A better understanding of how human immunodeficiency virus (HIV) coinfection affects the course of hepatitis C virus (HCV) infection is required to select patients with HIV who would benefit from current HCV therapy. Between June 1996 and March 2000, HCV RNA levels were quantified for 1,279 patients at the Louisiana State University Health Sciences Center; 28 of these patients were coinfected with HIV. HCV loads were quantified by the Bayer branched-DNA assay with a lower limit of detection of 0.2 Meq/ml. We compared the median HCV RNA levels of for patients coinfected with HIV and HCV and patients infected only with HCV who were in the same age range (23 to 55 years). The median HCV load for the 28 patients coinfected with HCV and HIV (17.8 Meq/ml) was significantly greater (P < 0.05) than that for similarly aged patients infected only with HCV (6.1 Meq/ml). The HCV load did not correlate with age or sex for either group of patients. A significant (R ‫؍‬ ؊0.4; P < 0.05) negative correlation was observed between HCV load and CD4 count in the coinfected group, for whom the CD4 counts at the time of HCV load analysis ranged from 6 to 1,773/mm 3 . The increased HCV load in patients coinfected with HCV and HIV compared to that in patients infected only with HCV and the inverse relationship of the HCV load to the CD4 count indicate that immunosuppression results in decreased control of HCV replication. In addition, we report significantly higher HCV loads among coinfected African Americans than Caucasians.

PROTEIN COMPONENT OF ENDOTOXINblood glucose must be maintained for a certain period before its reduction to stimulate HGH secretion.Oufr observation is difficult to interpret, but raises some questions on the regulatory manner of HGH secretion mlediated by glucose metabolism. If the stimulation of HGH secretion CUTS by intracellular glucose deprivation( 1-3) in the hypothalamus( 2,7) as proposed, glucose infused for a short period in most cases is unable to induce enough metabolic shift in the hypothalamic cells to stimulate HGH secretion, in spite of other definite responses such as plasna NEFA change. An alternative explanation may be that the direct stimulant of HGH secretion is not the extracellular or intracellular glucose itself, but the metabolites or other substances related to glucose metabolism, which are different quanrtitatively or qualitatively in the conditions of Short and long continuous glucose infusion. Since plasma NEFA change was similar in all cases, it is apparent that there is no conrelation between the rise of plasma HGH and the value of plasma NEFA. In these respects, our results may support the observation of Quabbe et aZ (8), who showed the absence of correlation between plasma HGH rise and blood glucose or plasma NEFA level during a 24-hour fast in normal subjects.Summary. Serial plasma HGH concentrations were measured, in 18 normal subjects, following continuous intravenous glucose in-fusion performed for periods of 3, 10, 20 and 30 minutes. In 5 of 8 cases infused for 3 minutes, no rise of plasma HGH was olbserved in spite of the rapid fall of blood glucose with (4 cases) or without (1 case) its reduction below the fasting level. The 3 other cases infused for 3 minutes and all 10 cases of 10, 20 and 30 minutes' infusion showed definite rise of plasma HGH at 90-180 minutes following the infusion. From the results obtained, it appears that the falling blood glucose per se is not a direct stimulus, and the reduction of blood glucose !below the fasting level is not necessarily a stimulus to HGH secretion.

A Boivin preparation of Brucella abortus, unlike common enterobacterial endotoxins, failed to depress water intake or increase numbers of hemolysin-producing spleen cells in mice, or to cause delayed inflammatory reactions in rabbit skin. Reactivity to the B. abortus endotoxin was found only in animals which were previously given the endotoxin with, but not necessarily in, complete Freund's adjuvant. Previous treatment with the endotoxin in saline or with only the adjuvant was ineffective. Sensitization appeared within 10 days and waned after 5 weeks. Passive sensitization was obtained with sensitized donor spleen cells but not with serum. Serum antibody titers did not correlate with the appearance and disappearance of sensitization.

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