Specific Viral Interference in Hela Cell Cultures Chronically Infected With Coxsackie B5 Virus

Crowell, Richard L.

doi:10.1128/jb.86.3.517-526.1963

Cited by 45 publications

(11 citation statements)

References 17 publications

(18 reference statements)

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“…The absence of interference to superinfection of rubella-infected cell strains with echovirus 11 confirms the finding of Goffe (42). Variability in resistance to superinfection of carrier cultures with related and unrelated viruses has been noted by others (43,45,46). Crowell (46) found specific resistance to related enteroviruses and this resistance was found to be an adsorption defect, which was not demonstrated to be the case in our rubella-infected cells.…”

Section: Discussionsupporting

confidence: 87%

Rubella Virus Carrier Cultures Derived From Congenitally Infected Infants

Rawls

Melnick

1966

The Journal of Experimental Medicine

110

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Spontaneous rubella carrier cultures derived from tissues of infants with congenital rubella were studied in an attempt to elucidate a possible mechanism for viral persistence observed in these infants. Chronically infected cells were found to have a reduced growth rate and the cultures appeared to have a shortened life span. The rubella carrier state was not dependent on serum inhibitors or rubella antibodies. Virtually every cell in the carrier population was found to be producing virus. The carrier cultures could not be cured by rubella antibodies. The rubella-infected cells were resistant to superinfection with vesicular stomatitis virus and herpes simplex virus but were susceptible to infection with echovirus 11. The replication of vesicular stomatitis virus was apparently blocked at an intracellular site, for the virus readily adsorbed to the chronically infected cells and entered into an eclipse phase; however no infectious virus developed. No evidence of interferon production by these cells could be obtained. It is postulated that clones of rubella-infected cells in vivo, with properties similar to those in carrier cultures developed in vitro from tissues of in utero infected infants, might explain the observed viral persistence noted in congenital rubella.

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Section: Discussionsupporting

confidence: 87%

Rubella Virus Carrier Cultures Derived From Congenitally Infected Infants

Rawls

Melnick

1966

The Journal of Experimental Medicine

110

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“…The finding that the monoclonal antibody Rmc CB3-CB3RD blocked receptors for some picornaviruses outside of the specific receptor family (i.e., E6 and coxsackievirus A21) was unexpected (6,8). In addition, the monoclonal antibody blocked attachment to RD cells of CB1-RD, CB3-RD, and CB5-RD variant viruses, which presumably use the same receptor site on HeLa and RD cells as well as a second site on HeLa cells.…”

Section: Discussionmentioning

confidence: 97%

“…These monoclonal antibodies include the one for receptors on HeLa cells for CB1, CB5, and CB6 obtained by Campbell and Cords (5), one for the receptor on HeLa, RD, and monkey kidney cells for the three poliovirus immunotypes obtained by Minor et al (30), one for receptors on HeLa cells for the major group of HRVs found by Colonno et al (5a), and the one reported herein, which has an extended receptor specificity to completely block receptors for CB1, CB3, CB5, E6, and coxsackievirus A21 on HeLa cells and CB1-RD, CB3-RD, and CB5-RD on RD cells. In general these monoclonal antibodies help to confirm the existence of separate receptor families for the different species of picornaviruses, which first were recognized by virus competition experiments (1,3,6,7,14,23,29,32,34).…”

Section: Discussionmentioning

confidence: 98%

“…The receptors for the different species of prototype picornaviruses differ in susceptibility to proteolytic enzymes (38), pH and heat inactivation (39), saturation by different picornaviruses (6,7,13,23,32), and blockade by anticellular serum (2). In addition, variant receptors in genetically dissimilar individuals may select variant viruses with altered tissue tropisms (9,33).…”

mentioning

confidence: 99%

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Monoclonal antibody that inhibits infection of HeLa and rhabdomyosarcoma cells by selected enteroviruses through receptor blockade

