Arbovirusis an informal name for anyvirusthat istransmittedbyarthropodvectors.The termarbovirusis aportmanteau word(arthropod-bornevirus).[1]Tibovirus(tick-bornevirus) is sometimes used to more specifically describe viruses transmitted byticks,asuperorderwithin the arthropods.[2]Arboviruses can affect both animals (including humans) and plants.[3]In humans, symptoms of arbovirus infection generally 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,butencephalitisandviral hemorrhagic fevermay also occur.[4]

Arbovirus infection
Tissue infected with theRift Valley fevervirus
SpecialtyInfectious disease

Signs and symptoms

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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 systemcan also be affected by infection, as encephalitis andmeningitisare 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 Aedesmosquitoes, 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 Culexmosquitoes, especiallyCulex tritaeniorhynchus Domestic pigsandwading birds Southeast and East Asia Yes
Rift Valley fever virus Rift Valley fever 2–6 days Fever, headache,myalgiaand liver abnormalities 4–7 days Hemorrhagic fever, meningoencephalitis 1% in humans; in pregnant livestock, 100% fatality rate for fetuses Culex tritaeniorhynchusandAedes vexans Micropteropus pusillusandHipposideros 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 Culexmosquitoes Passerinebirds 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 Aedesmosquitoes, especiallyAedes aegypti Primates Tropical and subtropical regions of South America and Africa Yes
  1. ^Infection provides lifelong immunity to the specific serotype causing illness, but temporary immunity to other serotypes.

Cause

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Transmission

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Many female mosquitoes, like those ofAedes albopictus,require a vertebrate blood meal in order for their eggs to develop.[8]

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.[9]For arboviruses, vectors are commonly mosquitoes, ticks,sandflies[10]and other arthropods that consume the blood ofvertebratesfor nutritious or developmental purposes.[11]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.[12]

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.[13][14]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 ofvirionspresent in the blood.[15]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.[16]

A flowchart showing the West Nile virus transmission cycle.

An example of this vector-host relationship can be observed in the transmission of the West Nile virus. Female mosquitoes of the genusCulexprefer to consume the blood ofpasserinebirds, making them the hosts of the virus.[17]When these birds are infected, the virus amplifies, potentially infecting multiple mosquitoes that feed on its blood.[15]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.[16][18]

In humans

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Person-to-person transmission of arboviruses is not common, but can occur.Blood transfusions,organ transplantation,and the use ofblood productscan transmit arboviruses if the virus is present in the donor's blood or organs.[19][20][21]Because of this, blood and organs are often screened for viruses before being administered.[21][22]Rarely,vertical transmission,or mother-to-child transmission, has been observed in infected pregnant[23]and breastfeeding women.[24]Exposure to used needles may also transmit arboviruses if they have been used by an infected person or animal.[25]This puts intravenous drug users and healthcare workers at risk for infection in regions where the arbovirus may be spreading in human populations.[21][23]

Virology

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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 Capsidshape 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 cellsandredandwhite blood cells 22genotypes
Chikungunya virus (CHIKV) +ssRNA 11.6 kilobases 60 - 70 nm Icosahedral Yes Membrane fusion Cell cytoplasm Budding Epithelial cells,endothelial cells,primaryfibroblastsandmacrophages Three genotypes
Dengue virus +ssRNA ~11,000nucleobases ~50 nm Icosahedral Yes Membrane fusion Cell cytoplasm Budding Langerhansand 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 Hepatocytesand white blood cells
Zika virus +ssRNA 10794 nucleobases 40 nm Icosahedral Yes Membrane fusion Cell cytoplasm Budding
  1. ^No significant distinct genetic populations exist due to the species having recent common ancestry.

Diagnosis

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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.[26]Definitivediagnosisis typically made in alaboratoryby employing some combination ofblood tests,particularlyimmunologic,serologicand/orvirologictechniques such asELISA,[26][27]complement fixation,[27]polymerase chain reaction,[27][28]neutralization test,[29]andhemagglutination-inhibition test.[30]

Classification

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In the past, arboviruses were organized into one of four groups: A, B, C, and D. Group A denoted members of the genusAlphavirus,[31][32]Group B were members of the genusFlavivirus,[33]and Group C remains as theGroup C serogroupof the genusOrthobunyavirus.[34]Group D was renamed in the mid-1950s to the Guama group and is currently theGuama serogroupin the genusOrthobunyavirus.[35]Currently, viruses are jointly classified according toBaltimore classificationanda virus-specific systembased on standardbiological classification.With the exception of theAfrican swine fever virus,which belongs to theAsfarviridaefamily of viruses, all major clinically important arboviruses belong to one of the following four groups:[citation needed]

