Human adenovirus infection in monkey cells: an example of host restriction at a step late in replication

Stephen G. Baum, R. I. Fox

Research output: Chapter in Book/Report/Conference proceedingChapter

5 Citations (Scopus)

Abstract

In the 1950's, attempts were made to adapt human adenoviruses to growth in monkey tissues for use in the production of vaccines. However, human adenovirus infection of monkey cells was found to be abortive, and the yield of infectious adenovirus did not exceed input levels. In contrast, when monkey cells were superinfected with SV40, adenovirus replication appeared to proceed normally through all steps, and the yield of adenovirus was increased by 103-105 fold over that in the abortive infection. The phenomenon of increasing adenovirus replication in monkey cells by superinfection with SV40 was called enhancement. For several years enhancement has been studied as a model of reversible host range restriction and the interaction of viral genomes. In addition, it was hoped that the study of restricted replication would provide information about the normal replicative cycle, in much the same way that the study of inborn errors of metabolism has contributed to knowledge of normal metabolic pathways. The authors' approach to this system has been to examine each step in adenovirus replication as it is known to occur in permissive human cells and to see if this process is carried out efficiently in the nonpermissive monkey cell. This paper discusses the evidence that the block to efficient replication is at a step following transcription of mRNA and, most probably, consists of a defect in the association of late RNA species with polyribosomes. This defect, in turn, interrupts the translation of late viral structural proteins. In addition, recent experiments indicate that adenovirus can produce a latent infection in monkey cells, possibly involving integration of viral DNA into host genome, and that this latent infection can be enhanced by SV40 for at least 30 days after initial infection. Therefore, the enhancement system also appears to serve as a model of the activation of latent or subclinical infection.

Original languageEnglish (US)
Title of host publicationSymposia on Quantitative Biology
Pages567-573
Number of pages7
Volume39
Edition1
StatePublished - 1974

Fingerprint

Human Adenovirus Infections
Adenoviridae
Haplorhini
Infection
Viral Structural Proteins
Human Adenoviruses
Inborn Errors Metabolism
Superinfection
Asymptomatic Infections
Polyribosomes
Viral Genome
Host Specificity
Viral DNA
Metabolic Networks and Pathways
Vaccines
Genome
RNA
Messenger RNA
Growth

ASJC Scopus subject areas

  • Medicine(all)

Cite this

Baum, S. G., & Fox, R. I. (1974). Human adenovirus infection in monkey cells: an example of host restriction at a step late in replication. In Symposia on Quantitative Biology (1 ed., Vol. 39, pp. 567-573)

Human adenovirus infection in monkey cells : an example of host restriction at a step late in replication. / Baum, Stephen G.; Fox, R. I.

Symposia on Quantitative Biology. Vol. 39 1. ed. 1974. p. 567-573.

Research output: Chapter in Book/Report/Conference proceedingChapter

Baum, SG & Fox, RI 1974, Human adenovirus infection in monkey cells: an example of host restriction at a step late in replication. in Symposia on Quantitative Biology. 1 edn, vol. 39, pp. 567-573.
Baum SG, Fox RI. Human adenovirus infection in monkey cells: an example of host restriction at a step late in replication. In Symposia on Quantitative Biology. 1 ed. Vol. 39. 1974. p. 567-573
Baum, Stephen G. ; Fox, R. I. / Human adenovirus infection in monkey cells : an example of host restriction at a step late in replication. Symposia on Quantitative Biology. Vol. 39 1. ed. 1974. pp. 567-573
@inbook{8ba02e9f2a28490d94c234ee1959cfec,
title = "Human adenovirus infection in monkey cells: an example of host restriction at a step late in replication",
abstract = "In the 1950's, attempts were made to adapt human adenoviruses to growth in monkey tissues for use in the production of vaccines. However, human adenovirus infection of monkey cells was found to be abortive, and the yield of infectious adenovirus did not exceed input levels. In contrast, when monkey cells were superinfected with SV40, adenovirus replication appeared to proceed normally through all steps, and the yield of adenovirus was increased by 103-105 fold over that in the abortive infection. The phenomenon of increasing adenovirus replication in monkey cells by superinfection with SV40 was called enhancement. For several years enhancement has been studied as a model of reversible host range restriction and the interaction of viral genomes. In addition, it was hoped that the study of restricted replication would provide information about the normal replicative cycle, in much the same way that the study of inborn errors of metabolism has contributed to knowledge of normal metabolic pathways. The authors' approach to this system has been to examine each step in adenovirus replication as it is known to occur in permissive human cells and to see if this process is carried out efficiently in the nonpermissive monkey cell. This paper discusses the evidence that the block to efficient replication is at a step following transcription of mRNA and, most probably, consists of a defect in the association of late RNA species with polyribosomes. This defect, in turn, interrupts the translation of late viral structural proteins. In addition, recent experiments indicate that adenovirus can produce a latent infection in monkey cells, possibly involving integration of viral DNA into host genome, and that this latent infection can be enhanced by SV40 for at least 30 days after initial infection. Therefore, the enhancement system also appears to serve as a model of the activation of latent or subclinical infection.",
author = "Baum, {Stephen G.} and Fox, {R. I.}",
year = "1974",
language = "English (US)",
volume = "39",
pages = "567--573",
booktitle = "Symposia on Quantitative Biology",
edition = "1",

