Objective: To evaluate the clinical application of a novel HIV-1 DNA reagent. Methods: HIV-1-infected and non-infected human blood samples were selected, as well as weakly positive samples, indeterminate samples, specific samples. Compared the result of HIV-1 DNA reagent with HIV-1 infection status (refer to the National Guideline for Detection of HIV/AIDS (2015)), the accuracy of the HIV-1 DNA reagent was evaluated in clinical application; Meanwhile, the commercially available RNA quantification kit was selected as reference reagent for parallel detection, and then the consistency and differences were evaluated between HIV-1 DNA reagent and RNA quantification reagent. Results: A total of 95 whole blood samples were tested by the HIV-1 DNA reagent. Taking the HIV-1 infection status as the reference standard, the result showed that the positive agreement rate was 100% (95%CI: 93.94%-100%), the negative agreement rate was 100% (95%CI: 90.26%-100%), and the overall agreement rate was 100% (95%CI: 96.19%-100%). The Kappa value was 1 (95%CI: 1.00-1.00). The HIV-1 DNA reagent could detect weakly positive samples and indeterminate samples of early infection, and could effectively distinguish false-positive samples tested by the Ag-Ab reagent. The specific samples had no false-positive result . Conclusions The result of HIV-1 DNA reagent were consistent with the HIV-1 infection status. It can be considered as equivalent to the HIV-1 detection reagent commercially available in our country. It can effectively identify the indeterminate samples in the early infection. Compared with the RNA quantification reagent, it can effectively detect HIV-1 DNA of virus reservoirs.

Postnatal heart maturation is the basis of normal cardiac function and provides critical insights into heart repair and regenerative medicine. While static snapshots of the maturing heart have provided much insight into its molecular signatures, few key events during postnatal cardiomyocyte maturation have been uncovered. Here, we report that cardiomyocytes (CMs) experience epigenetic and transcriptional decline of cardiac gene expression immediately after birth, leading to a transition state of CMs at postnatal day 7 (P7) that was essential for CM subtype specification during heart maturation. Large-scale single-cell analysis and genetic lineage tracing confirm the presence of transition state CMs at P7 bridging immature state and mature states. Silencing of key transcription factor JUN in P1-hearts significantly repressed CM transition, resulting in perturbed CM subtype proportions and reduced cardiac function in mature hearts. In addition, transplantation of P7-CMs into infarcted hearts exhibited cardiac repair potential superior to P1-CMs. Collectively, our data uncover CM state transition as a key event in postnatal heart maturation, which not only provides insights into molecular foundations of heart maturation, but also opens an avenue for manipulation of cardiomyocyte fate in disease and regenerative medicine.
Gene Expression Regulation ; Heart ; Myocytes, Cardiac/metabolism* ; Single-Cell Analysis ; Transcription Factors/metabolism*