The Malaysian giant freshwater prawn, Macrobrachium rosenbergii, is an economically important crustacean worldwide. However, production of this prawn is facing a serious threat from Vibriosis disease caused by Vibrio species such as Vibrio parahaemolyticus. Unfortunately, the mechanisms involved in the immune response of this species to bacterial infection are not fully understood. We therefore used a high-throughput deep sequencing technology to investigate the transcriptome and comparative expression profiles of the hepatopancreas from this freshwater prawn infected with V. parahaemolyticus to gain an increased understanding of the molecular mechanisms underlying the species’ immune response to this pathogenic bacteria. A total of 59,122,940 raw reads were obtained from the control group, and 58,385,094 reads from the Vibrio-infected group. Via de novo assembly by Trinity assembler, 59,050 control unigenes and 73,946 Vibrio-infected group unigenes were obtained. By clustering unigenes from both libraries, a total of 64,411 standard unigenes were produced. The standard unigenes were annotated against the NCBI non-redundant, Swiss-Prot, Kyoto Encyclopaedia of Genes and Genome pathway (KEGG) and Orthologous Groups of Proteins (COG) databases, with 19,799 (30.73%), 16,832 (26.13%), 14,706 (22.83%) and 7,856 (12.19%) hits respectively, giving a final total of 22,455 significant hits (34.86% of all unigenes). A Gene Ontology (GO) analysis search using the Blast2GO program resulted in 6,007 unigenes (9.32%) being categorized into 55 functional groups. A differential gene expression analysis produced a total of 14,569 unigenes aberrantly expressed, with 11,446 unigenes significantly up-regulated and 3,103 unigenes significantly down-regulated. The differentially expressed immune genes fall under various processes of the animal immune system. This study provided an insight into the antibacterial mechanism in M. rosenbergii and the role of differentially expressed immune genes in response to V. parahaemolyticus infection. Furthermore, this study has generated an abundant list of transcript from M.rosenbergii which will provide a fundamental basis for future genomics research in this field.

Fibroblast growth factors (FGFs) are crucial signaling proteins that govern numerous cellular activities, such as proliferation, differentiation, and tissue repair. Recent studies indicate that FGFs, particularly FGF-2, are pivotal in viral replication by altering the host cell environment to promote viral survival, replication, and immune evasion. Viruses rely on host cell components for their replication and often manipulate host signaling pathways, including FGF signaling, to optimize their environment for viral growth. Among the various FGFs, FGF-2 (basic FGF) stands out as particularly influential in viral replication due to its roles in angiogenesis, cell survival, and immune modulation. This chapter explores the molecular processes via which various FGFs affect viral life cycles, particularly highlighting FGF-2, which is notably important in promoting viral replication via its impact on cell survival, angiogenesis, and inflammation. Understanding FGF-mediated viral replication may offer new therapeutic targets for viral infections.

Over two years, the SARS-CoV-2 virus has evolved by producing several variants by RNA polymerase mutation. This mutation created many virus variants that five of them are designated by WHO. These are Alpha, Beta, Gamma, Delta, and Omicron, among them Alpha, Delta, and Omicron spread faster. Coronaviruses (CoVs) are enveloped in positive-sense RNA viruses and contain huge RNA virus genomes. RNA polymerase controls the replication in which the genomic material is copied, and it often makes errors that lead to create a new mutation. Most mutations create a virus that cannot replicate and spread among people. However, some mutations lead to a virus that can replicate and create a variant. This chapter will discuss the mechanism of the mutations during the last two years and the future of these mutations in SARS-CoV-2.

Lung cancer, particularly non-small cell lung cancer (NSCLC), remains a major clinical challenge because of its profound molecular heterogeneity, metabolic adaptability, and rapid development of therapeutic resistance. Although targeted therapies and immune checkpoint inhibitors have significantly improved patient outcomes, durable responses remain limited due to adaptive tumor evolution and metabolic rewiring. This chapter discusses disease-oriented drug repurposing as an emerging therapeutic framework that targets broader biological processes rather than isolated genetic alterations. By integrating findings from cancer metabolism, systems biology, network pharmacology, bioinformatics, and translational oncology, the chapter highlights how approved non-oncology drugs can be repurposed to modulate metabolic plasticity, tumor microenvironment dynamics, oxidative stress adaptation, autophagy, and resistance-associated signaling pathways. Particular emphasis is placed on combination therapeutic strategies, computational drug discovery, biomarker-guided approaches, and precision repurposing models. Collectively, disease-oriented repurposing represents a biologically rational and cost-effective strategy with substantial potential to improve therapeutic durability and overcome resistance in lung cancer, particularly when integrated with biomarker-guided patient selection, clinical validation, and careful consideration of translational barriers.