scholarly journals Stability of Human Immunodeficiency Virus Type 1 RNA in Cerebrospinal Fluid Determined with the AMPLICOR HIV-1 MONITOR Test, Version 1.5 (Ultrasensitive)

2002 ◽  
Vol 40 (10) ◽  
pp. 3863-3864 ◽  
Author(s):  
E. J. Singer ◽  
H. A. Aronow ◽  
S.-Y. Lee ◽  
C. H. Hinkin ◽  
T. Lazarus
2000 ◽  
Vol 38 (12) ◽  
pp. 4637-4639 ◽  
Author(s):  
Yi-Wei Tang ◽  
Joe T.-J. Huong ◽  
Robert M. Lloyd ◽  
Paul Spearman ◽  
David W. Haas

The source of human immunodeficiency virus type 1 (HIV-1) RNA in cerebrospinal fluid (CSF) during HIV-1 infection is uncertain. The sequence heterogeneity of HIV-1 RNA in simultaneous CSF and plasma samples was characterized for five patients at the baseline and during the first week of antiretroviral therapy by two commercial genotyping methodologies. In individual subjects, the sequences in CSF samples differed significantly from those in plasma. In contrast, the viral sequences in CSF at the baseline did not differ from the sequences in CSF during treatment. Similarly, viral sequences in plasma did not vary over this interval. This study provides evidence that HIV-1 RNA in CSF and plasma arise from distinct compartments.


1991 ◽  
Vol 32 (3) ◽  
pp. 259-268 ◽  
Author(s):  
Luigi M.E. Grimaldi ◽  
Antonella Castagna ◽  
Davide Maimone ◽  
Gian Vito Martino ◽  
Alberto Dolci ◽  
...  

1994 ◽  
Vol 36 (1) ◽  
pp. 32-39 ◽  
Author(s):  
W. Royal ◽  
O. A. Selnes ◽  
M. Concha ◽  
T. E. Nance-Sproson ◽  
J. C. McArthur

2000 ◽  
Vol 38 (5) ◽  
pp. 1920-1925 ◽  
Author(s):  
Fan Zhang ◽  
Surya Tetali ◽  
Xue Ping Wang ◽  
Mark H. Kaplan ◽  
Frans V. Cromme ◽  
...  

This study examined the clinical correlation between the presence of human cytomegalovirus (HCMV) pp67 mRNA in cerebrospinal fluid (CSF) and active HCMV central nervous system (CNS) disease in patients with human immunodeficiency virus type 1 (HIV-1). In total, 76 CSF specimens collected from 65 HIV-1-positive patients diagnosed with HCMV CNS disease, other non-HCMV-related CNS diseases, or no CNS disease were tested for the presence of HCMV pp67 mRNA using the NucliSens cytomegalovirus (CMV) pp67 assay (Organon Teknika, Durham, N.C.). The results were compared to those of a nested PCR for the detection of HCMV glycoprotein B DNA and to those obtained by viral culture (54 samples). CSF specimens collected from patients without HCMV CNS disease yielded the following results: pp67 assay negative, 62 of 62 specimens; culture negative, 41 of 41 specimens; and PCR negative, 56 of 62 specimens (6 specimens were positive). CSF specimens collected from patients with HCMV CNS disease yielded the following results: pp67 assay positive, 9 of 13 specimens; PCR positive, 13 of 13 specimens; and culture positive, 2 of 13 specimens. After resolution of the discordant results, the following positive and negative predictive values (PPV and NPV, respectively) for the diagnosis of HCMV CNS disease were determined. The PPV for PCR, pp67 assay, and culture were 68.4, 100, and 100%, respectively, and the NPV for PCR, pp67 assay, and culture were 100, 97.0, and 82.7%, respectively. The sensitivities for DNA PCR, pp67 assay, and culture for the detection of HCMV were 100, 84.6, and 18%, respectively, and the clinical specificities were 90.5, 100, and 100%, respectively. This study indicates that the detection of HCMV pp67 mRNA in CSF has good correlation with active HCMV CNS disease, whereas CSF culture is insensitive and qualitative DNA PCR may detect latent nonreplicating virus in CSF from patients without HCMV CNS disease.


2005 ◽  
Vol 79 (13) ◽  
pp. 7959-7966 ◽  
Author(s):  
Patrick R. Harrington ◽  
David W. Haas ◽  
Kimberly Ritola ◽  
Ronald Swanstrom

ABSTRACT Human immunodeficiency virus type 1 (HIV-1) invades the central nervous system (CNS) during primary infection and persists in this compartment by unknown mechanisms over the course of infection. In this study, we examined viral population dynamics in four asymptomatic subjects commencing antiretroviral therapy to characterize cellular sources of HIV-1 in the CNS. The inability to monitor viruses directly in the brain poses a major challenge in studying HIV-1 dynamics in the CNS. Studies of HIV-1 in cerebrospinal fluid (CSF) provide a useful surrogate for the sampling of virus in the CNS, but they are complicated by the fact that infected cells in local CNS tissues and in the periphery contribute to the population pool of HIV-1 in CSF. We utilized heteroduplex tracking assays to differentiate CSF HIV-1 variants that were shared with peripheral blood plasma from those that were compartmentalized in CSF and therefore presumably derived from local CNS tissues. We then tracked the relative decline of individual viral variants during the initial days of antiretroviral therapy. We found that HIV-1 variants compartmentalized in CSF declined rapidly during therapy, with maximum half-lives of approximately 1 to 3 days. These kinetics emulate the decline in HIV-1 produced from short-lived CD4+ T cells in the periphery, suggesting that a similarly short-lived, HIV-infected cell population exists within the CNS. We propose that short-lived CD4+ T cells trafficking between the CNS and the periphery play an important role in amplifying and maintaining HIV-1 populations in the CNS during the asymptomatic phase of infection.


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