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An arbovirus (from arthropod-borne virus) is a virus that is maintained in nature by biological transmission between susceptible vertebrate hosts and blood-feeding arthropods, which acquire the virus by feeding on a viremic host and transmit it by bite after the virus has replicated in the arthropod. The term describes an ecological and epidemiological category and not a taxonomic group. Arboviruses belong to several unrelated viral families, and most are RNA viruses. The only known arthropod-borne DNA virus is African swine fever virus. More than 500 arboviruses are listed in the International Catalogue of Arboviruses, and roughly 150 of them are known to infect humans. Their vectors include mosquitoes, ticks, sandflies, biting midges, and black flies.

Arboviruses cause some of the most important infectious diseases of humans and domestic animals, including dengue fever, yellow fever, Japanese encephalitis, West Nile fever, chikungunya, Zika fever, tick-borne encephalitis, Crimean-Congo hemorrhagic fever, Rift Valley fever, and Oropouche fever, and animal diseases such as bluetongue disease and African swine fever. Their distribution is determined by the ranges and ecology of their vectors and hosts, so it responds strongly to temperature, rainfall, land use, urbanization, trade, and travel.

The term "arbovirus" was formalized by a World Health Organization study group in 1957. The group defined arboviruses by their biological transmission through hematophagous arthropods, in contrast to purely mechanical transmission on contaminated mouthparts. Several related terms are used:

• Biological transmission means that the virus replicates in the arthropod before it is transmitted. The interval between ingestion of an infectious blood meal and the ability to transmit is the extrinsic incubation period (EIP).
• Mechanical transmission is the carriage of virus on the mouthparts of a feeding insect without replication. It is not a feature of arboviruses, although it occurs for some other viruses, such as myxoma virus.
• Robovirus (rodent-borne virus) and insect-specific virus are separate categories. Insect-specific viruses replicate in arthropods but not in vertebrate cells, and they are not arboviruses by definition.
• Zoonotic arboviruses circulate mainly among animals, and humans are infected incidentally. Anthroponotic arboviruses, such as dengue, Zika, chikungunya, and urban yellow fever viruses, can circulate between humans and vectors without an animal reservoir.

The concept that an insect could transmit a virus emerged from work on yellow fever. Carlos Finlay proposed in 1881 that mosquitoes transmit yellow fever, and the Yellow Fever Commission led by Walter Reed showed experimentally in Cuba in 1900 that Aedes aegypti carries a filterable agent that causes the disease. This was the first demonstration that a human disease was caused by a filterable agent and transmitted by an arthropod. Dengue was shown to be transmitted by mosquitoes in the early twentieth century.

The Rockefeller Foundation's virus program, from the 1930s, isolated yellow fever virus in mice and cell culture and led to the development of the live attenuated 17D vaccine by Max Theiler, for which he received the 1951 Nobel Prize in Physiology or Medicine. Systematic field programs in Africa, South America, and Asia in the 1940s to 1960s isolated hundreds of new viruses from mosquitoes, ticks, and vertebrates and established the ecological concept of the arbovirus. West Nile virus was isolated in 1937, Zika virus in 1947, and chikungunya virus in 1952.

Modern history includes the introduction of West Nile virus to New York in 1999, the spread of chikungunya across the Indian Ocean from 2004 and across the Americas from 2013, the Zika epidemic of 2015 to 2016, the growth of dengue to record levels in the 2020s, and the emergence of Oropouche virus as a cause of large outbreaks in the Americas in 2023 and 2024.

Arboviruses are distributed across at least seven families of RNA viruses and one family of DNA viruses. Within each family, arbovirus status is a property of some genera or lineages. The same family also includes viruses with no arthropod vector, as in the flaviviruses, in which tick-borne, mosquito-borne, no-known-vector, and insect-specific lineages are all present.

