Alphaviruses belong to group IV of the Baltimore classification of viruses, with a positive-sense, single-stranded RNA genome.

[1] There are 32 alphavirus species, which infect various vertebrates such as humans, rodents, fish, birds, and larger mammals such as horses, as well as invertebrates.

[2] Transmission between species and their vertebrate hosts (including human) occurs mainly via mosquitoes, making the alphaviruses a member of the collection of arboviruses – or arthropod-borne viruses.

[3] The alphaviruses are small, spherical, enveloped viruses with a genome of a single strand of positive-sense RNA.

The viral membrane-anchored surface glycoproteins are responsible for receptor recognition and entry into target cells through membrane fusion.

[4] Upon exposure of the virus to the acidity of the endosome, E1 dissociates from E2 to form an E1 homotrimer, which is necessary for the fusion step to drive the cellular and viral membranes together.

[5] The E2 glycoprotein functions to interact with the nucleocapsid through its cytoplasmic domain, while its ectodomain is responsible for binding a cellular receptor.

Most alphaviruses lose the peripheral protein E3, but in Semliki viruses it remains associated with the viral surface.

Four nonstructural proteins (nsP1–4) which are produced as a single polyprotein constitute the virus' replication machinery.

[6] The processing of the polyprotein occurs in a highly regulated manner, with cleavage at the P2/3 junction influencing RNA template use during genome replication.

Mutations in nsP2 that produce noncytopathic viruses or a temperature sensitive phenotypes cluster at the P2/P3 interface region.

These include prohibitin, phosphatidylserine, glycosaminoglycans and ATP synthase β subunit (ref needed).

Replication occurs within the cytoplasm, specifically in areas termed "spherules" separated by plasma membrane invaginations from the rest.

These two glycoproteins are the targets of numerous serologic reactions and tests including neutralization and hemagglutination inhibition.

A study of this taxon suggests that this group of viruses had a marine origin—specifically the Southern Ocean—and that they have subsequently spread to both the Old and New World.

Once a human is bitten by the infected mosquito, the virus can gain entry into the bloodstream, causing viremia.

Vector control with repellents, protective clothing, breeding site destruction, and spraying are the preventive measures of choice.

Alphaviruses can be engineered to create replicon vectors which efficiently induce humoral and T-cell immune responses.

The flaviviruses were formed into their own family when sufficient differences with the alphaviruses were noted due to the development of sequencing.