Abstract
Non-human primates (NHP) are an important source of viruses that can spillover to humans and, after adaptation, spread through the host population. Whereas HIV-1 and HTLV-1 emerged as retroviral pathogens in humans, a unique class of retroviruses called foamy viruses (FV) with zoonotic potential are occasionally detected in bushmeat hunters or zookeepers. Various FVs are endemic in numerous mammalian natural hosts, such as primates, felines, bovines, and equines, and other animals, but not in humans. They are apathogenic, and significant differences exist between the viral life cycles of FV and other retroviruses. Importantly, FVs replicate in the presence of many well-defined retroviral restriction factors such as TRIM5α, BST2 (Tetherin), MX2, and APOBEC3 (A3). While the interaction of A3s with HIV-1 is well studied, the escape mechanisms of FVs from restriction by A3 is much less explored. Here we review the current knowledge of FV biology, host restriction factors, and FV–host interactions with an emphasis on the consequences of FV regulatory protein Bet binding to A3s and outline crucial open questions for future studies.
Highlights
The first description of a foamy virus (FV) was reported in 1954 [1]
Since the original human foamy virus (HFV) isolate came from a person who might have had contact with chimpanzees in Kenya, the virus was probably acquired as a zoonotic infection
HFV has been renamed as the prototype foamy virus (PFV), it is debated whether the “real” origin of the virus isolate derived from in vivo cross-species transmission from chimpanzee or from a cell culture contamination [5]
Summary
The first description of a foamy virus (FV) was reported in 1954 [1]. It was found as a contaminant with an atypical cytopathic effect (CPE), eliciting the formation of multinucleated and vacuolated giant cells in primary kidney cell cultures from Old World monkeys of the Macacaceae family. In 1971, a viral agent with FV-like characteristics was identified from lymphoblastoid cells in cultures of a nasopharyngeal carcinoma (NPC) from a Kenyan patient [3] The origin of this human foamy virus (HFV) was discussed until 1994, when HFV was cloned and sequenced [4]. Molecular clock calibrations have revealed an extremely low rate of SFV evolution, 1.7 × 10−8 base substitutions per site per year, making FV the slowest-evolving virus documented so far These investigations revealed highly congruent relationships, indicating virus-host co-evolution for at least 30–40 million years [20,21]. Infection rates ranging from 70% to 100% are reported in adult animals [5,6,23], and high numbers of SFVcpz infections in wild-living chimpanzees across equatorial Africa were documented [14]. Humans are dead-end hosts of primate foamy viruses, and no human foamy virus has evolved so far [10,35,36]
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