<i>In Vivo</i>
            Cellular Tropism of Gorilla Simian Foamy Virus in Blood of Infected Humans

Rua, Réjane; Betsem, Edouard; Montange, Thomas; Buseyne, Florence; Gessain, Antoine

doi:10.1128/jvi.01801-14

Cited by 20 publications

(22 citation statements)

References 21 publications

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“…ϩ T, and B lymphocytes in the blood of infected humans (30). Our study also revealed natural polymorphisms in gag and bet between SFV strains originating from different chimpanzee subspecies and polymorphisms in U3 and tas at the interindividual level (31).…”

mentioning

confidence: 73%

Cocirculation of Two env Molecular Variants, of Possible Recombinant Origin, in Gorilla and Chimpanzee Simian Foamy Virus Strains from Central Africa

Richard

Rua

Betsem

et al. 2015

J Virol

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Simian 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 that env was the most variable gene. Furthermore, recombinant SFV strains, some of which involve sequences in the env gene, were recently identified. Here, we investigated the variability of the env genes of zoonotic SFV strains and searched for possible recombinants. We sequenced the complete env gene 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 two env variants 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.

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confidence: 73%

Cocirculation of Two env Molecular Variants, of Possible Recombinant Origin, in Gorilla and Chimpanzee Simian Foamy Virus Strains from Central Africa

Richard

Rua

Betsem

et al. 2015

J Virol

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“…By studying a larger cohort of humans infected with a gorilla strain of SFV in Cameroon, we demonstrated that CD8+, CD4+ T cells and CD19+ B lymphocytes were preferentially infected, compared to monocytes and NK cells ( Table 1). SFV DNA was detected in both memory and naive CD4+ T lymphocytes and SFV DNA levels in CD4+ T cells were positively correlated with the duration of the infection [27].…”

Section: Sfv Tropismmentioning

confidence: 94%

Origin, evolution and innate immune control of simian foamy viruses in humans

Rua

Gessain

2015

Current Opinion in Virology

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Most viral pathogens that have emerged in humans have originated from various animal species. Emergence is a multistep process involving an initial spill-over of the infectious agent into single individuals and its subsequent dissemination into the human population. Similar to simian immunodeficiency viruses and simian T lymphotropic viruses, simian foamy viruses (SFV) are retroviruses that are widespread among non-human primates and can be transmitted to humans, giving rise to a persistent infection, which seems to be controlled in the case of SFV. In this review, we present current data on the discovery, cross-species transmission, and molecular evolution of SFV in human populations initially infected and thus at risk for zoonotic emergence.

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“…Porcine circovirus type 2 (PCV2) spliced capsid mRNA (Cap mRNA) and viral DNA were detected in B lymphocytes from pigs, although no further studies were performed to determine if the presence of these nucleic acids corresponds to a productive infection, with release of viral progeny from these cells (20). The capacity of simian foamy viruses (SFVs) to transcribe genes in human B lymphocytes was also recently described (21). Interestingly, live rabies virus vaccines have been shown to infect murine and human B lymphocytes (22).…”

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confidence: 99%

Early Activation of Teleost B Cells in Response to Rhabdovirus Infection

Abós

Castro

Granja

et al. 2015

J Virol

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To date, the response of teleost B cells to specific pathogens has been only scarcely addressed. In this work, we have demonstrated that viral hemorrhagic septicemia virus (VHSV), a fish rhabdovirus, has the capacity to infect rainbow trout spleen IgMpositive (IgM ؉ ) cells, although the infection is not productive. Consequently, we have studied the effects of VHSV on IgM ؉ cell functionality, comparing these effects to those elicited by a Toll-like receptor 3 (TLR3) ligand, poly(I·C). We found that poly(I·C) and VHSV significantly upregulated TLR3 and type I interferon (IFN) transcription in spleen and blood IgM In mammals, Toll-like receptors (TLRs) recognize highly conserved structures of viral (TLR3, -7, -8, and -9) and bacterial (TLR1, -2, -4, -5, -6, -7, -8, and -9) origins. While TLR1, -2, -4, -5, and -6, together with TLR11 and TLR12 in mice and TLR10 in humans, are mostly expressed on the cell surface, a second group of TLRs, including TLR3, -7, -8, and -9, are localized within endosomal compartments and detect foreign nucleic acids (1). Recognition of pathogen-associated molecular patterns (PAMPs) through TLRs and other pattern recognition receptors (PRRs) leads to the activation and maturation of innate immune cells such as macrophages or dendritic cells (DCs). Additionally, once the presence of several TLR receptors on distinct populations of human and murine B cells was verified, further investigations concluded that B cells have evolved to directly sense microbes and that this TLR-mediated activation of B cells contributes to the establishment of an adequate humoral response (2). However, controversy remains as to what degree TLR signaling in B cells conditions the antibody response. On one hand, early studies showed that mice lacking B cell TLR signaling failed to mount an efficient antibody response (3). However, subsequent studies suggested a slightly different model in which these receptors play a role in the regulation of antibody class switching and in sustaining antibody secretion at late times after immunization in B cells (4), contributing to the amplification of the humoral response but not being completely responsible for it (5). In support of these observations, further studies demonstrated that the primary responses of some immunoglobulin (Ig) subclasses (i.e., IgG2a or IgG2c) were absolutely dependent on signaling through the adaptor protein MyD88, used by most TLRs, whereas other Ig classes were not (IgG1 and IgG3) or were much less (IgG2b and IgA) dependent on the MyD88 signaling cascade (6, 7). Interestingly, the conditional deletion of MyD88 in either DCs or B cells revealed that the antibody response to virus-like particles required TLR signaling in B cells, while the response to a soluble antigen was dependent on TLR signaling on DCs (8). This result reveals an ability of B cells to discriminate among antigens based on their physical form.

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In Vivo Cellular Tropism of Gorilla Simian Foamy Virus in Blood of Infected Humans

Cited by 20 publications

References 21 publications

Cocirculation of Two env Molecular Variants, of Possible Recombinant Origin, in Gorilla and Chimpanzee Simian Foamy Virus Strains from Central Africa

Cocirculation of Two env Molecular Variants, of Possible Recombinant Origin, in Gorilla and Chimpanzee Simian Foamy Virus Strains from Central Africa

Origin, evolution and innate immune control of simian foamy viruses in humans

Early Activation of Teleost B Cells in Response to Rhabdovirus Infection

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