Sodium and Potassium Transport in Herpes Simplex Virus-infected Cells

Abstract

SUMMARYSodium (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 S6Rb+ 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-l-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-l-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 (Km) of K ÷ transport in HSV-l-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-l-induced inhibition of host protein synthesis at 3 h post-infection as has been suggested in other virus systems.

Na and K Changes in Animal Virus-infected HeLa Cells

“…There was no evidence that either of these viruses induced significant Na-K changes in infected cells during one-step growth (C. N. Nair, unpublished observations). The absence of monovalent cation changes in association with herpes simplex virus-induced inhibition of protein synthesis in Vero cells has been reported by Hackstadt & Mallavia (1982). Thus, from the results of this and previous studies, it would appear that Na-K changes do not occur in infected cells soon enough to initiate inhibition of host protein synthesis caused by several viruses, and that such changes are not invariably associated with toxic effects produced in cultured cells by all animal viruses.…”

Modification of membrane permeability by animal viruses

“…These ionic alterations have been described not only for picornavirus-or togavirus-infected cells, but also for other systems, including cells infected by vesicular stomatitis virus (Garry and Waite, 19791, reovirus (Munoz et al, 1985a1, coronavirus (Rey et al, 1988), vaccinia virus (Norrie et al, 19821, influenza virus (Lopez Vancell et al, 1984;Carrasco and Lacal, 1983), herpesviruses (Hackstadt and Mallavia, 1982;Nokta et al, 1988), and SV40 (Eggleton and Norkin, 1981).…”

Rotavirus infection alters Na+ and K+ homeostasis in MA-104 cells

“…In other systems, changes in intracellular Na + and K ÷ levels are detected after viral inhibition of cellular protein synthesis. Therefore, they do not seem to be a primary cause of the observed inhibition (Hackstadt & Mallavia, 1982;Lacal & Carrasco, 1982;Mizzen et al, 1987;Francoeur & Stanners, 1978;Nair, 1984).…”