BackgroundThe prevalence of anemia among antiretroviral-naïve HIV-infected patients in China has not been well characterized. We conducted a cross-sectional study to estimate the prevalence of anemia among Chinese adults with newly diagnosed HIV/AIDS.MethodsOne thousand nine hundred and forty-eight newly diagnosed HIV-infected patients in China were selected during 2009 and 2010. Serum samples obtained from each individual were collected to measure hemoglobin levels. Demographics and medical histories were recorded. Factors associated with the presence of anemia were analysed by logistic regression.ResultsAmong the 1948 patients, 75.8% were male. Median age was 40 years (range: 18–80 years). The overall prevalence of anemia among HIV-infected patients was 51.9% (51.5% among men, 53.2% among women). The prevalences of mild anemia, of moderate anemia, of severe anemia were 32.4%, 17.0%, and 2.5%, respectively. The prevalence of anemia was higher among ethnic minority patients than among the Han patients (70.9% versus 45.9%). The prevalence of anemia increased with increasing age (49.6%, 53.5% and 60.1% among patients who were 18–39, 40–59, and ≥60 years of age respectively) and with decreasing CD4 count (14.0%, 22.4%, 50.7%, and 74.6% among patients with CD4 count of ≥350, 200–349, 50–199, and <50 cells/mm3 respectively). The logistic regression analysis showed that older age, lower CD4 count and minority ethnicity were significantly associated with an increased risk of anemia.ConclusionsAnemia is highly prevalent among Chinese adults with newly diagnosed HIV/AIDS, but severe anemia is less prevalent in this population. Older age, lower CD4 count and minority ethnicity are associated with an increased risk of anemia.

The roles of immunodeficiency and combined antiretroviral therapy (cART) in shaping the gut microbiota in HIV-1-infected subjects (HISs) have not been described thoroughly by time-series investigations. In this study, 36 antiretroviral-naïve HISs were enrolled to prospectively assess alterations in the fecal microbiota and plasma markers of microbial translocation and inflammation with cART. At baseline, the species α-diversity of the fecal microbiota was significantly lower in HISs with a CD4+ T cell count <300/mm3 than in HISs with a CD4+ T cell count >300/mm3 (Shannon index: Median 2.557 vs. 2.981, P = 0.006; Simpson index: Median 0.168 vs. 0.096, P = 0.004). Additionally, the baseline α-diversity indices correlated with CD4+ T cell counts (Shannon index: r = 0.474, P = 0.004; Simpson index: r = −0.467, P = 0.004) and the specific plasma biomarkers for microbial translocation and inflammation. After cART introduction, the species α-diversity of fecal microbiota in HISs with CD4+ T cell counts <300/mm3 was significantly restored (Shannon index: Median 2.557 vs. 2.791, P = 0.007; Simpson index: Median 0.168 vs. 0.112, P = 0.004), while the variances were insignificant among HISs with CD4+ T cell counts >300/mm3 (Shannon index: Median 2.981 vs. 2.934, P = 0.179; Simpson index: Median 0.096 vs. 0.119, P = 0.082). Meanwhile, with cART introduction, alterations in the gut microbial composition were more significant in the subgroup with CD4+ T cell counts >300/mm3, corresponding to increases in the specific plasma inflammatory markers. These findings implicated the interactive roles of immunodeficiency and cART for affecting gut microbiota in HIV-1-infected individuals, providing new insights into intestinal microbiome dysbiosis related to HIV-1 infection.

Neonatal herpes simplex virus type 1 (HSV-1) infections contribute to various neurodevelopmental disabilities and the subsequent long-term neurological sequelae into the adulthood. However, further understanding of fetal brain development and the potential neuropathological effects of the HSV-1 infection are hampered by the limitations of existing neurodevelopmental models due to the dramatic differences between humans and other mammalians. Here we generated in vitro neurodevelopmental disorder models including human induced pluripotent stem cell (hiPSC)-based monolayer neuronal differentiation, three-dimensional (3D) neuroepithelial bud, and 3D cerebral organoid to study fetal brain development and the potential neuropathological effects induced by the HSV-1 infections. Our results revealed that the HSV-1-infected neural stem cells (NSCs) exhibited impaired neural differentiation. HSV-1 infection led to dysregulated neurogenesis in the fetal neurodevelopment. The HSV-1-infected brain organoids modelled the pathological features of the neurodevelopmental disorders in the human fetal brain, including the impaired neuronal differentiation, and the dysregulated cortical layer and brain regionalization. Furthermore, the 3D cerebral organoid model showed that HSV-1 infection promoted the abnormal microglial activation, accompanied by the induction of inflammatory factors, such as TNF-α, IL-6, IL-10, and IL-4. Overall, our in vitro neurodevelopmental disorder models reconstituted the neuropathological features associated with HSV-1 infection in human fetal brain development, providing the causal relationships that link HSV biology with the neurodevelopmental disorder pathogen hypothesis.

