The family Arteriviridae presently includes a single genus Arterivirus. This genus includes four species as the taxonomic homes for equine arteritis virus (EAV), lactate dehydrogenase-elevating virus (LDV), porcine respiratory and reproductive syndrome virus (PRRSV), and simian hemorrhagic fever virus (SHFV), respectively. A revision of this classification is urgently needed to accommodate the recent description of eleven highly divergent simian arteriviruses in diverse African nonhuman primates, one novel arterivirus in an African forest giant pouched rat, and a novel arterivirus in common brushtails in New Zealand. In addition, the current arterivirus nomenclature is not in accordance with the most recent version of the International Code of Virus Classification and Nomenclature. Here we outline an updated, amended, and improved arterivirus taxonomy based on current data. Taxon-specific sequence cut-offs are established relying on a newly established open reading frame 1b phylogeny and pairwise sequence comparison (PASC) of coding-complete arterivirus genomes. As a result, the current genus Arterivirus is replaced by five genera: Equartevirus (for EAV), Rodartevirus (LDV + PRRSV), Simartevirus (SHFV + simian arteriviruses), Nesartevirus (for the arterivirus from forest giant pouched rats), and Dipartevirus (common brushtail arterivirus). The current species Porcine reproductive and respiratory syndrome virus is divided into two species to accommodate the clear divergence of the European and American “types” of PRRSV, both of which now receive virus status. The current species Simian hemorrhagic fever virus is divided into nine species to accommodate the twelve known simian arteriviruses. Non-Latinized binomial species names are introduced to replace all current species names to clearly differentiate them from virus names, which remain largely unchanged.
Three lymphoblastoid cell lines were established from splenic lymphocytes of a lymphomatous baboon (Papio hamadryas) by co-cultivation of the lymphocytes with X-irradiated cells of marmoset or baboon lymphoblastoid cell cultures; the baboon splenic lymphocytes failed to grow when cultured alone. A herpesvirus, associated with each cell line, was identified by immunofluorescence, molecular hybridization and electron microscopy. Antigenic comparison with Epstein-Barr virus (EBV) showed that the baboon herpesvirus and EBV shared cross-reacting viral capsid antigens (VCA): 20 of 20 (100%) anti-VCA (EBV)-positive human sera and 55 of 62 (89%) baboon sera reacted with the baboon lymphoblastoid cells and baboon sera stained EBV VCA in P3HR-1 and EB-3 cells. No nuclear antigen, as assayed by anti-complement immunofluorescence tests, was detected in baboon lymphoblastoid cells when human or baboon anti-VCA positive sera were used. Baboon anti-VCA-positive sera also failed to stain EBV nuclear antigens (EBNA) in Raji or P3HR-1 cells. Preliminary molecular hybridization studies showed only approximately 40% homology between viral DNA of baboon cell lines and DNA of EBV derived from P3HR-1 cells.
The discussion about the clinical risk of zoonoses in xenotransplantation has recently culminated in the demand for a moratorium on clinical organ transplantation using pig donors. The basis for this discussion was a recent report showing a possible trans-species transmission of pig endogenous retrovirus (PERV) by in vitro transfer to human cell lines. At present, it remains unclear if this could also happen in vivo or in the setting of xenotransplantation. Potential in vivo transfer of PERV after xenotransplantation was investigated in an experimental pig-to-baboon cell transplantation model. Baboons were immunosuppressed with highdose cyclophosphamide (total 45-150 mg/kg) and transplanted with primary porcine aortic endothelial cells (PAEC). Tissue samples (skin, lymph nodes, lung) and peripheral blood leukocytes of 15 baboons, taken about 12-24 months after transplantation of PAEC, were then analyzed by PCR and showed no PERV infection. PERV expression in PAEC was also analyzed: PERV mRNA and reverse transcriptase in the culture supernatant could be detected. In spite of the release of retroviral particles from cultured PAEC, transplantation of these cells into baboon recipients did not result in virus transmission, not even under heavy immunosuppression.
Two lymphoblastoid cell lines were established from baboons with lymphoid disease. Cells of these lines were positive for complement and Fc receptors but lacked sheep cell receptors, thereby indicating B-cell origin. The cells contained antigens which cross-reacted with Epstein-Barr virus (EBV), viral capsid antigen (VCA), early antigen (EA) and membrane antigen (MA). Both lines released virus with in vitro transforming activity for lymphocytes of several primate species including humans. Cells of the original lines and transformed cells showed no staining for EB nuclear antigen (EBNA). The virus was neutralized by anti-MA positive baboon and human sera. Baboon virus and EBV had different but overlapping in vitro host-cell ranges.
