History Of Parvovirus And Cancer

Since the discovery of parvoviruses, there has been significant advance on the relationship between parvoviruses and cancer. Epidemiological surveys in humans have revealed a correlation between serological evidence of parvoviral infection and lower incidence of certain human cancers (7,8). In vivo studies have demonstrated that animals infected with parvoviruses exhibited increased protection against chemical carcinogen- and virus-induced tumorigenesis (9). Several in vitro studies have also reported inhibition of cellular transformation by parvoviruses and interestingly, preferential killing of established tumor cell lines by parvovirus infection compared with normal cells (9). Results of these studies have led to the belief of possible interference with the induction of malignant transformation as well as survival and proliferation of tumor cells. Subsequent studies have provided molecular evidence on the role of NS proteins of parvoviruses in oncosuppression (10-12). More recently, it has also been shown with AAV that the nature of single-stranded genomic structure itself triggers cellular events in p53 mutant tumor cells leading to apoptosis (13).


Fig. 1. Genomic organization of prototypic parvovirus. The genome of parvoviruses comprise of approx a 5-kb single-stranded DNA packaged within a icosahedral capsid of 25 to 30 nm. The major promoter near the 5'-end encodes NS or Rep proteins as in APV and AAV respectively. The capsid proteins are derived from the VP gene situated at the right half of the genome and expressed by a promoter situated immediately upstream of the gene in the middle of the vector genome. Relative map units of the location of respective promoters are given above. P5, P19, and P40 represent promoters of AAV and P4 and P38 are corresponding promoters in APV. The size of alternately spliced NS/Rep and VP are indicated in parenthesis. TR represents the palindromic terminal repeat sequences.

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