The Mammalian Cell-Virus Relationship

Holland, John J.; McLaren, Leroy C.

doi:10.1084/jem.109.5.487

Cited by 116 publications

(22 citation statements)

References 17 publications

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“…sage of virus produced by RNA infection between the non-primate (parent) cell line and HeLa cells. In addition, poliovirus produced by RNA-infected domestic rabbit fibroblasts was inactivated by receptor material present in HeLa debris (2), as was the original poliovirus.…”

Section: Response Of Insusceptible Cells or Animals To Rna From Othermentioning

confidence: 99%

“…Maintenance medium was removed, infected monolayers were washed gently with isotonic (0.14 M) NaC1 solution, cells were scraped from glass and were suspended in 0.2 phosphate-buffered salt solution to a concentration of 3 to 4 X 107 cells per ml., and suspended cells were frozen and thawed 3 times to release intracellular virus. Initially, virus pools were centrifuged to remove cellular debris which could inactivate virus (2), but this precaution appeared unnecessary so long as pools were frozen immediately and stored at --20°C. The procedure yielded poliovirus at 0.4 to 1.0 X 10 I° PFU per ml, Coxsackie A-9 virus at 0.8 to 3.0 × 101°, Coxsackie B-1 at 0.9--2.0 X 1010, and ECHO 8 virus at 7 × 109 PFU per ml.…”

Section: Enterovirus I~na Infectivity For Insusceptible Cellsmentioning

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: Response Of Insusceptible Cells or Animals To Rna From Othermentioning

confidence: 99%

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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“…All three serotypes of poliovirus share a single distinct receptor (21). Poliovirus bound only to cells ofprimate origin and not to murine cell lines (22). The demonstration that transfection with poliovirus RNA leads to productive infection in receptor-deficient murine cells supported the concept that viral binding to cell surface receptors may be a major determinant of host range and tissue tropism (23).…”

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confidence: 56%

Strategies for the identification of icosahedral virus receptors.

Bass

Greenberg²

1992

J. Clin. Invest.

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The first step in virus infection of a host cell is attachment to the cell plasma membrane. This necessary but not always sufficient event in cell infection is important for several reasons. Specific receptor expression can be an important determinant of host range and cell and tissue tropism of a virus, although productive infection may be regulated at many other stages in viral replication as well. As an initial step in infection, virus binding offers an opportunity for chemical or immunologic intervention before the viral genome has reached relative sanctuary within the cell. Finally, characterization ofviral receptors can lead to the identification of new cell surface molecules whose normal function can then be determined.A variety of strategies has been employed to identify and characterize specific viral receptors. Most of these studies, however, have not definitively demonstrated that the putative receptor actually mediates infection ofthe cell. To fully establish that an interaction between a virus and a presumed receptor has biologic significance, it is necessary to demonstrate that such an interaction can initiate viral infection of the cell. The most stringent test of biologic significance is the transformation of receptor-negative nonpermissive cells to a permissive phenotype by molecularly engineered transfer ofgenetic material encoding a putative receptor. Recently these stringent criteria have been met for a small icosahedral virus, poliovirus (1) as well as for the enveloped viruses HIV (2) and Maloney murine leukemia virus (3).This review will concentrate on recent progress in the study of cell receptors for nonenveloped, icosahedral viruses (see Table I). Icosahedral viruses present unique questions concerning the early events ofviral infection, especially those ofviral entry. The review will not be exhaustive but will use selected examples to emphasize the methodologies and experimental strategies which have made this progress possible. Several more comprehensive recent reviews of viral receptors are available (4, 5).Although

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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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The Mammalian Cell-Virus Relationship

Cited by 116 publications

References 17 publications

The Mammalian Cell Virus Relationship

The Mammalian Cell Virus Relationship

Strategies for the identification of icosahedral virus receptors.

Infection of cultured human pancreatic B cells with reovirus type 3

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