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Infection and immunity1976; 14(2); 325-331; doi: 10.1128/iai.14.2.325-331.1976

Hemagglutination by equine infectious anemia virus.

Abstract: Equine infectious anemia (EIA) virus which was propagated on an equine dermal cell line agglutinated guinea pig erythrocytes. Viral fluids containing about 10(7.5) mean tissue culture infective doses/ml showed hemagglutinating (HA) titers ranging from 16 to 32 units/0.05 ml. Results of cesium chloride equilibrium density gradient centrifugation revealed that the hemagglutinin was inseparable from the virus particles. The hemagglutination reaction persisted over a wide range of temperature and pH, and the absence of divalent cations did not decrease its activity. The HA activity was stable at 4 degrees C but not at 56 degreesC. The activity was destroyed by virus-disrupting lipid solvents and moderately sensitive to a proteolytic enzyme. Neuraminidase enhanced HA activity slightly. Phospholipase C had no effect on HA titer, although it completely inactivated infectivity. It was relatively stable to ultraviolet irradiation. Thus, the hemagglutinin appears to be closely associated with virus particles, and its activity is dependent on the presence of its lipids and proteins. Hemagglutination was inhibited by sera from horses infected with EIA virus. Hemagglutinin receptors on the erythrocytes were inactivated by a proteolytic enzyme and formaldehyde but were not influenced by neuraminidase, sodium deoxycholate, or KIO4.
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Publication Date: 1976-08-01 PubMed ID: 9361PubMed Central: PMC420886DOI: 10.1128/iai.14.2.325-331.1976Google Scholar: Lookup
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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.

The research article investigates how the equine infectious anemia (EIA) virus affects guinea pig red blood cells. The findings reveal that the virus induces hemagglutination, a process which causes these cells to clump together. The exact mechanism behind this reaction involves numerous factors including temperature, pH, lipid and protein presence, and receptors on the erythrocyte surface.

Virus Propagation and Hemagglutination

  • The EIA virus was made to multiply on a type of horse skin cell line and could form clumps with red blood cells from guinea pigs.
  • The virus needs to reach a certain concentration in the cell culture to bring about these clumps. This hemagglutination was quantified using hemagglutinating units.

Characteristics of Hemagglutination

  • The researchers identified that the hemagglutination could not be separated from the actual virus particles using a technique called cesium chloride equilibrium density gradient centrifugation.
  • The hemagglutination remained effective across a large range of temperatures and environmental pH and did not require divalent cations, which are ions with double positive charge.

Stability of Hemagglutination Activity

  • The hemagglutination activity remained stable at a temperature of 4 degrees Celsius but was disrupted when exposed to a temperature of 56 degrees Celsius.
  • Hemagglutination activity could also be destroyed using virus-disrupting lipid solvents and was somewhat sensitive to an enzyme that can break down proteins.

Influence of Enzymes and Light on Hemagglutination

  • The enzyme neuraminidase slightly increased hemagglutination activity, but another enzyme called phospholipase C did not affect it, although it did inactivate the virus’s ability to infect cells.
  • Ultraviolet light had minimal impact on the hemagglutination activity.

Receptors on Red Blood Cells

  • The hemagglutination reaction could be stopped by serum (the liquid part of blood) from horses infected with the EIA virus.
  • The receptors involved in hemagglutination on the red blood cells could be inactivated by a protein-breaking enzyme and a chemical called formaldehyde, but were not affected by neuraminidase, sodium deoxycholate, or KIO4 (potassium periodate).

To summarize, the activity of hemagglutination by the EIA virus is reliant on both the lipid and protein components of the virus, and is associated with the virus particles. The virus’s ability to agglutinate red blood cells could be stopped by serum from EIA-infected horses and inactivation of receptors on the surface of red blood cells.

Cite This Article

APA
Sentsui H, Kono Y. (1976). Hemagglutination by equine infectious anemia virus. Infect Immun, 14(2), 325-331. https://doi.org/10.1128/iai.14.2.325-331.1976

Publication

Infection and immunity
ISSN: 0019-9567
NlmUniqueID: 0246127
Country: United States
Language: English
Volume: 14
Issue: 2
Pages: 325-331

Researcher Affiliations

Sentsui, H
    Kono, Y

      MeSH Terms

      • Animals
      • Chloroform / pharmacology
      • Complement Fixation Tests
      • Deoxycholic Acid / pharmacology
      • Equartevirus / immunology
      • Ether / pharmacology
      • Formaldehyde / pharmacology
      • Guinea Pigs
      • Hemagglutination / radiation effects
      • Hemagglutination Inhibition Tests
      • Hydrogen-Ion Concentration
      • Neuraminidase / pharmacology
      • Periodic Acid / pharmacology
      • Phospholipases / pharmacology
      • RNA Viruses / immunology
      • Species Specificity
      • Temperature
      • Trypsin / pharmacology
      • Ultraviolet Rays

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      Citations

      This article has been cited 6 times.
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