Phylogenies show that arthropod-borne status has arisen more than once and that vertebrate-only lineages exist in the same families. Among the orthoflaviviruses, the mosquito-borne and tick-borne groups are distinct clades. There are also viruses with no known vector, and insect-specific orthoflaviviruses such as cell-fusing agent virus, which are thought to be closer to the ancestral state. Evolutionary analyses suggest that the ancestors of the arthropod-borne flaviviruses were arthropod viruses that acquired the ability to infect vertebrates, and not the reverse. The mechanism and timing of such host-range expansions are not completely resolved.

Mosquitoes

Mosquitoes of the family Culicidae transmit most medically important arboviruses.

• Aedes aegypti is the main vector of dengue, Zika, chikungunya, and urban yellow fever viruses. It originated in Africa, is closely associated with human dwellings, breeds in small artificial water containers, bites mainly during the day, and prefers human blood. It spread globally through shipping from the sixteenth century onward.
• Aedes albopictus (the Asian tiger mosquito) is a less efficient but ecologically flexible vector of the same viruses. It has spread from Asia to every inhabited continent since the 1970s and 1980s, helped by the trade in used tires and by eggs that survive in diapause, and it tolerates cooler climates than Ae. aegypti.
• Culex species, such as Culex pipiens, Culex quinquefasciatus, Culex tarsalis, and Culex tritaeniorhynchus, maintain and transmit West Nile virus, Japanese encephalitis virus, St. Louis encephalitis virus, and others in cycles that involve birds and, for Japanese encephalitis, pigs.
• Haemagogus and Sabethes species are the main vectors of sylvatic yellow fever in South America, and Aedes africanus and related species have this role in Africa.
• Floodwater Aedes species (for example Aedes mcintoshi) and Culex species are vectors of Rift Valley fever virus.

Ticks

Ticks (Ixodidae, or hard ticks, and Argasidae, or soft ticks) are the vectors of tick-borne encephalitis virus (Ixodes ricinus and Ixodes persulcatus), Powassan virus (Ixodes species), Crimean-Congo hemorrhagic fever virus (Hyalomma species), severe fever with thrombocytopenia syndrome virus (Haemaphysalis longicornis), Colorado tick fever virus, and African swine fever virus (soft ticks of the genus Ornithodoros). Ticks feed for days, live for years, and can maintain virus through the molt (transstadial transmission). Several tick-borne viruses can also be transmitted between ticks that feed close together on a host, even without viremia in that host (co-feeding transmission).

Other vectors

• Sandflies (subfamily Phlebotominae) transmit sandfly fever viruses, Toscana virus, and the vesiculovirus Chandipura virus.
• Biting midges (Culicoides) transmit Oropouche virus, bluetongue virus, African horse sickness virus, epizootic hemorrhagic disease virus, and Schmallenberg virus.
• Black flies (Simuliidae) transmit some vesicular stomatitis virus strains.

Enzootic and epizootic cycles

Most arboviruses circulate in an enzootic (sylvatic) cycle among wild vertebrates and arthropods. The vertebrate hosts that amplify the virus develop viremia high enough to infect feeding arthropods and typically show little disease. Examples are birds for West Nile virus, wading birds and pigs for Japanese encephalitis virus, forest rodents for enzootic Venezuelan equine encephalitis virus, and non-human primates for sylvatic yellow fever, dengue, and Zika viruses. An epizootic cycle results when the virus reaches amplifying domestic animals, such as horses for epizootic Venezuelan equine encephalitis virus and ruminants for Rift Valley fever virus. Epizootics can produce large numbers of human cases.

Dead-end hosts and bridge vectors

Many zoonotic arboviruses infect humans, but humans develop too little viremia to infect vectors. They are dead-end hosts. A bridge vector is a vector that feeds on both the amplifying animal and humans and thereby links the enzootic cycle with human disease. West Nile virus illustrates the pattern: Culex mosquitoes that feed on birds in spring and early summer amplify the virus, and later feeding on mammals leads to human and equine cases.

Urban cycles

A few arboviruses can be maintained entirely in humans and Aedes mosquitoes. Dengue virus (four serotypes, DENV-1 to DENV-4), chikungunya virus, Zika virus, and yellow fever virus all have urban cycles, in which humans are amplifying hosts that develop high viremia. The four dengue serotypes arose independently from sylvatic cycles in non-human primates in Southeast Asia and West Africa. Urban cycles can produce explosive epidemics in cities with dense human populations and abundant Aedes aegypti. Yellow fever has an urban cycle that is controllable by vaccination and vector control, and a sylvatic cycle that cannot be eradicated.

