ABSTRACT: Nucleic acid testing (NAT)-based methods for the detection and quantification of human immunodeficiency virus Type 1 (HIV-1) RNA are used to increase transfusion safety and to diagnose and manage HIV-1-infected patients. We describe a novel HIV-1 recombinant form associated with lack of reactivity or substantial underestimation of viral load by commercial NAT assays.
We observed a repeat blood donor seroconverting to anti-HIV in whom HIV RNA was initially undetectable with routine NAT was observed. During donor follow-up, HIV RNA became detectable, but the viral load was 2 to 3 log lower than measured with other NATs targeting different genome regions. Genome sequencing revealed a novel B/F recombinant with mutations affecting primers and probe annealing accounting for the poor performance of routine NAT. A total of 553 HIV-1-infected patients attending the hospital clinic were subsequently tested prospectively using the routine assay and an in-house assay specifically designed to detect the B/F strains.
The routine assay substantially underestimated viremia (1-5 log) in 19 cases (3.5%), 11 (58%) of which were infected with the same B/F strain observed in the index donor samples. Two other non-B circulating recombinant forms of HIV-1 (A/G, B/G subtypes) were identified as poorly detected. Newly introduced NATs targeting two HIV-1 regions improved assay performance.
HIV-1 increasing heterogeneity affects the efficiency of NATs and consequently the safety of the blood supply as well as diagnosis and patient management.
Transfusion 11/2010; 51(4):719-30. · 3.22 Impact Factor
ABSTRACT: To analyze transient elastography-measured liver stiffness in patients with acute decompensated heart failure to describe variations in liver stiffness measurements and assess their relationship with the patients' clinical course and laboratory data.
This study was approved by the local institutional review board, and all of the subjects gave verbal informed consent. Twenty-seven hospitalized patients with heart failure with no signs of liver disease (mean age, 79 years ± 12 [standard deviation]; 12 men [mean age, 78 years ± 11], 15 women [mean age, 80 years ± 12]) underwent liver stiffness and N-terminal proβ brain natriuretic peptide (NTproβBNP) assessments at admission, and 24 patients underwent stiffness measurements at discharge. (Three patients had failed measurement at admission; two of whom did not undergo measurement at discharge and one patient who died had only an admission value obtained.) The predefined stiffness cutoff values were greater than 7.65 kPa for substantial fibrosis and greater than 13.01 kPa for cirrhosis. The control subjects were 21 patients unaffected by heart failure or liver disease. The two groups were compared by using two-tailed Wilcoxon, Mann-Whitney, or t tests, as appropriate.
Among the patients with heart failure, median liver stiffness at admission was 8.80 kPa (interquartile range, 5.92-11.90 kPa), greater than 7.65 kPa in 14 (58%) cases and greater than 13.01 kPa in five (21%). During hospitalization, liver stiffness decreased in 18 patients (including all five patients with baseline measurement > 13.01 kPa) and increased in five. Median liver stiffness (P < .003) and NTproβBNP (P < .001) levels both significantly decreased during hospitalization. Liver stiffness was less than 7.65 kPa in all control patients and did not significantly change during hospitalization (P = .261).
Most patients with acute decompensated heart failure have high liver stiffness values which, like NTproβBNP levels, tend to decrease with clinical improvement.
Radiology 10/2010; 257(3):872-8. · 5.73 Impact Factor
New England Journal of Medicine 09/2010; 363(10):993-4. · 53.30 Impact Factor