T cell recognition of common and type-specific herpes simplex virus (HSV) glycoproteins was measured in 72 subjects. T cells were stimulated with whole HSV-2 antigen and glycoproteins gB2, gD2, and gG2. T cell proliferation in response to HSV-2 antigen and gG2 was significantly higher in subjects with HSV-2 infection than in those with HSV-1 infection only; responses to gB2 and gD2 were the same. T helper (Th) type 1 and Th2 cytokine production in response to whole HSV-2 antigen, gB2, and gD2 was evaluated in 33 subjects. Interleukin (IL)-2 and interferon-gamma responses to most antigens were significantly higher among HSV-2-seropositive subjects than among seronegative subjects. IL-4 synthesis was negligible; IL-10 was produced in seronegative and seropositive persons, but HSV-2 antigen responses were significantly higher in HSV-2-seropositive persons. Naturally acquired immunity to HSV involves T cell recognition of common and type-specific glycoproteins, prominent Th1 responses, and discordant Th2 responses with little IL-4 but substantial IL-10 production.

We compared extracellular and intracellular acid-base states in paralyzed bullfrogs subjected to 4 h of anoxic submergence at 15 degrees C with or without maintenance of extracellular pH at preanoxic levels by bicarbonate infusion. We also assessed anaerobic metabolism under these conditions by measuring tissue lactate and glycogen concentrations in liver, heart, and skeletal muscle. Although bicarbonate infusion resulted in a significantly higher arterial blood pH (pHe) than saline infusion, intracellular pH (pHi) of heart and skeletal muscle, as determined by the DMO equilibration technique, were not significantly different after 4 h of anoxia. We were also unable to demonstrate any differences in anaerobic metabolic rate, since both tissue lactate accumulation and glycogen depletion were identical in bicarbonate- and saline-infused frogs in the tissues studied. We conclude that (1) alterations in the extracellular acid-base state by bicarbonate infusion are not necessarily reflected in the intracellular compartment, perhaps due to powerful intracellular buffering processes, and (2) maintenance of an alkaline extracellular pH during anoxia in bullfrogs does not influence the anaerobic metabolic rate. We could not, however, rule out a possible role for intracellular pH in regulating anaerobic metabolism during anoxia in frogs.