Non-vector transmission

Arboviruses can also spread without a vector in several ways, although these routes are usually secondary:

• Blood transfusion and organ transplantation (West Nile, dengue, Zika, and others), which leads to screening of blood donations in some countries.
• Vertical transmission from mother to fetus (Zika, dengue, chikungunya, and Oropouche viruses) or at delivery.
• Sexual transmission, best documented for Zika virus.
• Contact with infected animal tissue (Rift Valley fever and Crimean-Congo hemorrhagic fever viruses in livestock workers and slaughterhouse workers) and nosocomial spread of Crimean-Congo hemorrhagic fever virus.
• Foodborne transmission, such as tick-borne encephalitis virus in unpasteurized milk.
• Laboratory exposure by needlestick or aerosol.

Transmission within vectors

Arthropods may transmit virus to their offspring by transovarial transmission (as with La Crosse virus in Aedes triseriatus, and Rift Valley fever virus in floodwater Aedes), and by venereal transmission from male to female. Vertical transmission occurs at low frequency for most viruses and probably helps maintain some viruses during dry or cold seasons, but it is not sufficient to maintain most arboviruses without horizontal transmission.

Barriers to infection

After a mosquito ingests an infectious blood meal, the virus must infect the midgut epithelium, replicate, escape into the hemolymph, infect other tissues, and reach the salivary glands, from which it is released in saliva during feeding. The mosquito may block this process at several points. They are classically termed the midgut infection barrier, the midgut escape barrier, the salivary gland infection barrier, and the salivary gland escape barrier. The ability of a vector population to be infected and to transmit is called vector competence. It varies among species, among populations of one species, and among virus strains, and it depends on temperature and on the microbiota of the mosquito.

Arthropods are infected for life, usually without detectable pathology, which contrasts with the acute disease these viruses cause in vertebrates. Components of mosquito saliva also modulate the vertebrate immune response in the skin and may enhance infection.

Antiviral defenses of vectors

The main antiviral defense of mosquitoes is RNA interference. In the exogenous small interfering RNA pathway, Dicer-2 cleaves viral double-stranded RNA into short RNAs, which guide Argonaute-2 to cleave viral RNA. A PIWI-interacting RNA-like pathway also produces viral small RNAs in Aedes mosquitoes. The Toll, IMD, and JAK-STAT signaling pathways, autophagy, and other responses contribute. Arboviruses that evolved in the presence of these defenses cause persistent infection, and the balance between replication and RNA interference is thought to explain why arthropods tolerate infection.

Symbionts and insect-specific viruses

The intracellular bacterium Wolbachia occurs naturally in many insects and can reduce the replication of several RNA viruses in mosquitoes, an effect that has been used in control programs. Insect-specific viruses, which infect mosquitoes but not vertebrate cells, are common in wild mosquitoes, and in some experiments they interfere with the replication of arboviruses in the same cells. The ecological importance of this effect in nature is still being studied.

Arboviruses must replicate in two very different hosts, a vertebrate and an arthropod, which differ in body temperature, immune systems, and cellular receptors. This alternation is thought to constrain their evolution. Many arboviruses show strong purifying selection and lower rates of long-term change than viruses that infect only vertebrates, which has been explained by the need to maintain fitness in both hosts. Experiments show that serial passage in a single host, such as cell culture, leads to adaptation to that host and loss of fitness in the other. The high mutation rate of RNA viruses nevertheless allows rapid adaptation when ecological conditions change. Examples include:

• An E1 substitution (A226V) in chikungunya virus of the East, Central, and South African lineage that increased infection of Aedes albopictus and contributed to the large Indian Ocean epidemic of 2005 and 2006.
• Substitutions in the E2 protein in Venezuelan equine encephalitis virus that allowed an enzootic virus transmitted by Culex (Melanoconion) mosquitoes to infect equines at high viremia and to be transmitted by epizootic vectors.
• The replacement of the original North American genotype of West Nile virus by the WN02 genotype after 2001. WN02 carries an envelope V159A change, and it shortens the extrinsic incubation period in Culex mosquitoes.

