Official websites use. Share sensitive information only on official, secure websites. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Sensitive assays are needed for detection of residual HIV in patients with undetectable plasma viral loads to determine if eradication strategies are effective. The gold standard quantitative viral outgrowth assay QVOA underestimates the magnitude of the viral reservoir, while sensitive PCR-based assays lack the ability to distinguish replication competent from defective virus.
We sought to determine whether xenograft of leukocytes from HIV-1 infected patients with undetectable plasma viral loads into severely immunocompromised mice would result in viral amplification and measurable viral loads within the aberrant murine host.
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Successful xenograft of mice was confirmed by flow cytometry. We similarly detected SIV in macaquized mice by seven days post-xenograft. The MVOA has the potential to serve as a powerful tool to identify residual HIV-1 in patients with undetectable viral loads, such as those who have undergone promising cure therapies.
Unfortunately, the virologic and immunologic determinants of post-ART control of HIV replication are still unclear, particularly in tissues. All 15 animals initiated a five-drug ART regimen 60 days after infection, which was maintained for seven months. ART was then interrupted and RMs monitored for eight additional months. We assessed whether the host response to residual virus may be a sensitive measure of reservoir size by comparing anti-HIV antibody profiles in relation to several HIV reservoir assays.
Summary estimates of the overall association between HIV reservoir measures and HIV antibody levels adjusted for multiple comparisons were obtained using permutation testing. Epitope location envelope proteins and reverse transcriptase, an enzyme involved in the early steps of viral replication may determine the strength of this association. Future studies are needed to evaluate whether viral RNA or proteins are produced in cells with defective proviruses.
