JB
Home Help [Feedback] [For Subscribers] [Archive] [Search] [Contents]
This Article
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrowReprints and Permissions
Right arrow Copyright Information
Right arrow Books from ASM Press
Right arrow MicrobeWorld
Citing Articles
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Ankudas, M. M.
Right arrow Articles by Khoobyarian, N.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Ankudas, M. M.
Right arrow Articles by Khoobyarian, N.
J Bacteriol. 1962 December; 84(6): 1287-1291
Copyright © 1963, The Williams & Wilkins Company. All Rights Reserved.

RABBIT HEART CELL CULTURE, STRAIN RHF-1 II. 1 TO 4

Behavior of Adenovirus Types1

Milda M. Ankudas and Newton Khoobyarian

a Department of Microbiology, University of Illinois at the Medical Center, Chicago, Illinois

ABSTRACT

ANKUDAS, MILDA M. (University of Illinois, Chicago) AND NEWTON KHOOBYARIAN. Rabbit heart cell cultures, strain RHF-1. II. Behavior of adenovirus types 1 to 4. J. Bacteriol. 84:1287–1291. 1962.—In general, the findings indicate that adsorption to RHF-1 cells of adenovirus types 1, 2, and 4, but not type 3, precedes the events leading toward virus multiplication. Adenovirus type 3 attained maximal adsorption (90%) in 2 hr, with no evidence of virus multiplication. Under optimal conditions in the present experiments, the type 1 virus appeared to be released from the infected cells at a much slower rate than types 2 and 4. No correlation seemed to exist between the extent of cytopathic changes produced by type 1 in RHF-1 cells and the rise in virus infectivity during the logarithmic phase. On the other hand, the progression of cytopathic effect of type 2- and type 4-infected cells appeared to be a direct result of virus propagation. Further-more, the relative yield of virus per host cell, though small in quantity, was more or less similar for all three types. Histopathologically, no marked difference among the cells infected with types 1, 2, and 4 was clearly evident. Upon serial subculturing of these viruses in RHF-1 cells, a concomitant decrease in infectious virus, as well as complement-fixing antigen titers at each passage level, was also noted.


FOOTNOTES

1 Portion of a thesis submitted by Milda M. Ankudas in partial fulfillment of the requirements for the degree of Master of Science.


J Bacteriol. 1962 December; 84(6): 1287-1291
Copyright © 1963, The Williams & Wilkins Company. All Rights Reserved.







Home Help [Feedback] [For Subscribers] [Archive] [Search] [Contents]
Appl. Environ. Microbiol. Infect. Immun. Eukaryot. Cell
Mol. Cell. Biol. J. Virol. Microbiol. Mol. Biol. Rev.
ALL ASM JOURNALS

Copyright © 1962 by the American Society for Microbiology. All rights reserved.