Crowell¹,

Field²,

Schleif³

et al. 1986

J Virol

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BALB/c mice were immunized with HeLa cells, and their spleen cells were fused with myeloma cells to produce hybridomas. Initial screening of culture fluids from 800 fusion products in a cell protection assay against coxsackievirus B3 (CB3) and the CB3-RD virus variant yielded five presumptive monoclonal antibodies with three specificities: (i) protection against CB3 on HeLa, (ii) protection against CB3-RD on rhabdomyosarcoma (RD) cells, and (iii) protection against both viruses on the respective cells. Only one of the monoclonal antibodies (with dual specificity) survived two subclonings and was studied in detail. The antibody was determined to have an immunoglobulin G2a isotype and protected cells by blockade of cellular receptors, since attachment of [35S]methionine-labeled CB3 was inhibited by greater than 90%. The monoclonal antibody protected HeLa cells against infection by CB1, CB3, CB5, echovirus 6, and coxsackievirus A21 and RD cells against CB1-RD, CB3-RD, and CB5-RD virus variants. The monoclonal antibody did not protect either cell type against 16 other immunotypes of picornaviruses. The monoclonal antibody produced only positive fluorescence on those cells which were protected against infection, and 1251-labeled antibody confirmed the specific binding to HeLa and RD cells. The results suggest that this monoclonal antibody possesses some of the receptor specificity of the group 1B coxsackieviruses.

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“…Eclipsing of Adenovirus in Presence of Its Satellite.--In order to determine the event during the adenovirus replication cycle at which the satellite exerts its interfering effect, experiments were performed to determine if satellite virus interfered with adenovirus adsorption, penetration, or eclipse. The first two of these steps have been shown to be the sites of interference in other virus systems (18,19). In order to test viral eclipsing, it is important that cells be infected simultaneously.…”

Section: Quantitation Of a Denovirusmentioning

confidence: 99%

Adeno-Associated Satellite Virus Interference With the Replication of Its Helper Adenovirus

Parks

Casazza

Alcott

et al. 1968

The Journal of Experimental Medicine

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Adeno-associated satellite virus type 4 interferes with the replication of its helper adenovirus. No interferon-like soluble substance could be detected in satellite-infected cultures and other DNA- and RNA-containing viruses were not inhibited by coinfection with satellite virus under conditions which reduced adenovirus yields by more than 90% in monkey cells. Altering the concentration of adenovirus in the presence of constant amounts of satellite resulted in a constant degree of interference over a wide range of adenovirus inocula and suggested that adenovirus concentration was not a significant factor in the observed interference. The interference with adenovirus replication was abolished by pretreating satellite preparations with specific antiserum, ultraviolet light or heating at 80°C for 30 min. This suggested that infectious satellite virus mediated the interference. Satellite virus concentration was found to be a determinant of interference and studies indicated that the amount of interference with adenovirus was directly proportional to the concentration of satellite virus. 8 hr after adenovirus infection, the replication of adenovirus was no longer sensitive to satellite interference. This was true even though the satellite virus was enhanced as effectively as if the cells were infected simultaneously with both viruses. Interference with adenovirus infectivity was accompanied by reduced yields of complement-fixing antigen and of virus particles which suggested that satellite virus interfered with the formation and not the function of adenovirus products. When cells were infected either with adenovirus alone or with adenovirus plus satellite, the same proportion of cells plated as adenovirus infectious centers. However, the number of plaque-forming units of adenovirus formed per cell in the satellite-infected cultures was reduced by approximately 90%, the same magnitude of reduction noted in whole cultures coinfected with satellite and adenovirus. This suggested that all cells infected with the two viruses were producing a reduced quantity of adenovirus.

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Specific Viral Interference in Hela Cell Cultures Chronically Infected With Coxsackie B5 Virus

Cited by 45 publications

References 17 publications

Rubella Virus Carrier Cultures Derived From Congenitally Infected Infants

Rubella Virus Carrier Cultures Derived From Congenitally Infected Infants

Monoclonal antibody that inhibits infection of HeLa and rhabdomyosarcoma cells by selected enteroviruses through receptor blockade

Adeno-Associated Satellite Virus Interference With the Replication of Its Helper Adenovirus

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