Emergence results from the combination of ecological, climatic, and social changes together with adaptation. Urbanization, water storage, increased air travel, trade in used tires and plants, deforestation, irrigation, and changes in livestock management all alter vector habitats and contact between vectors and hosts.

For a vector-borne pathogen, the basic reproduction number R₀ in the classical Ross-Macdonald model is:

where m is the number of female vectors per host, a is the biting rate per vector per day, b is the probability that an infectious bite infects a host, c is the probability that a vector becomes infected by biting an infectious host, μ is the daily vector mortality rate, n is the EIP in days, and r is the host recovery rate. The term e^−_μn_ is the probability that a vector survives the EIP. The vector-dependent part of the expression is the vectorial capacity:

Biting rate enters as a square because a vector must bite twice, once to acquire the virus and once to transmit it. Because n and μ appear in an exponent, small changes in them have large effects. For example, with μ = 0.1 per day and n = 10 days, survival through the EIP is e⁻¹ ≈ 0.37, whereas with n = 5 days it is e^−0.5 ≈ 0.61. The herd immunity threshold in a susceptible population is p_c = 1 − 1/_R_₀. Because R₀ depends on the square root, reducing vector density by half reduces R₀ by only about 29 percent, which partly explains why vector control alone often fails to stop transmission.

For zoonotic arboviruses with multiple host species, the amplification term sums over host species k, and each species contributes according to its reservoir competence:

where b_k is susceptibility, c_k is infectiousness to vectors, and 1/_γ__k is the duration of infectious viremia. Poorly competent hosts that attract bites can reduce transmission, a dilution effect.

The EIP of a virus in a vector depends on temperature. Over a limited range, it is often approximated by a degree-day relation:

where D is the thermal sum required for development, T is temperature, and T_min is the lower developmental threshold.

Vectors are ectotherms, so their development, survival, biting rate, and the replication of virus within them respond to temperature. Trait-based models represent traits such as the biting rate and development rate with the Brière function:

where c is a scaling constant and T_min and T_max are the lower and upper limits of the trait. Survival often follows a quadratic curve. Combining the traits gives transmission that is a unimodal function of temperature. Estimated optima are about 29 °C for Aedes aegypti with dengue, Zika, and chikungunya viruses, about 26 °C for Aedes albopictus, and about 24 to 25 °C for Culex species with West Nile virus. Models therefore predict that warming extends transmission seasons and ranges in cool regions and may reduce transmission in the hottest regions.

Other environmental factors include:

• Rainfall and water: Rain creates breeding sites for floodwater mosquitoes, but heavy rain can flush larvae from urban drains, and drought can concentrate nutrient-rich water and force hosts together. Water storage in drought also supports Aedes aegypti.
• Climate oscillations: El Niño and the Indian Ocean Dipole are associated with outbreaks of Rift Valley fever in East Africa and of dengue in some regions.
• Land use and urbanization: Unplanned urban growth with inadequate water supply and waste management favors Aedes aegypti, and irrigation and rice cultivation favor Culex tritaeniorhynchus and Japanese encephalitis virus.
• Ticks: Tick-borne viruses depend on temperature, humidity, vegetation, and the abundance of hosts such as deer and rodents, and changes in the distribution of Ixodes ricinus and Hyalomma ticks have been reported.

Attributing a particular outbreak to climate change is difficult, because travel, trade, human behavior, immunity, vector control, and surveillance also change.