A type-C RNA virus has been isolated from various tissues of a lymphomatous baboon (sp. P hamadryas). Virus isolations were made by co-cultivating baboon cells from the inguinal and mesenteric lymph nodes, testes, kidneys and spleen with cells of canine or human origin. The isolated virus grew in canine, bat, rhesus, and human cells but not in cells of mouse, rat, cat or rabbit origin. The baboon isolate resemble a type-C virus when infected cells were examined by thin section in the electron microscope. In addition, the virus was capable of providing helper function by rescuing and transmitting the Moloney and Kirsten sarcoma virus genome from non-productively transformed cells. Antibody directed against the RD114 virus reverse transcriptase was very effective in inhibiting the baboon virus polymerase while while anti-mouse and woolly type-C virus polymerase antibodies had no significant inhibitory activity. Further analysis by immunodiffusion and competitive radioimmune assay revealed a close immunological relationship between this virus, RD114 and another type-C virus isolated from the placenta of a different species of baboon. Finally, three different classes of interspecies antigenic determinants have been demonstrated in mammalian type-C virus isolated from the placenta of a different species of baboon. Finally, three different classes of interspecies antigenic determinants have been demonstrated in mammalian type-C viruses.
Xenotransplantation of pig organs seems a promising way of overcoming the prevailing limitation on allotransplantation due to donor numbers. However, as porcine endogenous retroviruses (PERVs) can infect human cells in vitro, there is substantial concern regarding the risk of a PERV infection in xenogeneic transplant recipients. Cultured porcine endothelial cells, stimulated peripheral blood mononuclear cells, and pancreatic islet cells can release PERV infectious for human cells in vitro, but it is currently unknown whether PERV is released in vivo, whether these viral particles can infect the transplant recipient, and whether they are pathogenic. In a retrospective study 15 immunosuppressed baboons were tested for a specific immune response against PERV after transplantation of porcine endothelial cells, mononuclear blood cells, and lungs. Anti‐PERV antibody expression was analyzed with peptide‐based, enzyme‐linked immunosorbent assays and highly sensitive Western Blot assays. This xenotransplantation study using nonhuman primates found no evidence of PERV specific humoral immune response. Our data suggest that no productive PERV infection and no continuous PERV release takes place in the nonhuman primates analyzed in this study.
g Simian hemorrhagic fever (SHF) is lethal for macaques. Based on clinical presentation and serological diagnosis, all reported SHF outbreaks were thought to be caused by different strains of the same virus, simian hemorrhagic fever virus (SHFV; Arteriviridae). Here we show that the SHF outbreaks in Sukhumi in 1964 and in Alamogordo in 1989 were caused not by SHFV but by two novel divergent arteriviruses. Our results indicate that multiple divergent simian arteriviruses can cause SHF. In late August 1964, a viral hemorrhagic fever epizootic occurred among captive macaques at the Institute of Experimental Pathology and Therapy in Sukhumi, Georgia, Soviet Union. All 64 infected animals succumbed. The disease was named simian hemorrhagic fever (SHF), as the etiological virus was not related to any other virus known at the time (1-3). In November 1964, an epizootic with a highly similar clinical presentation and case fatality rate occurred among macaques at the National Institutes of Health (NIH) Primate Quarantine Unit in Bethesda, MD, killing a total of 223 animals. Outbreak investigations revealed that the macaques affected at both facilities had been imported from the same primate supplier in India, suggesting that the two outbreaks were related (4).A list of additional SHF outbreaks, the majority of which had connections to Indian suppliers of nonhuman primates, is provided in Table 1. The diagnosis of SHF during these additional outbreaks was based on the typical clinical and pathological presentation of sick macaques (4-6) and on serological assays such as indirect fluorescence assay (IFA) or complement fixation (CF) (7-10). Several observations suggested that different strains of SHFV may have caused the various outbreaks. For example, central nervous system (CNS) manifestations were much more commonly observed among macaques during the 1964 Sukhumi outbreak than during the 1964 Bethesda and 1967 Sukhumi outbreaks (11). The presence or absence of CNS involvement could be reproduced in macaques experimentally infected with clinical material from the different outbreaks (11). CF, IFA, and enzyme-linked immunosorbent assay studies performed with virus antigen or nonhuman primate sera from various outbreaks often yielded contradictory results, either confirming or refuting direct relationships between the etiological viruses (7-10, 12, 13). Unfortunately, virus isolation in cell culture was reported for only a few outbreaks, and with the exception of 1964 Bethesda isolate NIH LVR42-0/M6941, all of the isolates and most of the associated materials have been accidentally or deliberately destroyed (Table 1).The origin of SHFV is unclear, although various African nonhuman primates, such as patas monkeys (Erythrocebus patas) (14, 15), Guinea baboons (Papio papio) (14), and olive baboons (Papio anubis) (16), have been implicated as possible carriers. This hypothesis is strengthened by the recent discovery in apparently healthy African nonhuman primates of several novel and highly divergent simian arteriviruses, all of...
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