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The aim of this study was to determine if the distribution of Langerhans cells (LC) and interstitial dendritic cells (IDC) is altered in AIDS-associated oral Kaposi's sarcoma when compared to HIV-negative highly vascular oral lesions. Fifty-one cases of AIDS-associated oral Kaposi's sarcoma and 20 of highly vascular oral lesions were retrospectively retrieved. All cases of Kaposi's sarcoma were confirmed with immunoreactions against CD34 and HHV-8. Clinical data regarding sex, age and lesions location were obtained from pathology reports. Immunohistochemistry against CD207 (immature dendritic cells) and CD83 (mature dendritic cells) were done. LC were in the epithelium and IDC in the stroma. CD207+ cells predominated in the epithelium of the lesions, whereas CD83+ cells predominated in their stromal compartment. Kaposi's sarcoma had a lower CD207+ immature LC count (p=0.02) and an increased CD207+ IDC than highly vascular oral lesions (p<0.001). Moreover, Kaposi's sarcoma also showed an increased number of mature CD83+ IDC than highly vascular oral lesions (p<0.001). There were significant alterations in the distribution of LC and IDC in AIDS-associated Kaposi's sarcoma when compared to HIV-negative vascular oral lesions, suggesting that changes in their concentrations may play a role in the pathogenesis of Kaposi's sarcoma.
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http://dx.doi.org/10.1590/0103-6440201902599 | DOI Listing |
HIV-induced gut microbiota dysbiosis perpetuates mucosal barrier disruption and systemic inflammation despite antiretroviral therapy (ART), creating a tumor-permissive microenvironment. This review synthesizes evidence linking HIV-associated microbial alterations to oncogenesis through three convergent metabolic axes: (1) butyrate deficiency impairing epithelial energy metabolism and anti-tumor immunity; (2) tryptophan metabolism dysregulation compromising gut barrier integrity via depletion and -mediated phenylethylamine overproduction; and (3) vitamin B biosynthesis defects disrupting DNA repair and Th1/Th2 balance. Comparative profiling across HIV-associated malignancies-non-Hodgkin lymphoma, cervical cancer, hepatocellular carcinoma, and lung cancer-reveals conserved dysbiotic signatures: depletion of anti-inflammatory taxa (, ) and expansion of pro-inflammatory genera (, ).
View Article and Find Full Text PDFJ Med Virol
September 2025
Department of Interdisciplinary Oncology, School of Medicine, Stanley S. Scott Cancer Center of Excellence, Louisiana State University Health Sciences Center, New Orleans, Louisiana, USA.
Kaposi sarcoma (KS) remains a global health concern. In sub-Saharan Africa, where there is a high burden of HIV-1 infection, there is also a high prevalence of infection by the etiologic agent of KS, the KS-associated herpesvirus (KSHV). Despite the successes of antiretroviral treatment (ART), the burden of KS and other KSHV-associated malignancies among people living with HIV under ART remained high, stressing the need for a greater understanding of the immune response against KSHV infection.
View Article and Find Full Text PDFBiochem Biophys Res Commun
September 2025
Department of Clinical Laboratory Medicine, The First Affiliated Hospital of Shandong First Medical University & Shandong Provincial Qianfoshan Hospital, Jinan, Shandong, China; Department of Pathogen Biology, School of Clinical and Basic Medical Sciences, Shandong First Medical University & Shandon
Disulfiram (DSF), an FDA-approved therapeutic agent for alcohol dependence, has recently attracted considerable interest due to its broad-spectrum inhibitory effects against various viruses. Increasing evidence suggests that DSF can inhibit viral replication through two major mechanisms: the inhibition of viral protein catalytic activity and the ejection of Zn from viral proteins. This review comprehensively summarized the molecular mechanisms underlying DSF's antiviral activity against viruses such as severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), hepatitis C virus (HCV), influenza virus, human immunodeficiency virus (HIV), and Kaposi sarcoma-associated herpes virus (KSHV), with a particular focus on its dual targeting of Cys residues and Zn coordination sites.
View Article and Find Full Text PDFEur J Cancer
August 2025
Department of Dermatology, University Hospital Tübingen, Tübingen, Germany. Electronic address:
Introduction: For rare skin cancers, few data exist on the outcome of systemic therapies, particularly immune checkpoint inhibition (ICI). The present study analysed the real-world use of different systemic therapies including ICI, and its outcome in patients with advanced rare skin cancers.
Methods: This retrospective multicenter study included patients who received systemic therapy for advanced, non-resectable cutaneous angiosarcoma (AS), Kaposi sarcoma (KS), pleomorphic dermal sarcoma (PDS), or cutaneous adnexal carcinoma (CAC).
Unlabelled: Kaposi's sarcoma-associated herpesvirus (KSHV) orchestrates late gene transcription through viral transcriptional activators that hijack host RNA polymerase II machinery, maintaining selectivity for viral promoters. Among these, the KSHV protein ORF24 serves as a TATA-binding protein (TBP) mimic essential for recognizing viral late promoters, although the molecular mechanisms underlying its function remain poorly characterized. Here, we used AlphaFold3 to predict the structure of ORF24 in complex with DNA and validated key features in both transfected cells and during KSHV lytic replication.
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