}

TY - CHAP

T1 - Human adenovirus infection in monkey cells

T2 - an example of host restriction at a step late in replication

AU - Baum, Stephen G.

AU - Fox, R. I.

PY - 1974

Y1 - 1974

N2 - In the 1950's, attempts were made to adapt human adenoviruses to growth in monkey tissues for use in the production of vaccines. However, human adenovirus infection of monkey cells was found to be abortive, and the yield of infectious adenovirus did not exceed input levels. In contrast, when monkey cells were superinfected with SV40, adenovirus replication appeared to proceed normally through all steps, and the yield of adenovirus was increased by 103-105 fold over that in the abortive infection. The phenomenon of increasing adenovirus replication in monkey cells by superinfection with SV40 was called enhancement. For several years enhancement has been studied as a model of reversible host range restriction and the interaction of viral genomes. In addition, it was hoped that the study of restricted replication would provide information about the normal replicative cycle, in much the same way that the study of inborn errors of metabolism has contributed to knowledge of normal metabolic pathways. The authors' approach to this system has been to examine each step in adenovirus replication as it is known to occur in permissive human cells and to see if this process is carried out efficiently in the nonpermissive monkey cell. This paper discusses the evidence that the block to efficient replication is at a step following transcription of mRNA and, most probably, consists of a defect in the association of late RNA species with polyribosomes. This defect, in turn, interrupts the translation of late viral structural proteins. In addition, recent experiments indicate that adenovirus can produce a latent infection in monkey cells, possibly involving integration of viral DNA into host genome, and that this latent infection can be enhanced by SV40 for at least 30 days after initial infection. Therefore, the enhancement system also appears to serve as a model of the activation of latent or subclinical infection.

AB - In the 1950's, attempts were made to adapt human adenoviruses to growth in monkey tissues for use in the production of vaccines. However, human adenovirus infection of monkey cells was found to be abortive, and the yield of infectious adenovirus did not exceed input levels. In contrast, when monkey cells were superinfected with SV40, adenovirus replication appeared to proceed normally through all steps, and the yield of adenovirus was increased by 103-105 fold over that in the abortive infection. The phenomenon of increasing adenovirus replication in monkey cells by superinfection with SV40 was called enhancement. For several years enhancement has been studied as a model of reversible host range restriction and the interaction of viral genomes. In addition, it was hoped that the study of restricted replication would provide information about the normal replicative cycle, in much the same way that the study of inborn errors of metabolism has contributed to knowledge of normal metabolic pathways. The authors' approach to this system has been to examine each step in adenovirus replication as it is known to occur in permissive human cells and to see if this process is carried out efficiently in the nonpermissive monkey cell. This paper discusses the evidence that the block to efficient replication is at a step following transcription of mRNA and, most probably, consists of a defect in the association of late RNA species with polyribosomes. This defect, in turn, interrupts the translation of late viral structural proteins. In addition, recent experiments indicate that adenovirus can produce a latent infection in monkey cells, possibly involving integration of viral DNA into host genome, and that this latent infection can be enhanced by SV40 for at least 30 days after initial infection. Therefore, the enhancement system also appears to serve as a model of the activation of latent or subclinical infection.

UR - http://www.scopus.com/inward/record.url?scp=0016306603&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0016306603&partnerID=8YFLogxK

M3 - Chapter

C2 - 169092

AN - SCOPUS:0016306603

VL - 39

SP - 567

EP - 573

BT - Symposia on Quantitative Biology

ER -