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More about: Lack of serologic evidence for prevalent simian virus 40 infection in humans.

We read with great interest the article by Carter et al. (1). As reviewed by the authors of that article, a number of laboratories have reported detection of simian virus 40 (SV40) DNA in human cancers, suggesting the existence of a human SV40-like agent associated with malignant disease. However, Carter et al. have shown quite convincingly that antibodies to SV40 virus-like particles (VLPs) are rare, at least in some populations, in sera of both cancer-free humans and those with cancer. In their article, 6.6% of the sera studied appeared to have antibodies that reacted to SV40 VLPs. However, all of the sera in that group also had antibodies that reacted to VLPs of two ubiquitous human polyomaviruses, BKV and JCV, both of which share extensive homology with SV40. When sera, apparently positive for antibodies to SV40 VLPs, were preadsorbed with BKV or JCV VLPs, reactivity to SV40 VLPs was eliminated. In sera from monkeys infected with SV40, pre-adsorption with BKV and JCV VLPs did not eliminate reactivity to SV40 VLPs, which suggested that what appeared to be SV40 antibodies in the human sera were really antibodies directed to BKV or JCV. The lack of human antibodies to SV40-like VLPs in the study by Carter et al. (1) raises serious questions about the existence of an SV40-like agent in humans and its association with cancer. However, one explanation that has not been seriously considered is the possibility that SV40 DNA might be pseudotyped by BKV and/or JCV capsids. There is evidence (2–5) that SV40 DNA can be packaged in capsids of BKV, or its variant RFV, and also in JCV capsids. Beginning in the mid1980s and extending into the 1990s, we found (2–5) that blocks of BKV or JCV DNA sequences could substitute for SV40 sequences without loss of viability. Some of the hybrids contained the BKV or JCV late DNA coding region (capsid genes) in place of the late SV40 coding region, but the remainder of the viral DNA, including the T-antigen gene and the regulatory region, was SV40 (3–5). The existence of these infectious hybrid genomes demonstrated that both BKV and JCV capsids could package or pseudotype SV40 DNA. In addition, we found that, although human embryonic kidney (HEK) cells were resistant to wild-type (wt) SV40 infection, they were fully permissive for infection by a chimeric BKV/SV40 genome, from which SV40 T-antigen production was greatly enhanced, apparently by the BKV late region contained in the chimera (3,5). In more recent studies involving co-infection of HEK cells with wtSV40 (strain 776) and wtBKV (O’Neill FJ, Greenlee JE: unpublished data), we have found that SV40 DNA can persist in these non-