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Adaptation of equine abortion virus to Earle’s L cells in serum-free medium with plaque formation.
Abstract: The research article discusses the successful adaptation of the Equine Abortion Virus (EAV) to L-M 929 cells, the impact on infected cultures, and possible reasons for earlier unsuccessful attempts. It […]
Publication Date: 1962-07-01 PubMed ID: 14490220DOI: 10.3181/00379727-110-27558Google Scholar: Lookup The Equine Research Bank provides access to a large database of publicly available scientific literature. Inclusion in the Research Bank does not imply endorsement of study methods or findings by Mad Barn.
- Journal Article
Summary
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The research article discusses the successful adaptation of the Equine Abortion Virus (EAV) to L-M 929 cells, the impact on infected cultures, and possible reasons for earlier unsuccessful attempts. It also explores potential factors that might have influenced the results such as contamination and the toxicity of the medium to certain cell lines.
Adaptation of Equine Abortion Virus to L-M 929 Cells
- The research primarily focusses on the adaptation of EAV to L-M 929 cells, which is a particular type of cell line. Successful adaptation means that the virus can effectively infect these cells and replicate within them.
- Complement-fixation methods were used for the identification of the virus within these cells. Complement fixation is an immunological method used to measure the presence or absence of specific antibodies or antigens.
Impact on Infected Cultures
- The study reports cytopathic effects on the infected cultures. A cytopathic effect means the observable changes in a cell due to a viral infection, which can include cell death or dysfunction.
- These effects were measured using both TCID50 or plaque-counting methods. TCID50 is a measure of infectious virus titer, while plaque counting is a method used to measure the number of viruses.
Previous Unsuccessful Adaptation
- The research attempts to explain the failure of the virus to propagate in the original L cells in previous experiments. The cause remains unexplained, but it may have been related to the growth medium used at that time, which contained horse and human sera that could have had an inhibitory effect.
Possible Contamination and Toxicity Factors
- The researchers also considered the possibility of the L-cell strain used in their study being contaminated by HeLa cells. However, this seems unlikely because the L-M 929 strain has a distinct chromosomal marker that permits precise identification.
- Finally, the researchers noted that YELP medium is highly toxic to the HeLa cell line. Thus, the growth of these cells in this particular medium is extremely improbable.
Cite This Article
APA
RANDALL CC, LAWSON LA.
(1962).
Adaptation of equine abortion virus to Earle’s L cells in serum-free medium with plaque formation.
Proc Soc Exp Biol Med, 110, 487-489.
https://doi.org/10.3181/00379727-110-27558 Publication
Researcher Affiliations
MeSH Terms
- Acclimatization
- Adaptation, Physiological
- Herpesvirus 1, Equid
- Tissue Culture Techniques
- Viruses / ethnology
Citations
This article has been cited 12 times.- Kim SK, Shakya AK, O'Callaghan DJ. Immunization with Attenuated Equine Herpesvirus 1 Strain KyA Induces Innate Immune Responses That Protect Mice from Lethal Challenge. J Virol 2016 Sep 15;90(18):8090-104.
- GENTRY GA, LAWSON LA, RANDALL CC. REPLICATION OF A DEOXYRIBONUCLEIC ACID VIRUS IN THYMINE-DEFICIENT MAMMALIAN CELLS. J Bacteriol 1964 Nov;88(5):1324-8.
- RANDALL CC, WALKER BM. DEGRADATION OF DEOXYRIBONUCLEIC ACID AND ALTERATION NUCLEIC ACID METABOLISM IN SUSPENSION CULTURES OF L-M CELLS INFECTED WITH EQUINE ABORTION VIRUS. J Bacteriol 1963 Jul;86(1):138-46.
- Bowles DE, Holden VR, Zhao Y, O'Callaghan DJ. The ICP0 protein of equine herpesvirus 1 is an early protein that independently transactivates expression of all classes of viral promoters. J Virol 1997 Jul;71(7):4904-14.
- Chen M, Harty RN, Zhao Y, Holden VR, O'Callaghan DJ. Expression of an equine herpesvirus 1 ICP22/ICP27 hybrid protein encoded by defective interfering particles associated with persistent infection. J Virol 1996 Jan;70(1):313-20.
- Caughman GB, Lewis JB, Smith RH, Harty RN, O'Callaghan DJ. Detection and intracellular localization of equine herpesvirus 1 IR1 and IR2 gene products by using monoclonal antibodies. J Virol 1995 May;69(5):3024-32.
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- O'Callaghan DJ, Hyde JM, Gentry GA, Randall CC. Kinetics of viral deoxyribonucleic acid, protein, and infectious particle production and alterations in host macromolecular syntheses in equine abortion (herpes) virus-infected cells. J Virol 1968 Aug;2(8):793-804.
- Abodeely RA, Lawson LA, Randall CC. Morphology and entry of enveloped and deenveloped equine abortion (herpes) virus. J Virol 1970 Apr;5(4):513-23.
- Allen GP, McGowan JJ, Gentry GA, Randall CC. Biochemical transformation of deoxythymidine kinase-deficient mouse cells with UV-irradiated equine herpesvirus type 1. J Virol 1978 Oct;28(1):361-7.
- Aswell JF, Allen GP, Jamieson AT, Campbell DE, Gentry GA. Antiviral activity of arabinosylthymine in herpesviral replication: mechanism of action in vivo and in vitro. Antimicrob Agents Chemother 1977 Aug;12(2):243-54.
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