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Aedes aegypti (*Stegomyia aegypti*), commonly known as the yellow fever mosquito, is a diurnal, container-breeding mosquito of the family Culicidae (genus Aedes, subgenus Stegomyia) and the primary global vector of human urban arboviruses: the four types of dengue virus, yellow fever virus, Zika virus, and chikungunya virus. It can also transmit Mayaro virus in the laboratory, but Mayaro virus is mainly transmitted by forest-canopy mosquitoes (Haemagogus) and Aedes aegypti is not established as an important natural vector of it.

The species originated in Africa as a forest mosquito that bred in tree holes and fed on a range of animals. At some point in the last several thousand years, a form arose that lives alongside people, breeds in their water containers, and feeds mostly on them. This domestic form has spread to tropical, subtropical, and warm temperate cities on every continent except Antarctica. Five features make it an effective vector of urban epidemics:

1. A strong preference for humans. In urban settings it takes most of its blood meals from people, guided by odor receptors tuned to compounds found on human skin.
2. Daytime biting and indoor resting. It bites mainly in the morning and late afternoon and rests inside houses, which shelters it from the weather and means that bed nets, designed against night-biting mosquitoes, offer little protection.
3. Repeated blood feeding. Females often interrupt feeding and move between several people, and they often take more than one meal per batch of eggs. Each interruption is an opportunity to transmit virus.
4. Scattered, drought-resistant eggs. Females divide a batch of eggs among several containers and stick them to the walls above the waterline, where they can survive for months without water.
5. A high temperature optimum. Modeled transmission peaks near 29 °C, higher than for the other major vectors that have been modeled, which suits the species to warm cities and allows it to expand its range as the climate warms.

Aedes aegypti was described by Carl Linnaeus in 1762, in a work by Fredrik Hasselquist based on specimens from Egypt (hence aegypti), as Culex aegypti. The genus Aedes was established by Johann Wilhelm Meigen in 1818. Stegomyia is a subgenus that groups Aedes aegypti, Aedes albopictus, and related species. A 2004 revision proposed that Stegomyia be raised to a genus (giving Stegomyia aegypti), but the change has not been universally adopted, and most medical and entomological literature keeps Aedes aegypti. The species belongs to the class Insecta, the order Diptera (true flies), and the clade Pancrustacea, which includes insects and crustaceans.

Two forms are recognized, treated for a long time as subspecies: Ae. aegypti formosus (the forest form) and Ae. aegypti aegypti (the domestic form). They intergrade where they meet, and many researchers now avoid the formal names.

Adult Aedes aegypti are small to medium mosquitoes, about 4 to 7 mm long. They are dark with white markings. The diagnostic character of the species is a lyre-shaped pattern of pale scales on the upper surface of the thorax (the scutum), with two curved pale lines at the sides and two straight median lines. The legs have white bands at the bases of the tarsal segments, and the last segment of each hind leg is mostly white. The proboscis is dark. The pale scales are easily rubbed off in traps and in older females, so identification of damaged specimens relies on other characters or on molecular methods. Larvae have a short, dark breathing siphon with a single tuft of hairs and a comb of spines on the eighth abdominal segment. Eggs are black and about 0.5 mm long.

From forest to city

Genetic evidence indicates that Aedes aegypti arose in continental Africa, and its closest relatives include species of the western Indian Ocean islands (such as Ae. mascarensis).

• The forest form (Ae. aegypti formosus). Found in woodland and forest across Sub-Saharan Africa. It is darker than the domestic form and generally lacks pale scales on the first abdominal segment, although this character is variable. It rests and bites outdoors, feeds on a range of animals including monkeys and rodents, and lays eggs in natural water-holding cavities such as tree holes, bamboo stumps, and rock pools.
• The domestic form (Ae. aegypti aegypti). This form became dependent on the water that people store, probably during a period of regional drying that reduced natural breeding sites, with genomic studies pointing to the dry Sahel region of West Africa. The timing is debated, and estimates vary by thousands of years. Living beside stored water selected for feeding on the people who kept it, for resting indoors, and for laying eggs on the smooth walls of jars and pots. It is paler, usually with white scales on the first abdominal segment.

Between the sixteenth and nineteenth centuries, the domestic form left Africa. It reached the Americas aboard sailing ships, where eggs stuck to water casks could hatch during a voyage. It brought yellow fever, and later dengue, with it, and it caused epidemics from Brazil and the Caribbean as far north as Philadelphia and Boston. Genomic studies indicate that Asian and Pacific populations descend mainly from American ones. They spread in the nineteenth and twentieth centuries as steamship traffic grew after the opening of the Suez Canal in 1869. In rapidly growing West and Central African cities, the native forest form and the returning domestic mosquitoes interbreed, producing urban populations of mixed ancestry.