Background Genetic variability and liability to develop drug-resistant mutations are the main characteristics of HIV-1, which can not only increase the risk of antiretroviral treatment (ART) failure, but also can lead to the spread of resistant strains. We aim to investigate the distribution of HIV-1 genotypes and prevalence of pretreatment drug resistance (PDR) in ART-naïve HIV-1 infected patients in Shanghai China. Methods A cross-sectional study was performed among the newly diagnosed ART-naive HIV-1 infected patients during the period from January 2017 to November 2017 in Shanghai Public Health Clinical Center. The target fragment of 1316 bp in the pol gene spanning the reverse transcriptase and protease regions was amplified using a nested polymerase chain reaction. HIV-1 genotypes were determined by phylogenetic analysis, and PDR associated mutations were determined according to Stanford University HIV Drug Resistance Database ( http://hivdb.stanford.edu/ ). Results We successfully amplified pol gene sequences from blood samples of 317 patients, of whom 95.3% were male, and 68.8% were men who have sex with men. The median age was 33 years; and the median CD4 count was 275 cells/μL. The predominant HIV-1 genotype was circulating recombinant form (CRF) 01_AE (53.0%, 168/317), followed by CRF07_BC (29.7%, 94/317), B (7.6%, 24/317), CRF08_BC (1.9%, 6/317), CRF55_01B (1.9%, 6/317), CRF 59_01B (0.9%, 3/317). In addition, 5% (16/317) HIV-1 strains were identified as other subtypes or CRFs/URFs (unique recombinant forms). The overall prevalence of PDR was 17.4% (55/317). PDR frequency to non-nucleoside reverse transcriptase inhibitor (NNRTI, 16.4%) was much higher than that to nucleoside reverse transcriptase inhibitor (NRTI, 4.7%) and protease inhibitor (PI, 0.6%). The most common HIV-1 mutation pattern for NNRTI and NRTI were V179D/E (10.1%, 32/317) and M184 V (2.8%, 9/317), respectively. About half (49.1%, 27/55) of the HIV-1 strains with mutation presented as potential low-level resistant to NNRTI attributed to V179D/E. Conclusion The distribution of HIV-1 genotypes in Shanghai China is diverse and complex. The high prevalence of PDR highlights the significance of baseline HIV-1 drug resistance testing. Non-NNRTI-containing regimen may be the preferred initial therapy for newly diagnosed HIV-1 patients in Shanghai in the absence of PDR test results.

infection is increasingly observed in people living with human immunodeficiency virus (HIV) in eastern China, a nonendemic area. This study aimed to draw the clinician's attention to this disease by presenting the clinical characteristics and prognosis of penicilliosis among HIV-infected patients from this region. We retrospectively analyzed HIV-infected patients with culture-proven infection admitted during January 1, 2014-December 31, 2015, at the Shanghai Public Health Clinical Center. A total of 48 patients with confirmed HIV infection and penicilliosis were enrolled, which accounted for a mean of 3.2% (95% confidence interval: 2.4-4.2%) of yearly HIV infection admissions among patients from eastern China. Symptoms included fever, cough, and gastrointestinal complaints, whereas the most common sign was skin lesions. Anemia occurred in 87.5% (42/48) of the patients. The overall mortality rate was 16.7%. Low CD4 T-cell count and hemoglobin level were correlated with mortality. Based on these results, we concluded that penicilliosis should be considered in HIV-infected patients from eastern China who present with fever, cutaneous lesions, and anemia. The clinical characters and the prognosis of patients with penicilliosis are similar to those in endemic areas. More attention should be paid to penicilliosis patients with low CD4 T-cell count and/or low hemoglobin level.