Abstract
A number of viruses show a naturally extended tropism for tumor cells whereas other viruses have been genetically modified or adapted to infect tumor cells. Oncolytic viruses have become a promising tool for treating some cancers by inducing cell lysis or immune response to tumor cells. In the present work, rotavirus strains TRF-41 (G5) (porcine), RRV (G3) (simian), UK (G6-P5) (bovine), Ym (G11-P9) (porcine), ECwt (murine), Wa (G1-P8), Wi61 (G9) and M69 (G8) (human), and five wild-type human rotavirus isolates were passaged multiple times in different human tumor cell lines and then combined in five different ways before additional multiple passages in tumor cell lines. Cell death caused by the tumor cell-adapted isolates was characterized using Hoechst, propidium iodide, 7-AAD, Annexin V, TUNEL, and anti-poly-(ADP ribose) polymerase (PARP) and -phospho-histone H2A.X antibodies. Multiple passages of the combined rotaviruses in tumor cell lines led to a successful infection of these cells, suggesting a gain-of-function by the acquisition of greater infectious capacity as compared with that of the parental rotaviruses. The electropherotype profiles suggest that unique tumor cell-adapted isolates were derived from reassortment of parental rotaviruses. Infection produced by such rotavirus isolates induced chromatin modifications compatible with apoptotic cell death.
Highlights
A small decrease in the overall cancer rate has been reported for countries such as USA, the incidence of some particular cancers has shown an increasing rate [1]
Infectivity of isolates obtained after multiple passages of parental rotaviruses To determine the effect of multiple cell culture passages on the infectivity of parental rotavirus strains (TRF-41, RRV, UK, Ym, Wa, Wi61, M69, WT1, WT2, WT3, WT4, WT5 and ECwt), cell lines U937, AGS, Caco-2, Kato III, MCF-7, PC-3, REH, A549, and Sp2/0-Ag14 were separately infected with these parental strains
When the differential infectivity was measured in terms of the percentage of infected cells, the results showed that most tumor cell-passaged rotavirus were able to infect a higher proportion of tumor cells AGS, U937, Sp2/0-Ag14 and MCF-7 and Caco-2 than MA104 cells
Summary
A small decrease in the overall cancer rate has been reported for countries such as USA, the incidence of some particular cancers has shown an increasing rate [1]. Viruses exhibit cellular tropism which defines their ability to preferentially infect a specific tissue. A number of viruses have been shown to naturally extend their tropism to tumor cells [4]. Parvovirus, Newcastle disease virus (NDV), Moloney leukemia virus (MLV) and mumps virus (MV) are among the viruses showing natural preference for tumor cells, while viruses such as vesicular stomatitis virus (VSV), measles virus (MV), vaccinia virus (VV), adenovirus (AdV), and herpes simplex virus (HSV) have been genetically modified or adapted to infect tumor cells [5].
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