Comparison of the two forms of Aedes aegypti with Aedes albopictus

Genome and sex determination

The Aedes aegypti genome is about 1.3 billion base pairs arranged on three pairs of chromosomes, encoding roughly 15,000 protein-coding genes. It is nearly five times the size of the genome of Anopheles gambiae, mostly because about two thirds of it consists of repetitive sequences, in particular mobile elements. Several gene families have expanded, including those for odorant and gustatory receptors and for detoxification enzymes. The genome also contains fragments of RNA viruses (non-retroviral endogenous viral elements) within clusters that produce PIWI-interacting RNAs, which are thought to contribute to antiviral defense.

Unlike Anopheles and mammals, Aedes aegypti has homomorphic sex chromosomes, with no large visible difference between them. Sex is determined by a small male-determining region on one chromosome, which is present only in males.

• The gene Nix, identified in 2015 by Andrew Hall, Zhijian Tu, and colleagues, is the male-determining factor. It acts early in the embryo to direct male-specific splicing of doublesex and fruitless. Disrupting Nix feminizes genetic males, and expressing it in genetic females partly masculinizes them.
• A neighboring gene, myo-sex, encodes a muscle protein that is needed for male flight.

Aedes aegypti passes through four stages: egg, four larval stages (instars), pupa, and adult.

Eggs

A female Aedes aegypti matures about 60 to 150 eggs after a blood meal. She divides them among several containers (skip oviposition), which reduces the risk of losing the whole batch if one container dries or is emptied. Typical sites include water storage drums, washbasins, flower vases, pet bowls, discarded tires, and blocked gutters. She chooses sites by sight, preferring dark interiors, and by smell, in response to compounds from bacteria in the water and to substances from larvae already present. Each egg is cemented to the damp wall of the container just above the water line. It is pale at first and darkens to black within a couple of hours. Over the next two or three days, the embryo develops into a fully formed larva that remains inside the shell.

During embryonic development, the extraembryonic serosa secretes a waxy, waterproof cuticle. Once this has formed, the unhatched larva can survive drying for months (quiescence). This allows eggs to be transported between continents in dry tires and plant pots and to bridge a dry season. Hatching is triggered when the eggs are submerged and the oxygen level in the water falls, as happens in a container with decaying matter. The larva breaks the shell with a small egg burster. Not all eggs hatch at once, so some remain for later flooding.

Larvae and pupae

Larvae of Aedes aegypti hang at an angle below the water surface, with the tip of the siphon at the surface. When disturbed, they dive with a wriggling motion. They scrape bacteria, fungi, algae, and decaying leaf material from the walls and floor of the container. At 27 to 30 °C, they pass through four instars in about 5 to 7 days, followed by 1 to 2 days as a non-feeding pupa, so that development takes about a week in warm conditions and much longer in cool ones.

Containers are small systems with limited food, so competition among larvae is often intense, and it carries over into adult life:

• Starved larvae can delay development for weeks.
• Adults from crowded containers are smaller and emerge with lower energy reserves.
• Smaller females may feed sooner and more often, which raises the biting rate. Whether they are also more susceptible to infection is disputed, with studies reporting effects in both directions.

Adults

Adult Aedes aegypti are active by day, with peaks a few hours after sunrise and before sunset, and little activity in darkness, although artificial light can extend biting into the evening indoors. Unlike Anopheles, which form swarms at dusk, Aedes aegypti males gather around hosts, where they intercept females arriving to feed. A male detects a female by the sound of her wingbeat, and the two adjust their flight tones to converge on a shared harmonic before mating in flight. A substance transferred by the male reduces the willingness of the female to mate again.

Two features of adult feeding are epidemiologically important:

• Reliance on blood. Many mosquitoes feed regularly on plant sugars for flight energy. Several field studies of urban Aedes aegypti (for example in Thailand and Puerto Rico) found that it rarely feeds on sugar and uses blood for both egg production and energy.
• Interrupted feeding. The species is easily disturbed. It approaches from behind and below, bites the ankles and lower legs, and withdraws at the slightest movement. It then moves to another person nearby. A single female may therefore bite several people in completing one meal, and she often takes more than one meal per batch of eggs. An infected female can expose a whole household within a day.

