METHODS: Using 3 d of dietary records, FA intakes of 333 recruited patients were calculated using a food database built from laboratory analyses of commonly consumed Malaysian foods. Plasma triacylglycerol (TG) and erythrocyte FAs were determined by gas chromatography.
RESULTS: High dietary saturated fatty acid (SFA) and monounsaturated fatty acid (MUFA) consumption trends were observed. Patients on HD also reported low dietary ω-3 and ω-6 polyunsaturated fatty acid (PUFA) consumptions and low levels of TG and erythrocyte FAs. TG and dietary FAs were significantly associated respective to total PUFA, total ω-6 PUFA, 18:2 ω-6, total ω-3 PUFA, 18:3 ω-3, 22:6 ω-3, and trans 18:2 isomers (P < 0.05). Contrarily, only dietary total ω-3 PUFA and 22:6 ω-3 were significantly associated with erythrocyte FAs (P < 0.01). The highest tertile of fish and shellfish consumption reflected a significantly higher proportion of TG 22:6 ω-3. Dietary SFAs were directly associated with TG and erythrocyte MUFA, whereas dietary PUFAs were not.
CONCLUSION: TG and erythrocyte FAs serve as biomarkers of dietary PUFA intake in patients on HD. Elevation of circulating MUFA may be attributed to inadequate intake of PUFAs.
METHODOLOGY/PRINCIPAL FINDINGS: Syrian hamsters were euthanized between 4 and 48 hours post intranasal inoculation and tissues were collected and analyzed for the presence of viral RNA, viral antigen and infectious virus. Virus replication was first detected at 8 hours post inoculation (hpi). Nipah virus initially targeted type I pneumocytes, bronchiolar respiratory epithelium and alveolar macrophages in the lung and respiratory and olfactory epithelium lining the nasal turbinates. By 16 hpi, virus disseminated to epithelial cells lining the larynx and trachea. Although the pattern of viral dissemination was similar for both virus isolates, the rate of spread was slower for NiV-B. Infectious virus was not detected in the nervous system or blood and widespread vascular infection and lesions within lymphoid organs were not observed, even at 48 hpi.
CONCLUSIONS/SIGNIFICANCE: Nipah virus initially targets the respiratory system. Virus replication in the brain and infection of blood vessels in non-respiratory tissues does not occur during the early phase of infection. However, virus replicates early in olfactory epithelium and may serve as the first step towards nervous system dissemination, suggesting that development of vaccines that block virus dissemination or treatments that can access the brain and spinal cord and directly inhibit virus replication may be necessary for preventing central nervous system pathology.