scholarly journals Use of a NAT-based assay to improve the surveillance system and prevent transfusion-transmitted malaria in blood banks

2020 ◽  
Vol 19 (1) ◽  
Author(s):  
Daniele Rocha ◽  
Gisely Cardoso de Melo ◽  
José Marcelo Hipólito Carneiro ◽  
Marisa Ribeiro ◽  
Sthefanie Ribeiro ◽  
...  
Keyword(s):  
Nucleic Acid ◽  
Blood Donation ◽  
High Sensitivity ◽  
Nucleic Acid Amplification ◽  
Molecular Diagnostic ◽  
Hiv Rna ◽  
Immunodeficiency Virus ◽  
Blood Banks ◽  
Wide Availability

Abstract Background Malaria can be transmitted by blood transfusion through donations collected from asymptomatic donors. Transfusion-transmitted malaria (TTM) poses a great risk to blood services worldwide. A good screening tool for Plasmodium spp. detection in blood banks must have a high sensitivity for prevention of TTM. However, in Brazilian blood banks, screening for malaria still relies on microscopy. Methods In Brazil, screening for human immunodeficiency virus type 1 (HIV), RNA/DNA for hepatitis C (HCV) and hepatitis B (HBV) viruses is mandatory for every blood donation and uses nucleic acid amplification testing (NAT). The aim of this study was to evaluate the inclusion of an assay for malaria to identify Plasmodium sp. from total nucleic acid (TNA; DNA/RNA) by targeting the 18S rRNA gene of the parasite. Results Considering the limitations of microscopy and the wide availability of the Brazilian NAT platform in the screening of blood units for HIV, HCV, and HBV, a molecular diagnostic tool was validated for detection of Plasmodium sp. in blood banks; a pilot study showed that using this novel NAT assay could reduce the risk of TTM. Conclusion The prototype HIV/HCV/HBV/malaria NAT assay was effective in detecting infected candidate donors and has good prospects to be applied in routine screening for preventing TTM.

scholarly journals Relationship of Incremental Specimen Volumes and Enhanced Detection of Human Immunodeficiency Virus Type 1 RNA with Nucleic Acid Amplification Technology

2000 ◽  
Vol 38 (1) ◽  
pp. 85-89
Author(s):  
Donald J. Witt ◽  
M. Kemper ◽  
Andrew Stead ◽  
Christine C. Ginocchio ◽  
Angela M. Caliendo
Keyword(s):  
Human Immunodeficiency Virus ◽  
Nucleic Acid ◽  
Human Immunodeficiency Virus Type ◽  
Virus Type ◽  
Nucleic Acid Amplification ◽  
Copy Numbers ◽  
Nucleic Acid Amplification Technology ◽  
Immunodeficiency Virus ◽  
Hiv 1

ABSTRACT The relationship between specimen input volume and the frequency of reported human immunodeficiency virus type 1 (HIV-1) RNA copy numbers by nucleic acid amplification technology (the NASBA HIV-1 RNA QT system) was investigated. Results obtained with both clinical specimens and dilution panels indicated that both the absolute number of reported results and the reported HIV-1 RNA copy number were directly proportional to the specimen input volumes evaluated (0.1, 0.5, and 1.0 ml). Conversion of the reported HIV-1 RNA copy numbers to a constant 1.0-ml volume indicated that the numerical relationship among the specimen input volumes and the HIV-1 RNA copy numbers was multiplicative. The HIV-1 RNA copy numbers reported for the 0.5-ml input volume were approximately 5-fold increased over those reported for the 0.1-ml input volume, and those reported for the 1.0-ml input volume were 10-fold increased over those reported for the 0.1-ml input volume. For the specimen input volumes investigated, a common linear range of 264 to 5,400,000 HIV-1 RNA copies was observed. The use of increased specimen input volumes did not result in a loss of assay specificity, as the results reported for specimens from 50 seronegative blood donors were negative at all three specimen input volumes. In conclusion, an increase in the input volume of specimens analyzed by nucleic acid amplification technology can be useful for the enhanced detection of HIV-1 RNA.

scholarly journals Genotypic Changes in Human Immunodeficiency Virus Type 1 Associated with Loss of Suppression of Plasma Viral RNA Levels in Subjects Treated with Ritonavir (Norvir) Monotherapy

1998 ◽  
Vol 72 (6) ◽  
pp. 5154-5164 ◽  
Author(s):  
P. Scott Eastman ◽  
John Mittler ◽  
Reed Kelso ◽  
Chris Gee ◽  
Eric Boyer ◽  
...  
Keyword(s):  
Human Immunodeficiency Virus ◽  
Human Immunodeficiency Virus Type ◽  
Resistance Mutation ◽  
Virologic Response ◽  
Hiv Rna ◽  
Immunodeficiency Virus ◽  
Plasma Rna ◽  
Doubling Times ◽  
Rna Levels

ABSTRACT Ten subjects received 600 to 1,200 mg of the human immunodeficiency virus type 1 (HIV-1) protease inhibitor ritonavir per day. Following 2 weeks of therapy, plasma HIV RNA levels decreased by a mean of 1.57 (range, 0.89 to 1.96) log units. With continued therapy, HIV RNA levels began to rise in eight subjects. The initial rise in plasma RNA levels was temporally associated with the development and quantitative increase in the V82 resistance mutation. Doubling times of the V82A mutant virus were estimated to be 2.4 to 4.8 days. An L63P/A mutation was commonly present at baseline even in subjects with a durable virologic response. The concomitant acquisition of an L63P/A mutation with the V82A/F mutation at the time when plasma RNA levels rebounded suggests a role for the L63P/A mutation in improving the fitness of the V82A/F mutation. Subsequent additional genotypic changes at codons 54 and 84 were often associated with further increases in plasma RNA levels. Ongoing viral replication in the presence of drugs resulted in the appearance of additional genotypic changes, including the L90M saquinavir resistance mutation, and decreased phenotypic susceptibility. The relative fitness of the protease V82A ritonavir resistance mutation and reverse transcriptase T215Y/F zidovudine resistance mutation following drug withdrawal were estimated to be 96 to 98% that of the wild type. Durability of the virologic response was associated with plasma RNA levels at the nadir. A virologic response beyond 60 days was not observed unless plasma HIV RNA levels were suppressed below 2,000 copies/ml, consistent with estimates from V82A doubling times for selection of a single resistance mutation to dominate the replicating population.

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