Adult females disperse little, often remaining within about 100 meters of the place where they emerged, provided that people and containers are available. Transmission is therefore concentrated within households and neighborhoods, and it spreads over longer distances mainly through the movement of infected people.

How the mosquito finds people

The shift in Aedes aegypti from feeding on animals to feeding on humans involved changes in the sense of smell, acting at different distances:

1. Carbon dioxide from breath activates receptors on the maxillary palps, triggering upwind flight and making the mosquito more responsive to other cues.
2. Human body odor. Work by Carolyn McBride, Leslie Vosshall, and colleagues showed that the odorant receptor Or4 responds strongly to sulcatone, a compound that is emitted from human skin and is more abundant in human odor than in that of many other animals. The domestic form expresses more of this receptor and is more sensitive to the compound than the forest form.
3. Acids from sweat and skin bacteria, such as lactic acid, are detected by a separate family of ionotropic receptors. Sequencing of single neurons by Margaret Herre, Vosshall, and colleagues showed that many olfactory neurons of Aedes aegypti express several receptor types at once, which breaks the "one neuron, one receptor" rule found in other animals. This redundancy helps to explain why disabling one receptor does not abolish attraction to people.
4. Heat, humidity, and sight. Within about a meter, temperature and humidity sensors on the antennae, together with a preference for dark objects, guide the mosquito to land and probe.

Quantifying transmission

In Aedes aegypti, the Ross-Macdonald model describes vector-borne transmission. The vectorial capacity and the basic reproduction number per generation of transmission (host to vector to host) can be written as:

where m is the number of mosquitoes per person, a is the daily biting rate on humans, μ is the daily death rate of the mosquito, n is the extrinsic incubation period in days, b and c are the transmission probabilities from mosquito to human and from human to mosquito, and 1/_γ_ is the infectious period in humans. Many authors define R₀ per transmission step, which takes the square root of this expression, and the two conventions give different numerical values with the same threshold of 1. The term e^−_μn_ is the probability that a mosquito survives the incubation period. For μ = 0.1 per day, it is e⁻¹ ≈ 0.37 for a 10-day period and e^−0.6 ≈ 0.55 for a 6-day period, so that warming has a large effect.

Arboviral transmission differs from malaria in two respects. A person with dengue is infectious to mosquitoes for only about 4 to 7 days, compared with weeks to months for untreated malaria, which limits the opportunity for onward transmission. Against this, Aedes aegypti bites humans often and almost exclusively, and because the biting rate enters squared, this raises transmission substantially. The balance of these effects depends on the local mosquito density and the temperature.

The viruses

Major arboviruses transmitted by Aedes aegypti

Barriers inside the mosquito

To become infectious, an Aedes aegypti female must be infected by virus taken up in a blood meal, and the virus must pass several barriers:

1. Infecting the gut. The virus must reach and infect cells of the midgut, before the peritrophic matrix forms around the blood meal and while digestive enzymes are active.
2. Escaping the gut. After replication, new particles must cross the basal lamina, a dense layer of connective tissue around the gut, into the hemolymph. Escape is affected by the stretching of the gut as it fills and by enzymes that remodel the lamina. A second blood meal taken a few days after an infectious one can increase and speed up the dissemination of virus, which shortens the time to infectiousness by a few days in experiments.
3. Surviving the mosquito's defenses. The main antiviral defense is RNA interference, in which Dicer-2 cuts double-stranded viral RNA into small interfering RNAs that guide Argonaute-2 to destroy viral RNA. Flaviviruses, including dengue and Zika, produce a structured subgenomic RNA that counteracts this. A PIWI-interacting RNA pathway also produces viral small RNAs, and mosquitoes can make viral DNA forms that are integrated in the genome. The Toll, IMD, and JAK-STAT pathways produce antimicrobial effectors. Gut bacteria also matter. Some strains stimulate immunity, and individual studies report that particular bacteria reduce dengue infection, and that some fungi increase susceptibility.
4. Reaching the saliva. The virus infects the salivary glands and is released in saliva when the mosquito probes. Saliva contains many proteins, including vasodilators and anticoagulants, and it modulates the local immune response. In experiments, virus delivered in saliva produces higher infection than virus injected without it.

The domestic form of Aedes aegypti is found in the tropics and subtropics, in and around houses and in cities. In the Americas it ranges from the southern United States to northern Argentina. It is established in much of South and Southeast Asia, northern Australia, the Pacific islands, and tropical Africa. In Europe it was present until the 1950s, and it disappeared from the Mediterranean region, but populations were later found around the Black Sea, in Madeira, and in Cyprus. The factors that limit its range are winter cold (adults and eggs do not survive freezing) and, in dry regions, a lack of water containers.

