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Effect of electrical stimulation on HIV-1-infected HeLa cells cultured on an electrode surface

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Abstract.

Acquired immunodeficiency syndrome (AIDS) is a disease caused by infection with the human immunodeficiency virus (HIV). Although drug therapy for AIDS is available, problems such as side effects associated with drug therapy and the appearance of resistant HIV strains have arisen. Therefore, therapies based on new principles other than drug treatment are required. In the present study, the effect of electrical stimulation on HIV-1LAI chronically infected HeLa (P6 HeLa/HIV-1LAI) cells cultured on an electrode surface was examined. The results indicated that sensitivity to electrical stimulation was much higher in P6 HeLa/HIV-1LAI cells than in uninfected p6 HeLa cells. When electrical stimulation was applied at 1.0 V (vs. Ag/AgCl) for 20 min, the proportion of damage to cell membrane among P6 HeLa/HIV-1LAI cells, as evaluated by Trypan blue staining, was approximately 4 times higher than that for uninfected P6 HeLa cells. Furthermore, in comparison with uninfected P6 HeLa cells, the proliferation of P6 HeLa/HIV-1LAI cells was significantly suppressed after electrical stimulation. This technique was proven to selectively kill P6 HeLa/HIV-1LAI cells, when compared with uninfected control cells.

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Acknowledgements.

We gratefully acknowledge Ms. Y. Turu, Ms. A. Hara, Ms. S. Douki, and Ms. S. Mizukami of Kumamoto University College of Medical Science for their technical support.

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Authors and Affiliations

  1. Kumamoto University College of Medical Science, 4-24-1 Kuhonji, Kumamoto 862-0976, Japan

    M. Tominaga & E. Kumagai

  2. Department of Biodefence and Medical Virology, Kumamoto University School of Medicine, 2-2-1 Honjo, Kumamoto 860-0811, Japan

    E. Kumagai & S. Harada

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  1. M. Tominaga
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  2. E. Kumagai
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  3. S. Harada
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Correspondence to M. Tominaga.

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Tominaga, M., Kumagai, E. & Harada, S. Effect of electrical stimulation on HIV-1-infected HeLa cells cultured on an electrode surface. Appl Microbiol Biotechnol 61, 447–450 (2003). https://doi.org/10.1007/s00253-003-1225-7

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  • DOI: https://doi.org/10.1007/s00253-003-1225-7

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