It has been identified in a wide variety of primates, including prosimians, New World and Old World monkeys, as well as apes, and each species has been shown to harbor a unique (species-specific) strain of SFV, including African green monkeys, baboons, macaques, and chimpanzees.

Although the simian foamy virus is endemic in African apes and monkeys, there are extremely high infection rates in captivity, ranging from 70% to 100% in adult animals.

The cellular receptors have not been characterized, but it is hypothesized that it has a molecular structure with near ubiquitous prevalence, since a wide range of cells are permissible to infection.

[9] The Bet protein is required for viral replication, as it counteracts the innate antiretroviral activity of APOBEC3 family defense factors by obstructing their incorporation into virions.

Recently, a novel mechanism was reported where foamy virus accessory protein Bet (unlike HIV-1 Vif) impaired the cytoplasmic solubility of APOBEC3G.

The IP is also unique in that the virus has the capacity to transcribe mRNAs from it; usually the complex retroviruses exclusively express transcripts from the LTR.

[16] Once the virus has entered the interior of the cell, the retroviral core undergoes structural transformations through the activity of viral proteases.

Whereas most retroviruses deposit ssRNA(+) into the cell, SFV and other related species are different in that up to 20% of released viral particles already contains dsDNA genomes.

This is due to a unique feature of spumaviruses in which the onset of reverse transcription of genomic RNA occurs before release rather than after entry of the new host cell like in other retroviruses.

This gives rise to the unspliced full length mRNA that will serve as genomic RNA to be packaged into virions, or used as a template for translation of gag.

[10] The spliced mRNAs encode pol (PR, RT, RnaseH, IN) and env (SU, TM) that will be used to later assemble the viral particles.

Evidence for this interaction was discovered in 2001 when a deliberate mutation for a conserved arginine (Arg) residue at position 50 to alanine of the SFVcpz inhibited proper capsid assembly and abolished viral budding even in the presence of the envelope glycoproteins.

[19] Analysis of the glycoproteins on the envelope of the viral particle indicate that it is localized to the endoplasmic reticulum (ER), and that once it buds from the organelle, the maturation process is finalized and can leave to infect additional cells.

A dipeptide of two lysine residues (dilysine) was the identified motif that determined to be the specific molecule that mediated the signal, localizing viral particles in the ER.

[9] With little evidence to suggest that SFV infection causes illness, some scientists believe that it has a commensal relationship to simians.

SFV/SIV models have since been proposed to replicate the relationship between SFV and HIV in humans, a potential health concern for officials.

[27] The phylogenetic tree analysis of SFV polymerase and mitochondrial cytochrome oxidase subunit II (COII has been shown as a powerful marker used for primate phylogeny) from African and Asian monkeys and apes provides very similar branching order and divergence times among the two trees, supporting the cospeciation.

These results suggest SFV has been cospeciated with Old World primates for about 30 million years, making them the oldest known vertebrate RNA viruses.

A strong linear relationship was found between the branch lengths for the host and SFV gene trees, which indicated synchronous genetic divergence in both data sets.

The high SFV infection rates of chimpanzees provide an opportunity to monitor where humans are exposed to these viruses.

[citation needed] Persistence in the absence of disease, but in the presence of antibodies is a defining characteristic of FV infection.

In 1971, a viral agent with FV-like characteristics was isolated from lymphoblastoid cells released from a human nasopharyngeal carcinoma (NPC) from a Kenyan patient.

[29] The agent was termed a human FV because of its origin, and named SFVcpz(hu) as the prototypic laboratory strain.

In addition, phylogenetic analysis showed that the pol regions of the two genomes shared 89–92% of their nucleotides and 95–97% of the amino acids are identical between the human virus and various SFV strains.

This subspecies has a natural habitat in Kenya and thus was most likely the origin of this SFV variant, and the virus was probably acquired as a zoonotic infection.