No abstract

Simian foamy viruses (SFV) are ancient retroviruses of primates and have coevolved with their host species for as many as 30 million years. Although humans are not naturally infected with foamy virus, infection is occasionally acquired through interspecies transmission from nonhuman primates. We show that interspecies transmissions occur in a natural hunter-prey system, i.e., between wild chimpanzees and colobus monkeys, both of which harbor their own species-specific strains of SFV. Chimpanzees infected with chimpanzee SFV strains were shown to be coinfected with SFV from colobus monkeys, indicating that apes are susceptible to SFV superinfection, including highly divergent strains from other primate species.Simian foamy viruses (SFV) and their nonhuman primate hosts demonstrate coevolution (20). Despite the fact that SFV strains have been described for most Old World primate species, no human-specific foamy virus has yet been identified (16). However, zoonotic transmissions of SFV from various nonhuman primates to zookeepers and central African hunters or others having close contact with nonhuman primates are known to occur (5, 8-10, 21, 22). Such viruses have sequences that show a close relationship to SFV sequences from several nonhuman primate species (Fig. 1). Until now, it has been unclear whether such interspecies transmission can also take place when the hunter is naturally infected with its own species-specific SFV. Wild chimpanzees that regularly hunt and consume western red colobus monkeys (4) provide such a situation.Wild chimpanzees (Pan troglodytes verus) and western red colobus monkeys (Piliocolobus badius) sharing a rainforest habitat, the Taï National Park, Côte d'Ivoire, were tested for SFV infection. The chimpanzees have been under human observation for more than 25 years and are known individually as a result of a project focusing on wild chimpanzee behavior. Tissue samples were obtained from 14 chimpanzees that had died of anthrax, respiratory disease, or other causes (12,14,15). Samples of blood, collected in EDTA, from nine red colobus monkeys were obtained under anesthesia, and organ samples were collected from the remains of a further two that had been killed and eaten by chimpanzees (15). All represented adult animals.Using the SFV primers for the integrase gene (19), previous analyses revealed that 12 of the 14 chimpanzees harbored SFV strains (SFV cpz ) corresponding to strains described for the chimpanzee subspecies Pan troglodytes verus (details will be published elsewhere). Also 11 red colobus monkeys were tested positive for SFV using the same primers and standard conditions (96°C for 5 min; 40 cycles 96°C for 1 min, 56°C [first PCR] or 60°C [nested PCR] for 30 s, 72°C for 1 min; and a final elongation step at 72°C for 10 min). PCR products were purified using the QIAquick PCR purification kit (Qiagen) and sequenced directly in both directions without interim cloning.Phylogenetic analysis using the neighbor joining method (BioEdit, PHYLIP 3.572 package) of these 389-bp sequences ...

Viruses, and more particularly retroviruses, have been postulated to play a role in the pathogenesis of autoimmune diseases. In a search for spumaretrovirus infection markers, we screened a group of 29 patients with Graves disease and a representative healthy population (23 subjects) as a control. Southern blot hybridization under s ent conditions, of patients' DNA extracted from peripheral blood lymphocyes, with a spumaretrovirus-specific genomic probe derived from the human spumaretroirus (HSRV) prototype, gave a positive signal in 10 cases. Moreover, by PCR, HSRVrelated sequences were detected in the DNA of 19 patients (66%). Positive DNA samples in Southern blots were also positive in PCR for all regions tested (gag, bell, li2, long terminal repeat). Amplified (gag and bel2) products were cloned and sequenced; they showed hih homology with HSRV. On the other hand, all 23 control subjects were negative by both procedures. Sera from both populations were ex for the presence of antibodies reactive with antigens of the spumaretrovirus family. These sera were negative by several immunodetection techniques: ELISA, indirect immunofluorescence, serum neutralization, and Western blotting. These results strongly suggest the existence of an assoclation between Graves disease and the presence of HSRV-related infection markers.Several clinical, genetic, and pathophysiological features support the notion of a role for autoimmunity in the pathogenesis of some endocrine conditions, such as Graves disease. In fact, the association of this affliction with other well-defined autoimmune nosological eptities-altered HLA expression, the. presence of autoantibodies, and modifications of certain lymphocyte subpopulations-favor this concept (1, 2).The possible involvement of different viruses in the etiology of autoimmune diseases has been evoked in animal models and in humans. Among viral agents, endogenous (3) and exogenous (4-6; §) retroviruses have been considered as likely candidates to be associated with this category of disorders. Animal models have produced evidence sustaining this hypothesis. For instance, in the genome of the obese chicken, which spontaneously develops autoimmune thyroiditis, an avian leukosis virus (ev22) has been identified (3). Moreover, type C retroviral particles have been detected in

Characterization of human foamy virus (HFV) gag-encoded precursors and the search for a Gag-Pol polyprotein and mature proteins derived from proteolytic processing were carried out in HFV-infected cells and with purified preassembled cores and extracellular virus by Western blotting and radioimmunoprecipitation using antisera against synthetic peptides corresponding to putative Gag and protease proteins. Precursor proteins, Pr78gag/74gag and Pr135pol, were found in the nucleus of epithelial and fibroblast cells 3-4 days after HFV infection. Kinetic analysis of HFV Pr78gag and Pr74gag indicated that Pr78gag is a precursor to Pr74gag. South-Western blot analysis indicated that Pr78gag and Pr74gag have properties associated with nucleic acid binding protein although they lack the typical zinc-finger motifs found in retroviral nucleocapsid proteins. Western blot analyses of preassembled HFV cores isolated from the cytoplasm of infected cells and purified by sucrose gradient centrifugation demonstrated the presence of Pr78gag/74gag and Pr135pol, but no proteolytically processed Gag proteins were observed. The majority of extracellular HFV particles were found to have pentagon-shaped cores, as observed intracellularly, and are believed to be the immature extracellular form of the virus. The highest concentration of extracellular particles, estimated by EM, Western blot, and reverse transcriptase assays were found in sucrose gradient fractions having a density of 1.21-1.24 g/cm3. Western blot analysis revealed that Pr78gag/74gag and Pr135pol were the major viral proteins associated with these extracellular particles, as only small amounts of putative proteolytically cleaved capsid (p32) were observed. Our results support the notion that Pol is translated independent of Gag in HFV-infected cells.

The MT-2 cell line transformed by human T-cell leukemia virus type 1 (HTLV-1) contains one complete provirus and seven defective proviruses. Four defective genomes have an identical structure (LTR-MA-deltaCA-pX-LTR) with an open reading frame that spans from MA to pX, giving rise to a 3.4-kb (24S) RNA transcript encoding a chimeric Gag-pX protein, p28. MT-2 cells release two distinct types of virions. The major "classic" type of particle has a buoyant density of 1.155-1.16 g/cm3 and contains the standard HTLV-I structural proteins and reverse transcriptase (RT). In addition, about 5% of particles are "light," approximately 1.12 g/cm3, and contain p28, RT activity, and the 3.4-kb RNA transcript. RT-PCR and in vitro translation indicate that some of the classic HTLV-1 particles package 3.4-kb RNA as well as full-length 8.5-kb RNA. In addition to matrix features, the p28 protein has a motif resembling a zinc finger at the C-terminal, pX0 region, which may play a role in the assembly of the defective light virions.