Kaposi Sarcoma

He was treated with bictegravir/emtricitabine/tenofovir alafenamide, trimethoprim-sulfamethoxazole prophylaxis, fluconazole, and intravenous penicillin G. The patient showed early clinical improvement with resolution of ocular symptoms and a declining HIV viral load following initiation of therapy and before discharge. This case highlights biopsy-proven KS as the presenting manifestation of previously undiagnosed advanced HIV, with unilateral limb lymphedema and pulmonary nodules suggesting disseminated disease. Additionally, our case underscores the need for early HIV testing in patients with recurrent mucocutaneous candidiasis and unexplained lymphedema, and for prompt evaluation of concomitant opportunistic and sexually transmitted infections.

The discontinuation of rocatinlimab after confirmed and suspected cutaneous Kaposi's sarcoma cases, together with two cumulative cases reported in the amlitelimab program in patients with known risk factors, has changed the discussion from early promise to mechanism, risk, and therapeutic strategy. The central challenge is now to determine how the axis can be targeted, in which patients, and in what therapeutic context, to maximize clinical benefit while managing risk. Rather than signaling the end of the axis in atopic dermatitis, Kaposi's sarcoma may instead mark the limits of a first-generation development strategy and the beginning of a more selective approach built around molecule design, therapeutic context, and prospective risk mitigation.

Human Herpesvirus 8-associated multicentric Castleman disease is predominantly observed in HIV-positive patients, but there is evidence of its occurrence in human immunodeficiency virus-negative individuals, presenting distinct epidemiological and pathological characteristics. Early and precise diagnosis is essential, as the disease can progress rapidly and may lead to severe or fatal outcomes.

By integrating locus-specific chromatin proteomics with functional and mechanistic analyses, our work reveals how an RNA-binding protein HNRNPA2B1 recruits a histone-modifying enzyme to control EBV reactivation. These findings provide new insights into host-virus interactions that control EBV latency and reactivation and highlight the role of RNA-binding proteins in chromatin regulation that may be broadly relevant to other latent DNA viruses.

Notably, the E3 ubiquitin ligase TRIM37 (tripartite motif containing 37) facilitates the polyubiquitination of lysine residues at position 116 of PFN1, which serves as a critical recognition motif for the cargo receptor SQSTM1/p62 (sequestosome 1), which is pivotal for the subsequent autophagic degradation of ORF44. Overall, our findings revealed a previously uncharacterized antiviral function of PFN1, highlighting its potential as a novel therapeutic avenue for the treatment of KSHV-associated malignancies.

Immediate ART initiation significantly reduces infection-related cancer risk in PWH that persists long-term.

The phenotype arises independently of viral DNA replication, indicating early host remodeling. A screen of EBV early genes identifies BRRF1 as a key driver: through a CIY(Y/E) motif conserved in KSHV ORF49, BRRF1 engages the nuclear CCR4-NOT complex through its CNOT9 and CNOT1 subunits, hijacking this canonically cytoplasmic deadenylation hub for nuclear disruption of host splicing.

KDR was found to promote lytic replication, stimulate the release of pro-inflammatory cytokines, and upregulate cancer signaling pathways. As such, we propose a model in which elevated KDR in KS lesions supports a lytic program to ensure maintenance and spread of infected cells while also promoting the tumor microenvironment.

Proteomic analysis identified unique protein candidates altered in MZ-1- and SIM-1-treated KSHV-infected immortalized endothelial cells compared with (+)-JQ1-treated cells. In summary, our study develops an effective strategy against KSHV-infected immortalized endothelial cells using selective BRD PROTACs, which may help improve therapeutic outcomes for KSHV-related malignancies in the future.

Among PWH with cancer, cancer-specific mortality increased with lower CD4 counts, including for solid tumors not associated with HIV, e.g., prostate and lung cancer. These results highlight the role of immunity in control of cancer.

Consistently, the responsiveness of LCLs to diABZI aligned with STING pathway competence, with minimal effects on growth and viability when STING expression was low or deficient. Overall, this work links STING pathway competence to both antiviral control of KSHV reactivation and reduced lymphoma growth, suggesting a potential new approach to limit KSHV pathogenesis.

spatiAlytica outperformed strong agentic baselines, while using less time and tokens. Case studies across Kaposi's sarcoma, colorectal cancer, and ovarian cancer recapitulated known spatial patterns and uncovered progressive CD8 T-cell dysfunction during KS progression.