Peter J. Bartelloni

Effects of an experimental viral infection on plasma lipid and lipoprotein metabolism.

Abstract Sandfly fever was found to stimulate a series of changes in the plasma concentration of lipids and their transport lipoproteins when the disease was induced experimentally in healthy young adult men, who had been equilibrated for 17 days on a constant liquid diet containing 40 per cent of calories as fat. Plasma values for total and esterified cholesterol, phospholipids, free fatty acids, and free glycerol declined in conjunction with, or prior to, the onset of fever, as did both the cholesterol and protein components of the low density lipoproteins. Concentrations of these moieties remained depressed for varying periods thereafter. Plasma triglyceride values also fell initially but then rose above base line in early convalescence. These lipid changes seemed compatible with a concept, (1) that the use of triglycerides and other lipids as metabolic fuel was increased prior to and during the early febrile period, and (2) that mechanisms that mediated metabolic responses to even a mild self-limited virus infection took precedence over some of the ordinary demands of energy balance.

Changes in individual plasma amino acids following experimentally induced sand fly fever virus infection

Abstract Fasting concentrations of 21 individual plasma amino acids were determined in daily (7:30 a.m.) serial samples from eight volunteers infected with sand fly fever virus and compared to values obtained in six separate daily preexposure baseline measurements in each volunteer, as well as to serial measurements in three unexposed control subjects. By 47 hr after inoculation and before the onset of fever or other clinical indications of infection, most individual plasma amino acids were significantly depressed below preexposure values. These changes began before the marked decrement in protein intake during the illness. Such changes in plasma amino acids did not occur in control subjects. Reduction in amino acid concentrations persisted until after the lysis of fever and did not coincide in timing with alterations in white blood counts or serum Zn and Fe values. Urinary total nitrogen, urea, and alpha amino nitrogen were not altered during the course of sand fly fever in these subjects. Although food intake was reduced during sand fly fever, the magnitude of the amino acid depression was far greater than that reported during starvation or protein deprivation in non-infected subjects, and the sequence of changes in plasma valine, alanine, and glycine followed patterns different from those reported during starvation. It may be postulated that unusually large quantities of certain plasma amino acids were taken up by the cells of the liver and other visceral tissues during this infection. Plasma phenylalanine responded in a manner different from that of the other amino acids. It was decreased on day 2 after exposure to the virus but by day 4 and 5 was significantly increased above preinfection values. This resulted in a significant increase in the phenylalaninetyrosine ratio during the febrile phase of sand fly fever.