Structural and Evolutionary Analysis of an Orangutan Foamy Virus

Verschoor, Ernst J.; Langenhuijzen, Susan; Engel, Saskia van den; Niphuis, Henk; Warren, K.; Heeney, Jonathan L.

doi:10.1128/jvi.77.15.8584-8587.2003

Cited by 12 publications

(6 citation statements)

References 39 publications

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“…As illustrated schematically in Fig. 1D the YXXL motif is conserved between FV of different species and is duplicated in bovine FV and the recently characterized SFVora isolate (43). All primate FV isolates contain a PSAP motif, and a PPPX motif is found in all primate FV Gag proteins except for SFVagm, whereas both motifs are absent in FFV, bovine FV, and equine FV.…”

Section: Identification Of Late Domain Consensus Sequences In the Pfvmentioning

confidence: 99%

Characterization of Prototype Foamy Virus Gag Late Assembly Domain Motifs and Their Role in Particle Egress and Infectivity

Stange

Mannigel

Peters

et al. 2005

J Virol

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Foamy viruses (FV) are unusual among retroviruses since they require both Gag and Env structural proteins for particle egress. Recently significant progress has been made towards the mechanistic understanding of the viral release process, in particular that of retroviruses, and the viral domains and cellular pathways involved. However little is currently known about domains of FV structural proteins and cellular proteins engaged in this process. By mutational analysis of sequence motifs in prototype FV (PFV) Gag, bearing homology to known late assembly (L) domains, a PSAP motif with L domain function that was functionally interchangeable by heterologous L domains was identified. In contrast the inactivation of a PPPI motif had no significant influence on PFV particle release, although mutant viral particles displayed reduced infectivity. Similarly mutation of an evolutionary conserved YXXL motif revealed no classical L-domain function but resulted in release of noninfectious viruslike particles. Biochemical and electron microscopy analysis demonstrated that these mutant particles incorporated all viral structural proteins but contained aberrantly capsid structures, suggesting a role in capsid assembly for this PFV Gag sequence motif. In line with the mutational analysis, overexpression of dominant negative (DN) mutants and wild-type TSG101 but not the DN mutant of AIP-1/ALIX reduced PFV particle release and infectivity. Furthermore, DN mutants of Vps4A, Vps4B, and CHMP3 inhibited PFV egress and infectivity. Taken together these results demonstrate that PFV, like other viruses, requires components of the vacuolar protein sorting (VPS) machinery for egress and enters the VPS pathway through interaction with TSG101.Particle release from infected cells is one of the last steps in the retroviral replication cycle, which is accomplished by budding of viral particles across cellular membranes. On the viral side the orthoretroviral Gag polyprotein contains all the essential structural information for particle egress, and Gag expression by itself is sufficient for the release of viruslike particles (VLP). Although for some orthoretroviruses, such as Mason-Pfizer monkey virus (MPMV), coexpression of Env enhances viral particle release (37). In recent years significant advances have been made in the understanding of the mechanistic processes involved in the retroviral budding process. In particular the interaction domains of the viral Gag protein with essential cellular factors required during late stages of the budding process and involved in pinching off the viral particle from the cellular membrane have been identified. To date three consensus sequences of so-called viral late-budding or late-assembly (L) domains have been characterized. A P(T/ S)AP L-domain motif originally identified in the human immunodeficiency virus type 1 (HIV-1) Gag p6 domain (13), a PPXY L-domain motif first found in the Rous sarcoma virus (RSV) Gag p2b cleavage product (47) and a YPXL motif present in the equine infectious anemia virus (EIAV) G...

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Section: Identification Of Late Domain Consensus Sequences In the Pfvmentioning

confidence: 99%

Characterization of Prototype Foamy Virus Gag Late Assembly Domain Motifs and Their Role in Particle Egress and Infectivity

Stange

Mannigel

Peters

et al. 2005

J Virol

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“…The recognition that AIDS originated as a zoonosis heightened public health concerns associated with infection of humans by other simian retroviruses endemic in non-human primates (NHPs) (Switzer et al, 2004). These retroviruses include several strains of simian immunodeficiency virus (SIV) (Hahn et al, 2000;Peeters et al, 2002), simian T-cell lymphotropic virus types 1, 2 and 3 (STLV-1/2/3) (Meertens & Gessain, 2003;Meertens et al, 2001) and simian foamy retroviruses (SFVs or spumaretroviruses) (Bieniasz et al, 1995;Broussard et al, 1997;Hussain et al, 2003;Switzer et al, 2004;Verschoor et al, 2003).…”

mentioning

confidence: 99%

Natural simian foamy virus infection in wild-caught gorillas, mandrills and drills from Cameroon and Gabon

Calattini

Nerrienet

Mauclère

et al. 2004

Journal of General Virology

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A survey for the presence of simian foamy retroviruses (SFVs) was performed in 44 wild-caught apes and monkeys, including 27 gorillas, 11 mandrills and six drills, originating from south Cameroon or Gabon. Combined serological and/or nested-PCR assays indicated SFV infection among five Gorilla gorilla gorilla, seven Mandrillus sphinx and two Mandrillus leucophaeus. Sequences of a 425 bp fragment of the integrase gene were obtained for 11 animals. Phylogenetic studies indicated that strains from gorillas, mandrills and drills each formed a highly supported phylogenetic clade with, moreover, the existence of two different gorilla SFVs. This study demonstrates for the first time that these animals are naturally infected with specific SFVs. In the context of simian-to-human interspecies transmission, the results confirm that such viruses can also infect humans, as the SFVs identified in wild-caught animals were the same as those recently reported as infecting hunters living in the same geographical areas.

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“…This is a remarkable low rate of evolution for a virus with RT that is as error-prone as other retroviruses. It has been suggested that FV may replicate through clonal expansion, analogous to primate T-lymphotropic viruses (Leendertz et al, 2008;Verschoor et al, 2003), thereby avoiding the introduction of many RT-induced mutations over short timescales. However, although most tissues harbour latent provirus in naturally infected rhesus macaques, viral replication does take place in oral mucosa (Murray et al, 2008), which complicates an explanation of low evolutionary rates by clonal expansion.…”

mentioning

confidence: 99%

“…FV have been isolated and cloned from a variety of primate (for references see below) and non-primate hosts (Holzschu et al, 1998;Tobaly-Tapiero et al, 2000;Winkler et al, 1997). Evolutionary studies would benefit from the characterization of the FV genomic diversity, but to date, only a few primate FVs from macaques (SFVmac) (Kupiec et al, 1991), African green monkey (SFVagm) (Renne et al, 1992), orang-utan (SFVora) (Verschoor et al, 2003), chimpanzees (SFVcpz) (Herchenröder et al, 1994(Herchenröder et al, , 1995, spider monkey (SFVspm) (Thümer et al, 2007), marmoset and squirrel monkey (Pacheco et al, 2010) have been cloned and completely sequenced. Although the gorilla simian FV (SFVgor) has been previously isolated and partially sequenced (Bieniasz et al, 1995;Calattini et al, 2004Calattini et al, , 2007Wolfe et al, 2004), the complete sequence of the SFVgor represents the last missing piece of the FV genomic puzzle within the great apes.…”

mentioning

confidence: 99%