Prevention

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Vector controlmeasures, especiallymosquito control,are essential to reducing the transmission of disease by arboviruses. Habitat control involves drainingswampsand 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.Insecticidescan be applied inruralandurbanareas, 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 someorganophosphatesandorganochlorides(such asDDT) have been banned in many countries.Infertilemale mosquitoes have been introduced in some areas in order to reduce the breeding rate of relevant mosquito species.Larvicidesare also used worldwide in mosquito abatement programs.Temefosis a common mosquito larvicide.[36]

Tent made of mosquito netting

People can also reduce the risk of getting bitten by arthropods by employing personal protective measures such as sleeping undermosquito nets,wearingprotective clothing,applyinginsect repellentssuch aspermethrinandDEETto 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.[37]

Vaccination

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Vaccines are available for the following arboviral diseases:

  • Japanese encephalitis[38]
  • Yellow fever[39]
  • Tick-borne encephalitis[40]
  • Rift Valley Fever (only veterinary use)[41]

Vaccines are in development for the following arboviral diseases:

Treatment

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Because the arboviral encephalitides are viral diseases,antibioticsare not an effective form of treatment and no effectiveantiviral drugshave 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 andibuprofenas they can increase the risk of bleeding.[47][48]

Epidemiology

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Most arboviruses are located in tropical areas, however as a group they have a global distribution. The warm climate conditions found intropical areasallows for year-round transmission by the arthropod vectors. Other important factors determining geographic distribution of arthropod vectors include rainfall, humidity, and vegetation.[49]

Mapping methods such asGISandGPShave allowed for spatial and temporal analyses of arboviruses. Tagging cases or breeding sites geographically has allowed for deeper examination of vector transmission.[50]

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:// 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

History

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Year Event
1800s Dengue feverepidemicsoccur globally
1898–1914 First large scale effort to prevent arbovirus infection
takes place inFlorida,Havana,and thePanama Canal Zone
1901 First arbovirus, theyellow fevervirus, is discovered
1906 Dengue fevertransmission is discovered
1936 Tick-borne encephalitis virusis discovered
1937 Yellow fevervaccineis invented
1937 West Nile virusis discovered
1950s Japanese encephalitisvaccinesare invented
1980s Insecticidetreatedmosquito netsare developed
1999 West Nile virus reaches theWestern Hemisphere
Late 1900s Dengue feverspreads globally

Arboviruses were not known to exist until therise of modern medicine[broken anchor],with thegerm theoryand an understanding thatviruseswere distinct from othermicroorganisms.The connection betweenarthropodsanddiseasewas not postulated until 1881 whenCubandoctor and scientistCarlos Finlayproposed thatyellow fevermay be transmitted bymosquitoesinstead of human contact,[51]a reality that was verified by MajorWalter Reedin 1901.[52]The primary vector,Aedes aegypti,had spread globally from the 15th to the 19th centuries as a result ofglobalizationand theslave trade.[53]This geographic spreading causeddengue feverepidemicsthroughout the 18th and 19th centuries,[54]and later, in 1906, transmission by theAedesmosquitoes was confirmed, making yellow fever and dengue fever the first two diseases known to be caused by viruses.[55]

Thomas Milton Riverspublished the first clear description of a virus as distinct from a bacterium in 1927.[56][57]The discovery of theWest Nile viruscame in 1937,[58]and has since been found inCulexpopulations[59]causing epidemics throughoutAfrica,theMiddle East,andEurope.The virus was introduced into theWestern Hemispherein 1999, sparking a series of epidemics.[60]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,[61]and continues to cause at least 50 million infections per year, making Dengue fever the most common and clinically important arboviral disease.[62][63]

Yellow fever,alongsidemalaria,was a major obstacle in the construction of thePanama Canal.Frenchsupervision of the project in the 1880s was unsuccessful because of these diseases, forcing the abandonment of the project in 1889.[64]During theAmericaneffort 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 inFloridaandHavanaby reducingmosquitopopulations 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.[65]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.[66]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 ofmalariaduring 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.[64][67]

See also

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