tasked with overseeing the health of the workers. He had past success in eradicating the disease inFlorida andHavana by reducingmosquito populations through draining nearby pools of water, cutting grass, applying oil to the edges of ponds and swamps to killlarvae, and capturing adult mosquitoes that remained indoors during the daytime.[69]Joseph Augustin LePrince, the Chief Sanitary Inspector of theCanal Zone, invented the first commerciallarvicide, a mixture ofcarbolic acid,resin, andcaustic soda, to be used throughout theCanal Zone.[70] 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 ofmalaria 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.[68][71]
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