The Mammalian Cell-Virus Relationship

Abstract

HeLa cell cultures have been reported previously to be resistant to infection by Coxsackie A9 virus (1, 2). Similar results have been reported for a number of other stable cell strains derived from human tissues (3-6). In contrast, this virus has been reported to infect primary cell cultures of human and monkey cells (1,3,(7)(8)(9). The resistance of HeLa cells to A9 virus infection was shown by Takemoto and Habel (10) to be relative, since virus-carrier cultures could be produced. Even in the presence of relatively large amounts of virus and in the absence of antibody in the medium, only a small proportion of the cells were infected at any time. We have reported previously that natural resistance of non-primate cells to enterovirus infection is related to the absence of cellular receptors active in the primary adsorption of these viruses (11-13). Evidence that resistance to Coxsackie A9 infection had been acquired by human cells in continuous culture prompted similar studies on the mechanism of resistance to this virus.The present investigation demonstrates that established human cell cultures are also resistant because of absence of receptor, and it will be shown that enteroviruses differ with regard to cell receptor specificity and cofactor requirements for viral attachment. Materials and MethodsCell Origin and Cultivation.--Cell strains established in continuous culture from human, rabbit, and mouse tissue, and maintained at the University of Minnesota as previously described (11,14) were studied. The human epidermoid carcinoma strain KB (15) also was studied. Human cell strains were propagated in 20 per cent human serum (HuS), diluted in Hanks's balanced salt solution (BSS), supplemented with 0.1 per cent yeast extract as YEM medium (16).

Studies on the Interaction Between Coxsackievirus A9 and Hela Cells

“…McLaren, Holland and Syverton (1960) reported that the resistance of HeLa cells to CA 9 virus infection is correlated with the absence of the receptor active in the primary adsorption of this virus. Takemoto and Habel (1959) showed that the resistance of HeLa cells to CA 9 virus infection was relative, since virus carrier cultures could be established and even when a relatively large amount of virus was present, only a small proportion of the cells was infected at any time.…”