PubMed · 8623144
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D N Mendelson, S G Sandler. 1996. Testing for human immunodeficiency virus p24 antigen.. https://doi.org/10.1046/j.1537-2995.1996.36496226156.x
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Human immunodeficiency virus (HIV) RNA testing is the gold standard for monitoring antiretroviral therapy in HIV-infected patients. However, equipment and reagent costs preclude widespread use of the assay in resource-limited settings. The Perkin-Elmer Ultrasensitive p24 assay and the Cavidi Exavir Load assay both offer potentially simpler, less costly technologies for monitoring viral load. These assays were compared to the Roche Amplicor HIV-1 Monitor Test, v1.5, using panels of clinical samples (subtype B) from HIV-positive subjects and HIV-spiked samples (subtypes A, C, D, CRF_01AE, CRF_02AG, and F). The Ultrasensitive p24 assay detected 100% of the spiked samples with virus loads of >250,000 copies/ml and 61% of the clinical samples with virus loads of 219 to 288,850 copies/ml. Detection rates were improved substantially if an external lysis buffer was added to the procedure. The Cavidi assay detected 54 to 100% of spiked samples with virus loads >10,000 copies/ml and 68% of the clinical samples. These detection rates were also greatly improved with a newly implemented version of this kit. Coefficients of variation demonstrate good reproducibility for each of these kits. The results from the Cavidi v1.0, Cavidi v2.0, and Perkin-Elmer, and the Perkin-Elmer Plus external buffers all correlated well with the results from the Roche Monitor Test (r = 0.83 to 0.96, r = 0.84 to 0.99, r = 0.58 to 0.67, and r = 0.59 to 0.95, respectively). Thus, the use of these two assays for monitoring patients, together with less-frequent confirmation testing, offers a feasible alternative to frequent HIV RNA testing in resource-limited settings.
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Human herpesvirus-8 (HHV-8) is etiologically associated with Kaposi's sarcoma (KS), body cavity-based lymphoma (BCBL), and multicentric Castleman's disease (MCD). These HHV-8-associated diseases arise predominantly in acquired immunodeficiency syndrome (AIDS) patients. Human interleukin-6 (huIL-6) elevated in the serum of AIDS patients is suggested to stimulate the growth of KS and BCBL and to augment the symptoms of MCD. To determine whether huIL-6 stimulates HHV-8 replication directly, expression of the HHV-8 ORF-50 immediate-early gene (transcription activator) and ORF-26 late lytic gene (a capsid protein) was assessed in a BCBL-1 cell line stimulated by huIL-6 by means of real-time reverse transcription-polymerase chain reaction. huIL-6 induced both ORF-50 and ORF-26 expression, and the maximal ORF-50 expression appeared earlier than that of ORF-26. The data indicate that huIL-6 reactivates HHV-8 in BCBL-1 cells through inducing ORF-50. We also confirmed the previously reported activities of HHV-8-encoded huIL-6 homologue (viral interleukin-6 [vIL-6]) on human immunodeficiency virus (HIV) replication in U1 cell line and huIL-6 production by MT-4 T cells, and utilizing monoclonal antibodies to the huIL-6 receptor components, we elucidated that gp130 is the signaling molecule necessary for these vIL-6 activities. These data suggest the possible existence of interaction between HIV and HHV-8 via IL-6, and that the blockade of IL-6 signal by anti-IL-6R antibody or anti-gp130 antibody can constitute a strategy to treat HIV/HHV-8 dually infected patients.