Temperature

Aedes aegypti evolved in hot climates, and modeled transmission by it peaks at a higher temperature than for Aedes albopictus and for malaria.

Temperature limits for transmission, as modeled (approximate 95 percent intervals in parentheses)

The difference of about 4 °C between the optima for malaria and for the _Aedes_-borne viruses is relevant to climate projections. Much of tropical Africa, Asia, and Latin America has mean temperatures of 25 to 28 °C. Further warming is projected to move parts of these regions past the malaria optimum and toward the peak for dengue, which would shift part of the burden from rural malaria toward urban arboviral disease, although the real outcome depends on many other factors, including urbanization, water supply, and vaccination. The models are fitted to laboratory data, and the intervals are wide.

Development time and daily temperature variation

The time needed for dengue virus to develop in Aedes aegypti falls steeply with temperature. Experimental estimates are roughly 20 days or more at 20 °C (longer than most mosquitoes live in the field), about 10 to 14 days at 25 °C, about a week at 30 °C, and 5 to 6 days at 32 °C. Daily temperature variation modifies this, as shown experimentally by Louis Lambrechts, Thomas Scott, and colleagues. Where mean temperatures are already warm, large daily swings reduce infection and survival. Where mean temperatures are cool, large swings can increase transmission, because the virus develops faster during warm afternoons.

Rainfall, drought, and cities

Unlike mosquitoes that breed in puddles, Aedes aegypti does not simply become more abundant as rainfall increases.

1. Rainy seasons fill outdoor containers such as tires, waste plastic, and gutters, increasing the number of breeding sites.
2. Drought can also increase risk. When piped supplies fail, households store water in open drums and buckets. These containers are warm and constantly refilled, and high temperatures shorten the incubation period of the virus. Droughts associated with El Niño have preceded large outbreaks in several regions, although this is only one of several factors.
3. Cities are warmer than their surroundings, by roughly 2 to 5 °C in some cases, because of paved surfaces, waste heat, and the loss of vegetation, and this adds to global warming.

The species and local dengue transmission have extended upslope in the tropics, for example in the Andes and in the highlands of Mexico, and Kathmandu, at about 1,400 m, has had dengue epidemics in recent years. Locally acquired dengue has occurred in France, Italy, and Spain, but in Europe it has been transmitted mostly by Aedes albopictus.

Surveillance of Aedes aegypti relies on counting stages of the mosquito and on testing for virus. Ovitraps (containers with a surface for egg laying), larval surveys, and adult traps (such as the BG-Sentinel trap, with a lure imitating human odor, and gravid traps) are used. Larval indices such as the house index, the container index, and the Breteau index (positive containers per 100 houses) are in use, but they correlate poorly with the risk of disease. The pupae-per-person index is considered a better measure of adult production. Mosquitoes can be tested for virus in pools by RT-PCR. Data from human cases, notified by health services and by sentinel sites, are used together with entomological data, and citizen science platforms collect photographs of mosquitoes.

The eradication campaign and the limits of fogging

Between 1947 and 1970, the Pan American Health Organization, under Fred Soper, attempted to eliminate Aedes aegypti from the Americas to prevent urban yellow fever. Inspection teams went house to house, removing containers and spraying surfaces with DDT. By the early 1960s, the mosquito had been eliminated from most countries of South and Central America. Several countries, including the United States and Venezuela, did not complete the work, and commitment faded after 1970, so the mosquito returned. Resistance to DDT, rapid and unplanned urban growth, the spread of disposable plastics, and the movement of goods all contributed. By 2000, it had again occupied nearly all of the region, which now has all four dengue types in circulation and had the chikungunya and Zika epidemics of 2013 and 2015.

Municipal responses to outbreaks often still rely on spraying insecticide as a fog from vehicles or aircraft. Evidence that this reduces dengue transmission is limited, for several reasons: the mosquitoes rest indoors, where little aerosol reaches, the spray does not affect eggs, larvae, or pupae, so adult numbers recover quickly, and many populations are resistant to the insecticides used.

Insecticide resistance

In Aedes aegypti, household sprays, municipal fogging, and the larvicide temephos have selected for resistance by several mechanisms at once.

