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Mice were monitored for weight loss for 5 days and organs were isolated to measure viral load in naïve and immunized mice.
The successful employment of quantitative PCR to measure viral load in clinical medicine has not only advanced our understanding of pathogenesis of many viral diseases but also provided useful markers for predicting outcome and/or monitoring therapeutic responses [1].
It therefore seems necessary to measure viral load for multiple occasions before deciding to treat.
We used quantitative real-time reverse transcription PCR to measure viral load in serum from 24 patients in Kosovo who had acute Crimean-Congo hemorrhagic fever.
For VZV, as well as for other herpes viruses, a variety of methods, techniques and protocols have been used to measure viral load at many institutions [ 57].
The children were monitored at least every 3 months with physical examinations, and blood sample collection to measure viral load (VL) and CD4+ cell count.
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As part of this continuum of care model, a number of intertwining goals are to identify newly infected or at-risk individuals, diagnosis, link to care, retain in care, prescribe medication, and measure viral loads and suppression.
We studied the emergence of an SIV Gag cytotoxic T cell immune escape variant in pigtail macaques expressing the Mane-A*10 MHC I allele using a quantitative RT-PCR to measure viral loads of escape and wild type variants.
The latency boundary was only calculated when serial measurements were nonlinear (R² < 0.85) by selecting the highest and lowest measured viral load and adding or subtracting 0.5 log HPV copies/cell.
For this secondary outcome of viral load, we considered observed suppression as a measured viral load less than 20 copies/μl.
It should be noted that the measured viral load does not account for potential differences in the ratio of integrated to episomal viral DNA between samples.
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