White Spot Syndrome Virus (WSSV) is one of the most devastating viral pathogens affecting shrimp, causing severe economic losses to the global farmed shrimp trade. The globalization of live shrimp trade and waterborne transmission have facilitated the rapid spread of WSSV across major shrimp-producing countries since its initial emergence. The present review gives an updated account of WSSV biology, pathology, transmission dynamics, and recent developments in control measures. The virus, a double-stranded DNA virus of the Nimaviridae family, utilizes advanced immune evasion strategies, resulting in severe mortality. Shrimp lack adaptive immunity and hence rely predominantly on innate immunity, which is insufficient to mount an effective response against severe infections. Traditional disease control measures such as augmented biosecurity, selective breeding, and immunostimulants have, despite extensive research, achieved only limited success. New biotechnological tools such as RNA interference, CRISPR-Cas gene editing, and nanotechnology offer tremendous potential for disease mitigation. In parallel, the development of DNA and RNA vaccines targeting WSSV structural proteins, such as VP28, holds significant promise for stimulating the shrimp immune system. This review highlights the urgent need for a convergent approach to sustainable disease management in global shrimp aquaculture, with interdisciplinarity playing a pivotal role in shaping the future of WSSV control.

Background: The triple-negative breast cancer (TNBC) microenvironment undergoes progressive reprogramming, transitioning from an early immune-active state to a late immune-suppressed state. While tumor cell plasticity has been extensively studied, the temporal molecular remodeling of T cells in vivo remains poorly defined. Results: Transcriptional analysis of T cells within 4T1 TNBC tumors, harvested at one-, three-, and six-weeks post-tumor implantation in the mammary fat pads of BALB/c mice, revealed a decline in transcriptomic signatures associated with T cells from 194 at one week to 156 at six weeks, with a significant late-stage loss or reduction of transcripts related to T cell receptors (TCR), natural killer T, and gamma delta T cells. Furthermore, changes in various temporal signature genes specific to T cell cytokines and transcription factors reflected temporal T cell polarization to CD4 ⁺ type 1 T helper and type 1 CD8 ⁺ cytotoxic T cell responses at one week, CD8 ⁺ cytotoxic follicular T cell skewing at three weeks, and interleukin 17/22 producing CD8 ⁺ T cell transition at six weeks. The antigen-presenting cell (APC) transcripts deteriorated at six weeks, characterized by reduced expression of co-stimulatory and APC genes. Despite an early dominance of M1-like macrophage genes (e.g., IL-12α/β ), persistent expression of arginase 1 ( ARG1 ) and other M2-associated genes indicated a stable tolerogenic niche. Conclusions: The temporally coordinated immune shifts, such as progressive decline in transcripts associated with T cell functions, TCRs, APCs, and sustained macrophage-driven immunosuppression, suggest tumor-driven adaptation toward immune evasion and identify potential windows for stage-specific immunotherapeutic intervention.

Background and Objectives: Cancer evolves via interconnected mechanisms, including changes in extrachromosomal DNA (ecDNA), genetic instability, and interactions with the tumor microenvironment (TME). These mechanisms allow for some clones to evolve metastatic traits, evade the immune system, and resist chemotherapy. However, how cancer cells evolve in vivo remains poorly understood. This study investigates the in vivo changes in gene expression of triple-negative breast cancer (TNBC) cells implanted in BALB/c mice. Methodology: We analyzed RNA-seq data from 4T1 TNBC cells and tumors at different growth stages (1-, 3-, and 6-week) to identify differentially expressed genes, protein-protein interactions, and ecDNA alterations. We also assessed how ecDNA and genomic instability proteins interact with anti-TNBC drugs Results: Our results reveal early transcriptional shifts within one week of tumor implantation, showing rapid acclimation. Changes in gene expression continued over time, with significant molecular reprogramming observed at six weeks under in vivo environmental pressures, including ecDNA alterations and immune evasion. The shift from the earlier generation (1 week) to the later generation (6 weeks) suggests cumulative alterations in key oncogenic pathways related to tumor progression. Additionally, we found that mutations in ecDNA and genomic instability proteins influence drug binding affinity, suggesting that adaptive changes may impact chemotherapy response. Conclusions and Implications: This study provides new insights into how TNBC tumors may evolve over time and novel ecDNA-related mechanisms of possible tumor adaptation, highlighting potential biomarkers for tumor aggression and immune evasion, which could help develop more effective therapeutic strategies against TNBC.