The Mammalian Cell-Virus Relationship

McLaren, Leroy C.; Holland, John J.; Syverton, Jerome T.

doi:10.1084/jem.109.5.475

Cited by 162 publications

(21 citation statements)

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“…RNA preparations were ribonucleasesensitive, and equally capable of infecting primate and non-primate cells. Nonprimate cells have been shown unable to adsorb similar quantities of intact virus (1). Such adsorption as occurs to yield cell-associated virus is not sufficient to cause infection.…”

Section: Discussionmentioning

confidence: 99%

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The Mammalian Cell Virus Relationship

Holland

McLaren

Syverton

1959

The Journal of Experimental Medicine

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201

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Primate cells naturally susceptible to poliovims infection possess specific surface receptors that permit poliovirus to be adsorbed quantitatively, received within the cell, eclipsed with loss of infectivity, replicated, and released with accompanying cytopathic effect. Conversely, non-primate cells are naturally insusceptible to poliovirus infection, do not possess active receptors, adsorb only a small fraction of supplied poliovirus, fail to eclipse or replicate measurable amounts of the cell-associated virus, and undergo no cytopathic change (1, 2). It was of interest to learn whether the specific capacity of primate ceils to receive, replicate, and release poliovirus was conditioned wholly by presence of specific receptors. Preliminary findings indicated lack of receptors required for cell infection by poliovirus could be surmounted by use of viral RNA (3).The present communication describes production of infectious poliovirus and other enteroviruses by non-primate cells exposed to viral ribonucleic acid, comparative efficiency of non-primate and primate cells for such virus production, and properties of the produced virus. Materials and MethodsCell Culture Methods.--Cell sources, cultural methods, solutions, and media have been described previously (I, 4).

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Section: Discussionmentioning

confidence: 99%

“…HeLa or smnion monolayers were rinsed, exposed for 30 minutes at room temperature to virus at multiplicities greater than 20, overlaid with 5 per cent calf serum in yeast extract medium (YEM) (1), and incubated at 37°C. for 10.5 hours.…”

Section: Enterovirus I~na Infectivity For Insusceptible Cellsmentioning

confidence: 99%

The Mammalian Cell Virus Relationship

Holland

McLaren

Syverton

1959

The Journal of Experimental Medicine

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201

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“…It is known that some viruses will grow in cultured cells derived from animals that are resistant to infection [20][21][22][23][24]. Differences in susceptibility to in vitro and in vivo infection may be related to the host defence mechanisms, induction of viral receptors, and/or the requirement for cell division.…”

Section: Discussionmentioning

confidence: 99%

Infection of cultured human pancreatic B cells with reovirus type 3

et al. 1981

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Summary. The capacity of reovirus type 3 to infect insulin-producing B cells was studied in human pancreatic cell cultures. Antibody to reovirus was labelled with fluorescein isothiocyanate and antibody to insulin was labelled with tetramethyl rhodamine isothiocyanate. By using a double-labelled immunofluorescent antibody technique, it was shown that only about 6% of the insulin-containing human B cells in culture became infected when inoculated with unpassaged reovirus type 3. However, by repeated passage of the virus in human pancreatic B cell cultures, the percentage of infected B cells increased to 27%, and the virus titre in cultures rose from 8.0 x 104 pfu/ml in the first passage, to 4.9 x 106 pfu/ml in the 5th passage. As measured by radioimmunoassay, the intracellular immunoreactive insulin began to decrease at 24h after infection. This decrease roughly paralleled the increase in virus titre. In contrast, there was relatively little change in immunoreactive insulin in cultures inoculated with unpassaged reovirus type 3. These studies show that the ability of reovirus type 3 to infect human B cells is enhanced by serial passage in human pancreatic cell cultures and that the infection resulted in the destruction of B cells and release of insulin.Key words: Virus-induced diabetes mellitus, human pancreatic B cell cultures, double-labelled immunofluorescent antibody staining, reovirus type 3, virus passage. study, it was shown that a Coxsackie virus B4 variant, isolated from the pancreas of a 10-year-old child who died of diabetic ketoacidosis, produced diabetes in mice by infecting and destroying B ceils [7].It is difficult, however, to demonstrate in vivo that viruses replicate in human B cells and produce diabetes in man. As a practical model, an in vitro system has been developed to determine if viruses are capable of infecting human B cells. By use of a double-labelled immunofluorescent antibody technique, it has been shown that human B cells grown in culture were susceptible to infection by mumps [8], Coxsackie virus B3 [9], and Coxsackie virus B4 [7].We have previously shown that reovirus type 3, passaged in murine pancreatic B cell cultures, produced an insulitis when inoculated into 1 to 2 week old mice [10]. In the present investigation, the double-labelled immunofluorescent antibody technique has been used to determine whether or not human B ceils grown in culture were permissive to reovirus type 3, and whether the capacity of the virus to infect human B cells was enhanced by repeated passage in human B cell cultures. Radioimmunoassay for immunoreactive insulin was used to evaluate the effect of the infection on intracellular and extracellular insulin. Materials and Methods Pancreatic B Cell CulturesThe possibility that viruses might cause some cases of insulin-dependent diabetes (IDD) by infecting and destroying pancreatic B cells has received considerable attention. Of the numerous viruses implicated, mumps and members of the Coxsackie virus B group (particularly B4) have been most often suggest...

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“…Cell 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.…”

Section: Methodsmentioning

confidence: 99%

“…of fluid. Numbers of free virus particles or infected cells (infectious centers) were counted as plaque-forming units (PFU) per milliliter, as previously described (11).…”

mentioning

confidence: 99%

The Mammalian Cell-Virus Relationship

McLaren

Holland

Syverton

1960

The Journal of Experimental Medicine

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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).

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The Mammalian Cell-Virus Relationship

Cited by 162 publications

References 21 publications

The Mammalian Cell Virus Relationship

The Mammalian Cell Virus Relationship

Infection of cultured human pancreatic B cells with reovirus type 3

The Mammalian Cell-Virus Relationship

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