Huibo Yan

Background: HIV/AIDS remains a leading infectious disease burden globally. While highly active antiretroviral therapy has transformed HIV into a manageable chronic condition, contemporary trends and attributable risk factors among reproductive-age adults in China—a critical demographic for epidemic control—remain poorly characterized. This study provides an updated comprehensive assessment of HIV/AIDS burden in this population using Global Burden of Disease Study 2023 data, which incorporates methodological refinements and post-pandemic data not available in earlier versions. Methods: We extracted age-standardised incidence, prevalence, mortality and disability-adjusted life-years (DALYs) for Chinese adults aged 15–49 years from GBD 2023. Joinpoint regression estimated annual percent change and identified significant trend inflection points. Population attributable fractions were analysed for unsafe sex, drug use, and intimate-partner violence. ARIMA models forecasted burden trends to 2035 with 95% uncertainty intervals. Results: Between 1990 and 2023, age-standardised rates increased substantially: incidence +301% (from 0.82 to 3.29 per 100,000), prevalence +774% (4.84 to 42.29), mortality +1,623% (0.13 to 2.24), and DALYs + 1,439% (7.96 to 122.48). Males showed consistently steeper increases than females across all metrics (all p < 0.05). Unsafe sex accounted for 70% of HIV/AIDS mortality in 2023. ARIMA projections indicate that while male incidence will plateau at ~5.0 per 100,000 by 2035, female metrics will continue rising (incidence +21%, prevalence +30%), widening the sex disparity. Conclusion: China’s HIV epidemic has transitioned to a chronic disease burden. Notably, this burden shows pronounced sex differences. Mortality is rising among people living with HIV, particularly among women. These trends highlight urgent needs for gender-differentiated prevention strategies. Our findings provide measurable targets for China’s National HIV/AIDS Action Plan (2024–2030) and SDG 3.3 monitoring. They further demonstrate how standardized burden estimation supports precision public health.

Excessive host immune responses contribute to severe malaria with high mortality. Here, we show that PRL2 in innate immune cells is highly related to experimental malaria disease progression, especially the development of murine severe malaria. In the absence of PRL2 in myeloid cells, Plasmodium berghei infection results in augmented lung injury, leading to significantly increased mortality. Intravital imaging revealed greater neutrophilic inflammation and NET formation in the lungs of PRL2 myeloid conditional knockout mice. Depletion of neutrophils prior to the onset of severe disease protected mice from NETs associated lung injury, and eliminated the difference between WT and PRL2 CKO mice. PRL2 regulates neutrophil activation and NET accumulation via the Rac-ROS pathway, thus contributing to NETs associated ALI. Hydroxychloroquine, an inhibitor of PRL2 degradation alleviates NETs associated tissue damage in vivo. Our findings suggest that PRL2 serves as an indicator of progression to severe malaria and ALI. In addition, our study indicated the importance of PRL2 in NET formation and tissue injury. It might open a promising path for adjunctive treatment of NET-associated disease.