Cerebrospinal fluid characteristics of infants who present to the emergency department with fever: establishing normal values by week of age.

UNLABELLED: BACKGROUND This study describes differences in the values of cerebrospinal fluid (CSF) white blood cell (WBC), glucose, and protein counts in infants less than 60 days of age with fever who were not proven to have viral or bacterial meningitis. METHODS: Three independent retrospective medical record reviews were conducted using a population of infants less than 60 days of age who presented to the Emergency Department with fever. Full-term infants were included if a lumbar puncture was performed within 24 hours of admittance and bacterial or viral meningitis was not identified as the cause of fever. RESULTS: A total of 1091 infants were included and grouped by week of age. Significant trends were found for CSF WBC and CSF protein with the highest values observed during the first week of life. Mean for CSF WBC was 8.63 cells/mm for infants aged 0 to 1 week and decreased for each age group ending with infants 8 weeks of age having a mean of 2.22 cell/mm. For CSF protein, a similar trend was observed. No significant differences were found for CSF glucose. CONCLUSIONS: Significant differences exist for infants by week of age for CSF WBC and CSF protein. These values can be used to assist in interpreting laboratory findings and making management decisions for infants less than 60 days of age.

Fatty acid synthase is up-regulated during hepatitis C virus infection and regulates hepatitis C virus entry and production.

UNLABELLED: Hepatitis C virus (HCV) is a major human pathogen that causes serious illness, including acute and chronic hepatitis, cirrhosis, and hepatocellular carcinoma. Using a mass spectrometry-based proteomics approach, we have identified 175 proteins from a cell culture supernatant fraction containing the HCV genotype 2a (JFH1) virus, among which fatty acid synthase (FASN), the multifunctional enzyme catalyzing the de novo synthesis of fatty acids, was confirmed to be highly enriched. Subsequent studies showed that FASN expression increased in the human hepatoma cell line, Huh7, or its derivative, upon HCV infection. Blocking FASN activity by C75, a pharmacological FASN inhibitor, led to decreased HCV production. Reduction of FASN by RNA interference suppressed viral replication in both replicon and infection systems. Remarkably, FASN appeared to be selectively required for the expression of claudin-1, a tight junction protein that was recently identified as an entry coreceptor for HCV, but not for the expression of another HCV coreceptor, CD81. The decrease in Claudin-1 expression resulting from FASN inhibition was accompanied by a decrease in transepithelial electric resistance of Huh7 cells, implying a reduction in the relative tightness of the cell monolayer. Consequently, the entry of human immunodeficiency virus-HCV pseudotypes was significantly inhibited in C75-treated Huh7 cells. CONCLUSION: As far as we know, this is the first line of evidence that demonstrates that HCV infection directly induces FASN expression, and thus suggests a possible mechanism by which HCV infection alters the cellular lipid profile and causes diseases such as steatosis.