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Archives of virology1979; 60(3-4); 279-289; doi: 10.1007/BF01317499

Characterization of the infection of equine fibroblasts by equine infectious anemia virus.

Abstract: Equine dermal fibroblasts persistently infected with equine infectious anemia virus (EIAV) show no alterations in cell morphology or growth kinetics when compared to uninfected cells. The percentage of cells immunofluorescent positive for viral proteins fluctuated, depending upon the stage of the cell cycle, while production of extracellular virus was uniform throughout the cell cycle, increasing only as the cell number increased. This was shown in log versus stationary phase cultures as well as in cultures synchronized by sterum starvation. The establishment of productive infection did not require host cell DNA synthesis. Normal levels of progeny virus were produced in cultures pretreated with mitomycin C and placed in serum-containing medium. Serum-starved cultures, however, did not support EIAV replication as well as other cultures, presumably because synthesis of provirus was inhibited.
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Publication Date: 1979-01-01 PubMed ID: 228638DOI: 10.1007/BF01317499Google Scholar: Lookup
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  • P.H.S.

Summary

This research summary has been generated with artificial intelligence and may contain errors and omissions. Refer to the original study to confirm details provided. Submit correction.

This research shows that equine dermal fibroblasts (cells in horse skin) infected with equine infectious anemia virus (EIAV) behave similarly to uninfected cells in terms of growth and appearance. The production of the virus by the infected cells is steady, regardless of the cell’s stage of growth, but the presence of the viral proteins varies. This study also found that the virus doesn’t need the host cell’s DNA synthesis to establish an infection and can still grow in cultures treated to inhibit cell division.

Virus Effect on Fibroblasts

  • The infected equine dermal fibroblasts, fibroblasts being a type of cell found in connective tissue, do not show any noticeable changes either in their physical appearance or their rate of growth when compared to non-infected cells.
  • The researchers found that the virus can establish a productive infection without a need for cellular DNA synthesis, that means it can multiply and spread without needing the cells to divide and replicate their DNA.

Fluctuation in Viral Protein Presence

  • The research showed a fluctuation in the amount of cells that tested positive for the virus’s proteins based on the cell’s stage in the cell cycle, a series of events that lead to cell division and replication. In other words, whether or not a cell showed signs of the virus was dependent on if the cell was dividing or preparing to divide.

Influence of Cell Growth Stage on Virus Production

  • The researchers found that the production of the virus was constant throughout all the stages of the host cells’ cycles. This means that the cells were releasing the virus consistently, regardless of the cell’s stage of growth.
  • However, the volume of virus production increased as the number of cells increased. This was seen both in cultures with increasing cell numbers and stationary cell numbers, showing that virus production increased with cell density rather than cell division.

Effect of Serum Starvation

  • The study also discovered that EIAV replication was less effective in serum-starved cultures, suggesting that the virus’s synthesis of its own DNA substitute (provirus) was hindered under these conditions.
  • Serum starvation is a method used to synchronize the cells’ growth and observe cellular behavior during different stages of the cell cycle. Essentially, researchers limit the nutrients available to keep the cells in a controlled state of non-division.
  • However, even after treating these cultures with mitomycin C, a drug used to inhibit cell division, the infected cells didn’t show a serious decrease in virus production once returned to normal, nutrient-rich conditions. This indicates that the virus can continue its lifecycle even under conditions detrimental to cell division.

Cite This Article

APA
Klevjer-Anderson P, Cheevers WP, Crawford TB. (1979). Characterization of the infection of equine fibroblasts by equine infectious anemia virus. Arch Virol, 60(3-4), 279-289. https://doi.org/10.1007/BF01317499

Publication

Archives of virology
ISSN: 0304-8608
NlmUniqueID: 7506870
Country: Austria
Language: English
Volume: 60
Issue: 3-4
Pages: 279-289

Researcher Affiliations

Klevjer-Anderson, P
    Cheevers, W P
      Crawford, T B

        MeSH Terms

        • Antigens, Viral / analysis
        • Cell Cycle
        • Cell Line
        • DNA / biosynthesis
        • Fibroblasts
        • Infectious Anemia Virus, Equine / growth & development
        • Infectious Anemia Virus, Equine / immunology
        • Mitomycins / pharmacology
        • Skin
        • Virus Replication

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        Citations

        This article has been cited 7 times.
        1. Wardle R, Pullman JA, Haldenby S, Ressel L, Pope M, Clegg PD, Radford A, Stewart JP, Al-Saadi M, Dyer P, Peffers MJ. Identification of Equid herpesvirus 2 in tissue-engineered equine tendon. Wellcome Open Res 2017;2:60.
          doi: 10.12688/wellcomeopenres.12176.2pubmed: 29152595google scholar: lookup
        2. Maury W, Thompson RJ, Jones Q, Bradley S, Denke T, Baccam P, Smazik M, Oaks JL. Evolution of the equine infectious anemia virus long terminal repeat during the alteration of cell tropism. J Virol 2005 May;79(9):5653-64.
          doi: 10.1128/JVI.79.9.5653-5664.2005pubmed: 15827180google scholar: lookup
        3. Maury W, Wright PJ, Bradley S. Characterization of a cytolytic strain of equine infectious anemia virus. J Virol 2003 Feb;77(4):2385-99.
          doi: 10.1128/jvi.77.4.2385-2399.2003pubmed: 12551976google scholar: lookup
        4. Maury W, Oaks JL, Bradley S. Equine endothelial cells support productive infection of equine infectious anemia virus. J Virol 1998 Nov;72(11):9291-7.
          doi: 10.1128/JVI.72.11.9291-9297.1998pubmed: 9765477google scholar: lookup
        5. McGuire TC, Tumas DB, Byrne KM, Hines MT, Leib SR, Brassfield AL, O'Rourke KI, Perryman LE. Major histocompatibility complex-restricted CD8+ cytotoxic T lymphocytes from horses with equine infectious anemia virus recognize Env and Gag/PR proteins. J Virol 1994 Mar;68(3):1459-67.
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        6. Sellon DC, Fuller FJ, McGuire TC. The immunopathogenesis of equine infectious anemia virus. Virus Res 1994 May;32(2):111-38.
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        7. Shively MA, Banks KL, Greenlee A, Klevjer-Anderson P. Antigenic stimulation of T lymphocytes in chronic nononcogenic retrovirus infection: equine infectious anemia. Infect Immun 1982 Apr;36(1):38-46.
          doi: 10.1128/iai.36.1.38-46.1982pubmed: 6281191google scholar: lookup
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