scholarly journals Identification of Recombination in the Envelope Gene of Simian Foamy Virus Serotype 2 Isolated from Macaca cyclopis

2013 ◽  
Vol 87 (15) ◽  
pp. 8792-8797 ◽  
Author(s):  
T. A. Galvin ◽  
I. A. Ahmed ◽  
M. Shahabuddin ◽  
T. Bryan ◽  
A. S. Khan
1982 ◽  
Vol 44 (2) ◽  
pp. 720-724 ◽  
Author(s):  
A B Benzair ◽  
A Rhodes-Feuillette ◽  
R Emanoïl-Ravicovitch ◽  
J Peries

2018 ◽  
Vol 6 (3) ◽  
Author(s):  
Subhiksha Nandakumar ◽  
Eunhae H. Bae ◽  
Arifa S. Khan

ABSTRACTThe full-length sequence of simian foamy virus serotype 3 (SFV-3) strain FV2014, an African green monkey (Chlorocebus aethiops) isolate, was obtained using high-throughput sequencing. SFVcae_FV2014 consisted of 13,127 bp and had a genomic organization similar to those of other SFVs but was distinct from SFV strain LK3, isolated from the same monkey species.


2015 ◽  
Vol 89 (24) ◽  
pp. 12480-12491 ◽  
Author(s):  
Léa Richard ◽  
Réjane Rua ◽  
Edouard Betsem ◽  
Augustin Mouinga-Ondémé ◽  
Mirdad Kazanji ◽  
...  

ABSTRACTSimian foamy virus (SFV) is a ubiquitous retrovirus in nonhuman primates (NHPs) that can be transmitted to humans, mostly through severe bites. In the past few years, our laboratory has identified more than 50 hunters from central Africa infected with zoonotic SFVs. Analysis of the complete sequences of five SFVs obtained from these individuals revealed thatenvwas the most variable gene. Furthermore, recombinant SFV strains, some of which involve sequences in theenvgene, were recently identified. Here, we investigated the variability of theenvgenes of zoonotic SFV strains and searched for possible recombinants. We sequenced the completeenvgene or its surface glycoprotein region (SU) from DNA amplified from the blood of (i) a series of 40 individuals from Cameroon or Gabon infected with a gorilla or chimpanzee foamy virus (FV) strain and (ii) 1 gorilla and 3 infected chimpanzees living in the same areas as these hunters. Phylogenetic analyses revealed the existence of twoenvvariants among both the gorilla and chimpanzee FV strains that were present in zoonotic and NHP strains. These variants differ greatly (>30% variability) in a 753-bp-long region located in the receptor-binding domain of SU, whereas the rest of the gene is very conserved. Although the organizations of the Env protein sequences are similar, the potential glycosylation patterns differ between variants. Analysis of recombination suggests that the variants emerged through recombination between different strains, although all parental strains could not be identified.IMPORTANCESFV infection in humans is a great example of a zoonotic retroviral infection that has not spread among human populations, in contrast to human immunodeficiency viruses (HIVs) and human T-lymphotropic viruses (HTLVs). Recombination was a major mechanism leading to the emergence of HIV. Here, we show that two SFV molecular envelope gene variants circulate among ape populations in Central Africa and that both can be transmitted to humans. These variants differ greatly in the SU region that corresponds to the part of the Env protein in contact with the environment. These variants may have emerged through recombination between SFV strains infecting different NHP species.


1979 ◽  
Vol 8 (5) ◽  
pp. 308-320 ◽  
Author(s):  
Alice Rhodes-Feuillette ◽  
Fortuna Saal ◽  
Jacqueline Lasneret ◽  
Pierre Dubouch ◽  
Jorge Périès

Epidemiologia ◽  
2021 ◽  
Vol 2 (1) ◽  
pp. 46-67
Author(s):  
Antoinette C. van der Kuyl

Old World monkeys (OWM), simians inhabiting Africa and Asia, are currently affected by at least four infectious retroviruses, namely, simian foamy virus (SFV), simian immunodeficiency virus (SIV), simian T-lymphotropic virus (STLV), and simian type D retrovirus (SRV). OWM also show chromosomal evidence of having been infected in the past with four more retroviral species, baboon endogenous virus (BaEV), Papio cynocephalus endogenous virus (PcEV), simian endogenous retrovirus (SERV), and Rhesus endogenous retrovirus-K (RhERV-K/SERV-K1). For some of the viruses, transmission to other primates still occurs, resulting, for instance, in the HIV pandemic. Retroviruses are intimately connected with their host as they are normally spread by close contact. In this review, an attempt to reconstruct the distribution and history of OWM retroviruses will be made. A literature overview of the species infected by any of the eight retroviruses as well as an age estimation of the pathogens will be given. In addition, primate genomes from databases have been re-analyzed for the presence of endogenous retrovirus integrations. Results suggest that some of the oldest retroviruses, SERV and PcEV, have travelled with their hosts to Asia during the Miocene, when a higher global temperature allowed simian expansions. In contrast, younger viruses, such as SIV and SRV, probably due to the lack of a primate continuum between the continents in later times, have been restricted to Africa and Asia, respectively.


2007 ◽  
Vol 13 (9) ◽  
pp. 1314-1320 ◽  
Author(s):  
Sara Calattini ◽  
Edouard B.A. Betsem ◽  
Alain Froment ◽  
Philippe Mauclère ◽  
Patricia Tortevoye ◽  
...  

Retrovirology ◽  
2011 ◽  
Vol 8 (S1) ◽  
Author(s):  
Jayashree S Nandi ◽  
Anil K Chhangani ◽  
Surendra M Mohnot

2001 ◽  
Vol 75 (15) ◽  
pp. 6857-6864 ◽  
Author(s):  
Scott W. Eastman ◽  
Maxine L. Linial

ABSTRACT In contrast to all retroviruses but similar to the hepatitis B virus, foamy viruses (FV) require expression of the envelope protein for budding of intracellular capsids from the cell, suggesting a specific interaction between the Gag and Env proteins. Capsid assembly occurs in the cytoplasm of infected cells in a manner similar to that for the B- and D-type viruses; however, in contrast to these retroviruses, FV Gag lacks an N-terminal myristylation signal and capsids are not targeted to the plasma membrane (PM). We have found that mutation of an absolutely conserved arginine (Arg) residue at position 50 to alanine (R50A) of the simian foamy virus SFV cpz(hu) inhibits proper capsid assembly and abolishes viral budding even in the presence of the envelope (Env) glycoproteins. Particle assembly and extracellular release of virus can be restored to this mutant with the addition of an N-terminal Src myristylation signal (Myr-R50A), presumably by providing an alternate site for assembly to occur at the PM. In addition, the strict requirement of Env expression for capsid budding can be bypassed by addition of a PM-targeting signal to Gag. These results suggest that intracellular capsid assembly may be mediated by a signal akin to the cytoplasmic targeting and retention signal CTRS found in Mason-Pfizer monkey virus and that FV Gag has the inherent ability to assemble capsids at multiple sites like conventional retroviruses. The necessity of Env expression for particle egress is most probably due to the lack of a membrane-targeting signal within FV Gag to direct capsids to the PM for release and indicates that Gag-Env interactions are essential to drive particle budding.


Sign in / Sign up

Export Citation Format

Share Document