Diagnosis of neurosyphilis is currently based on the cerebrospinal fluid (CSF) assessments and CSF-Venereal Disease Research Laboratory (CSF-VDRL) is the traditional “gold standard.” In the real world, CSF assessments and CSF-VDRL are not always available. This study aimed to identify noninvasive predictors of neurosyphilis based on real-world clinical parameters and diagnostic criteria in populations with different HIV status. In this retrospective cohort study, syphilis patients with different HIV statuses hospitalized for neurosyphilis screening were retrospectively recruited at an infectious disease hospital. Neurosyphilis was defined by real-world diagnostic criteria. Logistic regression and receiver operating characteristic curve analysis were used to investigate and evaluate predictors of neurosyphilis. In total, 528 patients were enrolled, including 143 syphilis patients without HIV infection and 385 HIV/syphilis-co-infected patients. One hundred twelve and 304 neurosyphilis patients were identified in the HIV-negative and HIV-positive groups, respectively. A high serum toluidine red unheated serum test (TRUST) titer was a robust predictor of neurosyphilis in all participants. An age ≥50 years old [adjusted odds ratio (aOR) = 5.062, 95% confidence interval (CI), 1.449–17.680] in the HIV-negative group and CD4 ⁺ T cell count <330/μL (<300 as reference, aOR = 0.552, 95% CI, 0.315–0.966) in the HIV-positive group were predictors of asymptomatic neurosyphilis. In real-world situations, for asymptomatic syphilis patients, relatively old age and a high serum TRUST titer in HIV-negative populations, and CD4 ⁺ T cells 1:64 in HIV-positive populations might predict neurosyphilis.

Backgroud The role of HIV infection in precipitating different clinical features in Cryptococcal meningitis (CM) patients remains controversial. Methods One hundred and twelve CM patients living with HIV/AIDS (CM+HIV+ patients) and 112 CM patients living without HIV/AIDS (CM+HIV- patients) were enrolled after propensity score matching. Demographic characteristics, symptoms, routine blood tests, biochemical and cerebrospinal fluid (CSF) profiles were compared between the two groups. Kaplan–Meier analysis and Cox proportional hazards model was used to assess 10-week mortality. Results CM+HIV+ patients frequently occurred in young (mean age 40.3±10.5) and male (89.3%) populations who also experienced leukopenia, neutropenia, lymphocytopenia, thrombocytopenia, and hypoalbuminemia, less headaches (66.9%) and higher cryptococcemia (23.2%) (all P < 0.050); they also had higher glucose (2.6±1.1 mmol/L), increased smear positivity (78.8%) and decreased white blood cells [8.0 (2.0-28.0)×106/L] in initial CSF assay (all P< 0.050). The 10-week cumulative survival rate was 84.6% for CM+HIV+ patients and 88.5% for CM+HIV- patients (P = 0.345). Age < 35.0 years old (Hazard ratio (HR) 3.0 (1.0-8.9), P=0.046), intracranial pressure (ICP) > 250.0 mmH2O (HR: 4.8(1.1-21.6), P=0.041) and treatment lacking amphotericin B [HR: 6.5(1.9-21.4), P=0.003] were independent risk factors for 10-week mortality in CM+HIV+ patients. Conclusions There are significant clinical differences in cryptococcal meningitis patients living with or without HIV/AIDS. However, the 10-week survival rate was similar between the two groups. Younger population, high ICP and treatment lacking amphotericin B were independent risk factors for 10-week mortality of Chinese CM+HIV+ patients.

Progressive multifocal leukoencephalopathy (PML) is a rare demyelinating disease of the central nervous system caused by JC virus (JCV) and is difficult to diagnose. We report on a male HIV-positive patient with PML finally diagnosed by 3 times lumbar punctures and 2 times brain biopsies. Negative results of JCV-PCR in cerebrospinal fluid (CSF) do not rule out the diagnosis of PML when clinical manifestations and neuroimaging features suspected PML. It is necessary to obtain new CSF and make repeat tests and even perform brain biopsy.

Background: As a malignant tumor derived from vascular endothelial cells, Kaposi’s sarcoma (KS) is quite common in AIDS patients. Nonspecific clinical symptoms often lead to timely diagnosis or wrong treatment, leading to recurrent disease and poor prognosis. Anti-retroviral therapy (ART) could significantly reduce its morbidity and aggressiveness. As one of the ARTs, liposome anthracyclines are the preferred chemotherapy regimen for disseminated KS with multiple organs or tissue invasion. The curative effect is highly related to the degree of immunosuppression. This is the first case of AIDS with Kaposi’s sarcoma, who was cured after ART and two consecutive chemotherapy with doxorubicin liposome without recurrence. This case may provide new ideas and methods for the clinical management of AIDS with Kaposi’s sarcoma. Case Description: The patient, a male aged 60 years, was hospitalized on 21/11/2018 following having a cough, expectoration, and difficulty breathing. He was infected with HIV eight years ago and presented symptoms of blood-stained sputum. The patient complained that he had not received ART before. After admission, he was diagnosed as KS with disseminated AIDS after multiple biopsies and histopathological examinations. The patient was treated with ten months of ART (lamivudine+tenofovir+dolutegravir) and 14 times of chemotherapy with doxorubicin liposome (20 mg/m², three times per week, seven times per course of treatment). The patient’s disease was finally alleviated, and there was no recurrence during the follow-up. Conclusion: The reconstitution of immune function and consecutive chemotherapy with doxorubicin liposome play a vital role in treating KS. In addition, for the early general symptoms of AIDS patients, such as thrombocytopenia and hemorrhagic purple papules, it is necessary to increase vigilance and obtain the results of histopathological verification as soon as possible to diagnose KS patients at an earlier stage and realize clinical intervention in time.

Background: People living with HIV (PLWH) exhibit a markedly elevated risk of developing atherosclerotic cardiovascular disease (ASCVD), a phenomenon not entirely attributable to conventional risk factors, thereby indicating the existence of an immune-mediated residual risk. Trained immunity may represent a critical underlying mechanism. Objective: This review explores the potential of HIV infection-induced trained immunity, examining its underlying mechanisms and its role in the pathophysiology of ASCVD. Methods: PubMed databases were searched for articles on the association between trained immunity and HIV infection and ASCVD. Results: HIV triggers trained immunity through various mechanisms: viral proteins like Nef reprogram monocytes, microbial translocation via LPS activates the TLR4-NF-κB pathway, CMV co-infection boosts T-cell activity, and IgA-ADCP causes cross-activation. Some ART regimens (PI/INSTI) promote metabolic training, while CCR5 antagonists may counteract it. Clinical studies and the REPRIEVE trial show immune training markers (sCD14, sCD163) are linked to coronary issues and cardiovascular events, with statins unable to fully reduce monocyte/macrophage inflammation. Strategies include metabolic interventions, anti-IL-1β therapy, epigenetic drugs, optimizing ART, and nanobiological. Importantly, this review distinguishes between canonical innate trained immunity—driven by monocytes, macrophages, and vascular cells—and T-cell immunometabolic dysfunction, which, while coexisting in HIV infection, represents a distinct adaptive immune process. The former is our primary mechanistic focus for ASCVD. Conclusion: Trained immunity plays a pivotal role in the residual risk associated with HIV-associated ASCVD. From a mechanistic perspective, trained monocytes and macrophages contribute to foam cell formation by hindering cholesterol efflux. Concurrently, trained endothelial cells maintain vascular inflammation and enhance monocyte adhesion, collectively expediting the progression of plaque development. Elucidating the underlying regulatory mechanisms and undertaking intervention trials constitute prospective avenues for translational research.