Resistance mechanisms in Aedes aegypti

Newer methods

Modern Aedes aegypti control programs evaluate several targeted interventions:

• Targeted indoor spraying and spatial repellents. Because the mosquitoes rest on lower wall surfaces, in closets, and under furniture, spraying only these places with a non-pyrethroid insecticide (targeted indoor residual spraying, developed by Gonzalo Vazquez-Prokopec and colleagues) reduced mosquito numbers in trials while using less insecticide. Spatial repellents release volatile compounds, such as transfluthrin, that reduce biting in a space, and trials in Peru and elsewhere have reported reductions in infection, although results differ among trials.
• Larval control and autodissemination. Water drums can be treated with bacterial larvicides, such as Bacillus thuringiensis israelensis, or with insect growth regulators, such as pyriproxyfen. Hidden containers can be reached indirectly by traps that dust visiting females with pyriproxyfen or a fungus, which they carry to other containers during skip oviposition.
• Wolbachia replacement. Wolbachia does not occur naturally in Aedes aegypti. Strains introduced into it (_w_Mel and _w_AlbB) spread through the population by cytoplasmic incompatibility, and they reduce the ability of the mosquito to transmit dengue and related viruses. Once established above a threshold of roughly 20 to 35 percent, the infection can persist without further releases. In a randomized trial in Yogyakarta, Indonesia, it reduced symptomatic dengue by 77 percent and hospital admissions by 86 percent. It has since been deployed in Brazil, Colombia, Australia, Vietnam, and Malaysia. In northern Queensland, local dengue transmission has been rare or absent for years after deployment, although this was not a randomized trial.
• Population suppression. Releasing only _Wolbachia_-carrying males (the incompatible insect technique), with or without low-dose irradiation, makes wild females lay inviable eggs, and it has suppressed mosquito populations and dengue cases in Singapore and elsewhere.
• Genetic methods. Releases of male Aedes aegypti carrying a gene that kills their female offspring (OX513A and later strains) have been tested in Brazil, the Cayman Islands, Panama, and Florida. Other systems, such as CRISPR-based precision-guided sterile insect technique (pgSIT), and gene drives are at the laboratory stage.

Vaccines

Vector control against Aedes aegypti is increasingly combined with vaccination. The live attenuated yellow fever vaccine, developed by Max Theiler in the 1930s, gives long-lasting protection after one dose. For dengue, the vaccine Dengvaxia was limited to people who had a previous infection, because of a higher risk of severe disease in those who had not, and its production was later discontinued. TAK-003 was recommended by the World Health Organization in 2023 for children in areas of high transmission, and a single-dose vaccine developed in Brazil (Butantan-DV) has shown high efficacy in a phase 3 trial and has been approved in Brazil. Two chikungunya vaccines have been approved, a live attenuated vaccine, for which use in older adults has been restricted because of safety reports, and a virus-like particle vaccine.

Why is *Aedes aegypti* a more efficient urban dengue vector than *Aedes albopictus*?

*Aedes aegypti* exhibits strict anthropophily, resting indoors and taking over 90% of its blood meals from humans via upregulated sulcatone-sensitive Or4 odorant receptors. Furthermore, *Aedes aegypti* females rarely feed on plant sugars and instead take multiple interrupted blood meals per gonotrophic cycle. Because the human biting rate (*a*) is squared in the Ross-Macdonald vectorial capacity equation, this high-frequency human feeding amplifies transmission far beyond that of the more opportunistic, outdoor-resting *Aedes albopictus*.

How do *Aedes aegypti* eggs survive prolonged drought and intercontinental transport?

During embryogenesis, about 12 to 16 hours after oviposition, the extraembryonic serosa of *Aedes aegypti* secretes a chitin-containing, lipid-rich waterproof serosal cuticle beneath the chorion. This barrier drastically reduces water permeability, allowing the fully developed unhatched first-instar larva to enter quiescence and survive desiccation for 4 to 6 months. Hatching is subsequently triggered when flooding submerges the egg and microbial respiration lowers dissolved oxygen concentrations below a critical threshold.

How does *Wolbachia* infection block dengue virus replication in *Aedes aegypti*?

Artificially transinfected *Wolbachia* strains (*w*Mel and *w*AlbB) colonize *Aedes aegypti* somatic and reproductive tissues, where they compete directly with flaviviruses for intracellular cholesterol and endoplasmic reticulum membranes required to form viral replication complexes. In addition, *Wolbachia* primes mosquito innate immune pathways, elevating basal reactive oxygen species (ROS) and antimicrobial peptides while disrupting host RNA-binding proteins, which collectively prevent dengue virions from reaching the salivary glands.

• Dengue fever
• Mosquito-borne disease
• Vector control
• Aedes albopictus
• Wolbachia
• Yellow fever
• Zika fever