AIDS reviews最新文献

Almost 40 years have passed since the first case of what is known as AIDS was documented. In these 40 years, AIDS has always been a research challenge and hot spot. Researchers and scientists have made tremendous progress in basic and clinical research on HIV. In particular, the widespread use of antiretroviral therapy (ART) has made it less of a deadly disease today and more of a manageable one. In the post- ART era when ART can significantly improve the immunity of people living with HIV (PLWH) and extend their life, the incidence of non-AIDS-defined cancers is greatly increased. Factors related to immunosuppression do not seem to explain this problem sufficiently. This suggests that besides immunosuppression, there are other mechanisms that may also contribute to the increased incidence of cancer in PLWH. Here, we summarized and discussed four possible mechanisms for the increased incidence of cancers in PLWH: immunosuppression, oncogenic viral infection, chronic infection, inflammatory damage, and the direct impact of HIV.

HIV-1 infection usually progresses to AIDS within 10 years in antiretroviral therapy untreated individuals, but there is a group of infected individuals, known as controllers, who maintain low plasma HIV-1 RNA levels and normal CD4+ T-cell counts for many years. Evidence suggests that the mechanisms of viral control in these individuals are heterogeneous. In this review, we highlight the viral and host factors, particularly host immunological and immunogenetic factors that are associated with controller status. Despite the broad heterogeneity within controllers, there is compelling evidence that cytotoxic CD8+ T lymphocyte responses act as the main driver of control in the majority of these individuals, especially in those with protective HLA-I alleles. Further investigation of controllers without protective HLA-I alleles is required as it seems that this subset exhibits more durable control of HIV-1 disease progression. Understanding the immune defense mechanisms in controllers provides hope for harnessing these responses in the general population, either for protective or therapeutic vaccines or to achieve a functional cure in infected individuals.

Pulmonary arterial hypertension (PAH) occurs more frequently in patients with HIV infection than in general population. The predictive value of HIV-related factors and traditional cardiovascular factors with PAH is inconsistent across studies. The objective is to determine the roles of HIV-related risk factors and traditional cardiovascular risk factors in the development of PAH in adults with HIV. We searched Pubmed/Medline, Embase, Web of Science, and Google Scholar to identify studies published between January 1, 2000 and February 23, 2021 on risk factors associated with PAH among people living with HIV (PLWH). Ten studies were included for final analysis. PLWH with PAH had higher mean age (weighted mean difference [WMD] = 2.27, 95% confidence interval [CI] 0.31 ~ 4.24), and lower mean CD4 cell count (WMD = -95.8, 95% CI -153.41 ~ -38.2). Meanwhile, they were more likely to have detectable viral load (odds ratio [OR] = 1.36, 95% CI 1.16 ~ 1.60), to accompany arterial hypertension (OR = 2.02, 95% CI 1.51 ~ 2.71) and less likely to receive antiretroviral therapy (ART) (OR = 0.84, 95% CI 0.72 ~ 0.99). Besides, more intravenous drug users were observed in HIV-infected adults with PAH (OR = 2.25, 95% CI 1.51 ~ 3.33). HIV infection itself and ART impact PAH in two opposite ways. Traditional cardiovascular factors such as arterial hypertension, and older age are also important to the development of PAH. Screening HIV-related factors and traditional cardiovascular factors may help to target and manage patients at risk.

Highly active antiretroviral therapy (HAART) strongly inhibits HIV replication. However, many patients show suboptimal immune recovery (SIR), as defined by virological suppression (i.e. low viral load) with a CD4⁺ T-cell count of ≤ 200 cells/mm³, after HAART initiation. Here, we performed a systematic evaluation of the SIR prevalence among HIV-infected patients in cohort studies. We searched PubMed, Cochrane Library, Embase, CNKI, Wanfang database, and Chinese Biomedicine Database for cohort studies about HIV-infected participants whose CD4⁺ T-cell count was ≤ 200 cells/mm³ but still had virological suppression after HAART initiation. The SIR prevalence from each of those cohort studies was pooled into a random-effect meta-analysis. We obtained two kinds of pooled post-HARRT initiation SIR prevalence: one among participants with virological suppression (11 cohort studies involving 18,672 participants), and the other among all HIV-infected participants (seven cohort studies involving 12,063 participants). The pooled SIR prevalence among HIV-infected patients with virological suppression after HAART initiation was 43% (95% confidence interval [CI], 34-51%) at 6 months post-HAART initiation and 10% (95% CI, 5-18%) at 36 months post-HAART initiation; among all HIV-infected patients after HAART initiation, it was 17% (95% CI, 0-55%) and 5% (95% CI, 2-10%) at 6 and 36 months post-HAART initiation, respectively. The SIR prevalence among HIV-infected patients is high at 6 months post-HAART initiation, but its prevalence gradually reduces over time under continuous HAART. Thus, it is important to follow-up on variations in the CD4⁺ T-cell count and viral load.