Lack of evidence for infection with simian immunodeficiency virus in bonobos.

Abstract

213 IN THE DISCUSSION ON THE ORIGIN of the human immunodeficiency virus type 1 (HIV-1) it has been hypothesized by E. Hooper in his book The River that the oral polio vaccine (OPV) could be held responsible for the introduction of the simian immunodeficiency chimpanzee virus (SIVcpz) into humans, leading to its human counterpart, HIV-1.1 This theory suggests that oral polio vaccine stocks would have been prepared in chimpanzee kidney tissue contaminated with SIV. During the African vaccination trials in the 1950s these allegedly SIV-contaminated OPVs would have then been administered to people in what is now the Democratric Republic Congo. However, this OPV/HIV hypothesis has recently lost a great deal of its credibility due to the work of Korber et al.,2 Salemi et al.,3 Rambaut et al.,4 Blancou et al.,5 and Berry et al.6 The first three studies show that HIV-1 group M infection in humans originated before the 1930s and thus predates the oral polio vaccination trials, while the last two studies confirm that macaque kidney tissue had been used for the preparation of the early batches of the OPV, and the absence of chimpanzee mitochondrial (mt)DNA and HIV/SIVCPZ-like sequences in these vaccines. However, as R. Weiss7 mentioned, it could still be argued whether “chimpanzee kidney cells” and bonobo kidney tissue “could have been used locally in Africa to amplify the batches of the OPV,” as insinuated by E. Hooper.1,8,9 As E. Hooper stated in his book, bonobos (Pan paniscus) have been reported earlier by us and others,10,11 to be at the origin of another zoonotic human retrovirus, human T-cell lymphotropic virus type II (HTLV-II). Thus, bonobos and the use of their tissues may pose a potential risk for cross-species transmission of other etiologic agents. SIV infection has been reported in various African monkey species, but no data about the serostatus in bonobos have been published yet. The fact that SIV infection has been described in two subspecies of the bonobo’s closest related simian species, the common chimpanzee or Pan troglodytes,12–14 raises the question of whether bonobos are also a natural host for SIV. This is especially interesting since the natural habitat of the affected P.t. troglodytes and P.t. schweinfurthii subspecies neighbors that of the bonobo, which is situated in the Central Congo basin, between the Congo River, the Lomami and the Kasai/Sankuru Rivers, and the Lake Tumba/Lac Ndombe area (Fig. 1). To assess the prevalence of SIV in bonobos, we have performed a serologic survey of 26 bonobos, of which 14 were wild caught and 12 were born in captivity. Thirteen animals were housed at the Yerkes primate center in Atlanta, Georgia, 7 in a breeding center of the Antwerp Zoo in Belgium, 2 in the Leipzig Zoo in Germany, and 4, saved from poachers, were housed in an orphanage in Congo Brazzaville. The bonobo plasma/serum samples were screened with either the Genetic Systems HIV-1/-2 peptide EIA (Redmond, WA), the Abbott AxSYM HIV-1/2 microparticle EIA (Abbott Laboratories, Delkenheim, Germany), or an in-house SIV antigen ELISA using SIVmac251 purified viral lysate (Advanced Biotechnologies Incorporated, Columbia, MD). All test results were negative. Additional screening of all 26 bonobo samples with the INNOLIA HIV (Innogenetics, Ghent, Belgium) confirmation test, a line immunoblot assay more sensitive for divergent SIV strains than commercial Western blots,15 found no reactivity in all 26 bonobos. Previously, these animals were screened for infection with another simian retrovirus, the simian T-cell lymphotropic virus type I/II (STLV) using an HTLV-I/-II particle agglutination test (Serodia-HTLV, Fujirebio, Japan) and/or an