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Sodium and Potassium Transport in Herpes Simplex Virus-infected Cells

Ted Hackstadt

Department of Bacteriology and Public Health, Washington State University, Pullman, Washington 99164, U.S.A.

Sodium (Na⁺) and potassium (K⁺) flux in African green monkey kidney cells (Vero) was examined following infection by herpes simplex virus type 1 (HSV-1). A decline in the rate of K⁺ uptake at 5 h post-infection was shown using ⁸⁶Rb⁺ as a K⁺ tracer. In contrast, host protein synthesis was inhibited by 3 h post-infection. The decrease in rate of K⁺ transport to levels 70 to 90% of that of mock-infected cells did not, however, reflect an inability of HSV-1-infected cells to maintain normal intracellular concentrations of Na⁺ and K⁺. At 7 h post-infection, intracellular Na⁺ and K⁺ concentrations were determined to be 26.6 ± 9.4 mM- and 33.3 ± 10.3 mM-Na⁺ and 130.1 ± 4.7 mM- and 137.1 ± 3.2 mM-K⁺ in mock-infected and HSV-1-infected cells respectively. Intracellular Na⁺ did not increase above control levels over at least a 9 h period following HSV-1 infection. The Michaelis constant (K_m) of K⁺ transport in HSV-1-infected or mock-infected Vero cells at 6 h post-infection was determined to be the same with calculated values of 1.38 ± 0.51 mM and 1.79 ± 0.42 mM respectively. A virus-induced alteration of intracellular Na⁺ and K⁺ concentrations cannot, therefore, account for the HSV-1-induced inhibition of host protein synthesis at 3 h post-infection as has been suggested in other virus systems.

Keywords: HSV, membrane, Na⁺, K⁺ ATPase, monovalent cations

Present address: Laboratory of Microbial Structure and Function, Rocky Mountain Laboratories, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Hamilton, Montana 59840, U.S.A.

Received 25 August 1981; accepted 6 January 1982.