You are not currently logged in.
Access your personal account or get JSTOR access through your library or other institution:
If You Use a Screen ReaderThis content is available through Read Online (Free) program, which relies on page scans. Since scans are not currently available to screen readers, please contact JSTOR User Support for access. We'll provide a PDF copy for your screen reader.
Activation of Endogenous Type C Virus in BALB/c Mouse Cells by Herpesvirus DNA
Ann L. Boyd, Jeffery G. Derge and Berge Hampar
Proceedings of the National Academy of Sciences of the United States of America
Vol. 75, No. 9 (Sep., 1978), pp. 4558-4562
Published by: National Academy of Sciences
Stable URL: http://www.jstor.org/stable/68592
Page Count: 5
Since scans are not currently available to screen readers, please contact JSTOR User Support for access. We'll provide a PDF copy for your screen reader.
Preview not available
Several virion and nonvirion DNAs were tested for the ability to activate endogenous type C virus in BALB/c-derived mouse cells using the calcium precipitation technique. The DNAs from all herpesviruses tested activated xenotropic type C virus synthesis. These included DNAs from herpes simplex virus types 1 and 2, Epstein-Barr virus, human cytomegalovirus, SA8 virus, infectious bovine rhinotracheitis virus, pseudorabies virus, and herpes saimiri virus (M-DNA). In contrast, DNAs from vaccinia virus, simian virus 40, primate cells, bacteria, mycoplasma, and salmon sperm showed no ability to activate type C virus when tested under the same conditions. Several herpesviruses and vaccinia virus, which were highly infectious for the BALB/c cells used, were tested for their ability to activate type C virus after UV irradiation. All herpesviruses tested were positive, while vaccinia virus was negative. Unirradiated simian virus 40 also showed no ability to activate type C virus. Activation of type C virus by DNA from herpes simplex virus was observed after shearing or sonication of the DNA to an average size of 3 × 106 daltons, but was not observed with DNA sonicated to an average size of 1 × 106 daltons. Alkali denaturation of DNA from herpes simplex virus or treatment with DNase, but not RNase, destroyed its ability to activate type C virus, as did crosslinking of the DNA with 4,5′,8-trimethylpsoralen (psoralen) and light.
Proceedings of the National Academy of Sciences of the United States of America © 1978 National Academy of Sciences