Arboviruses are often grouped by the clinical syndromes they cause in humans:

• Febrile illness with or without rash and arthralgia: dengue, Zika, chikungunya, Ross River, Mayaro, Sindbis, Oropouche, and sandfly fever viruses. Chikungunya and some other alphaviruses cause severe and persistent joint pain.
• Neuroinvasive disease: meningitis, encephalitis, and paralysis caused by West Nile virus, Japanese encephalitis virus, St. Louis encephalitis virus, tick-borne encephalitis virus, Powassan virus, La Crosse virus, and the equine encephalitis alphaviruses.
• Hemorrhagic fever: yellow fever, severe dengue, Rift Valley fever, Crimean-Congo hemorrhagic fever, Kyasanur Forest disease, and Omsk hemorrhagic fever.
• Congenital and perinatal disease: Zika virus, and probably Oropouche and some others.

Most infections with most arboviruses are asymptomatic or mild. The risk of severe disease depends on the virus, the age and immune status of the person, and, for dengue, prior infection with a different serotype.

After inoculation in the skin, many arboviruses replicate in dendritic cells, keratinocytes, and fibroblasts, spread to lymph nodes, and cause viremia. Disease results from direct viral injury, from the host inflammatory response, or both. The innate immune system, in particular type I interferon signaling, is critical in controlling early replication, and several arboviruses encode proteins that antagonize it. For example, the NS5 protein of Zika and dengue viruses degrades human STAT2. Neuroinvasive viruses cross the blood-brain barrier or enter through peripheral nerves.

In dengue, a person infected with one serotype develops lasting immunity to that serotype and a transient period of cross-protection to the others. After that period, secondary infection with a different serotype is associated with a higher risk of severe disease. This is attributed in part to antibody-dependent enhancement, in which non-neutralizing or weakly neutralizing cross-reactive antibodies promote infection of Fc receptor-bearing cells, and in part to the effects of cross-reactive T cells and of the secreted NS1 protein on the vascular endothelium. Severe dengue peaks at the time when fever resolves and viremia is falling, and it is characterized by increased vascular permeability.

Clinical diagnosis is unreliable because many arboviral illnesses resemble each other and other infections such as malaria, leptospirosis, and rickettsial disease, and because several arboviruses circulate together. Laboratory diagnosis uses:

• Nucleic acid detection by RT-PCR of blood in the first days of illness, and of urine, cerebrospinal fluid, or other samples in some conditions. Viremia is brief in many infections, especially for neuroinvasive disease, in which virus is usually no longer detectable when symptoms of neurological disease appear.
• Antigen detection, notably the NS1 antigen test for dengue, which is positive early.
• Serology: IgM antibody capture ELISA, which becomes positive within days to a week, and rising IgG titers in paired samples. Cross-reactivity within a genus (for example among orthoflaviviruses and after vaccination) is common, so a plaque reduction neutralization test is used for confirmation.
• Virus isolation in cell culture or by sequencing, used in specialized laboratories and for surveillance.

Surveillance combines human case reporting with monitoring of vectors and animals. Methods include sentinel chicken flocks, reports of dead birds and equine cases, trapping of mosquitoes with CO₂-baited light traps and gravid traps, ovitraps for Aedes, and testing of mosquito pools by RT-PCR. For M equal-sized pools of s mosquitoes with Y positive pools, the maximum likelihood estimate of infection prevalence is:

For Aedes species, entomological indices such as the container index, house index, and Breteau index are used, although their relation to human risk is weak. For _Culex_-borne viruses, a vector index, which is the sum over species i of the mean females per trap-night N_i multiplied by the infection prevalence P_i, is used:

Genomic sequencing and phylogenetic analysis are used to track introductions and spread, and wastewater and environmental surveillance are being explored for some viruses.

Vector control

• Source reduction: removal, covering, or treatment of water containers, improved water supply and drainage, and community engagement. This is the basis of control for Aedes aegypti.
• Larvicides: Bacillus thuringiensis israelensis (Bti), Lysinibacillus sphaericus, insect growth regulators such as methoprene and pyriproxyfen, and spinosad.
• Adulticides: space spraying with ultra-low-volume formulations of pyrethroids or organophosphates during outbreaks, and indoor residual spraying for some vectors. Insecticide resistance, in particular to pyrethroids, is widespread in Aedes aegypti and Culex populations.
• Biological and genetic approaches: Release of Aedes aegypti carrying Wolbachia (strains _w_Mel and _w_AlbB) reduces the capacity of the mosquito to transmit dengue virus. A cluster-randomized trial in Yogyakarta, Indonesia, found a reduction in symptomatic dengue of about 77 percent in the treated areas, and large reductions have been reported in other programs. Other methods, including the sterile insect technique, the incompatible insect technique, and genetically modified male mosquitoes, have been evaluated.
• Livestock and wildlife measures: ear tags and dips for ticks, vaccination of animals, and in some cases management of the host population.

Personal protection

Repellents (DEET, picaridin, IR3535, and oil of lemon eucalyptus), long clothing, window screens, insecticide-treated clothing and nets, avoidance of vectors at peak feeding times, and inspection for ticks after exposure are used. Because Aedes aegypti bites in the daytime, bed nets are less effective than for malaria.

Vaccines

Antiviral therapy

No specific antiviral treatment is approved for most arboviral diseases, and management is supportive. For dengue, careful fluid management during the critical phase reduces mortality. For Crimean-Congo hemorrhagic fever and severe fever with thrombocytopenia syndrome, ribavirin and favipiravir have been used, and evidence of benefit is limited. Candidate antivirals and monoclonal antibodies are in development.

Emergence has several recurring drivers: introduction of vectors and viruses by trade and travel, urban growth, deforestation and land-use change that increase contact between people and sylvatic cycles, changes in climate, loss of immunity in populations, and adaptation of the virus to new vectors. Examples include the spread of West Nile virus in the Americas, the global expansion of dengue and chikungunya, the Zika epidemic, the emergence of Oropouche virus, local transmission of dengue and chikungunya in southern Europe, the spread of bluetongue and Schmallenberg viruses in livestock in Europe, and the expansion of tick-borne encephalitis and Crimean-Congo hemorrhagic fever in parts of Europe. Ongoing discovery of new viruses by metagenomic sequencing of mosquitoes and ticks has revealed many viruses of unknown significance for human health.

• Dengue fever
• Zika fever
• West Nile fever
• Yellow fever
• Chikungunya
• Vector (epidemiology)
• Mosquito-borne disease
• Tick-borne disease

Why are almost all arboviruses RNA viruses rather than DNA viruses?

Almost all arboviruses possess RNA genomes because RNA-dependent RNA polymerases lack proofreading exonuclease activity, generating high mutation rates (10⁻⁴ to 10⁻³ substitutions per nucleotide per replication cycle) and diverse intrahost quasispecies. This genetic plasticity enables rapid adaptation across two physiologically divergent host environments—homeothermic vertebrates (37–42 °C, adaptive immunity, interferon signaling) and poikilothermic arthropods (ambient temperature, RNA interference)—whereas only one known arbovirus, African swine fever virus, uses a double-stranded DNA genome.

How do mosquitoes tolerate lifelong arbovirus infection without dying?

Arthropod vectors survive lifelong arbovirus infection because their primary antiviral defense—the exogenous small interfering RNA (exo-siRNA) pathway mediated by Dicer-2 and Argonaute-2—cleaves viral double-stranded RNA replicative intermediates to cap viral titers below cytopathic thresholds without clearing the virus completely. Unlike vertebrate hosts, where cytolytic viral replication and proinflammatory cytokine cascades cause acute tissue pathology, mosquito midgut and salivary gland cells maintain a persistent, non-lytic steady state that preserves vector flight and feeding fitness.

Why does ambient temperature have a nonlinear effect on arbovirus transmission?

Arbovirus transmission follows a unimodal thermal curve because rising temperature accelerates both the mosquito biting rate (a) and viral replication across the midgut barrier—shortening the extrinsic incubation period (n)—while simultaneously increasing daily adult mosquito mortality (μ) above thermal optima. In the Ross-Macdonald vectorial capacity equation, transmission peaks around 24–25 °C for _Culex_-borne West Nile virus and 29 °C for _Aedes aegypti_-borne dengue and Zika viruses, before collapsing above 34–35 °C as vector lifespan falls shorter than the extrinsic incubation period.