Crustacean aquaculture, dominated by shrimp, is a highly profitable food-producing sector in the world. However, a variety of biotic and abiotic stressors can have adverse effect on the immune system of shrimp making them susceptible to diseases. Although a vertebrate-like adaptive immune system is lacking in shrimp, an efficient innate immune system renders protection against invading pathogens. The innate immune system comprises two distinct but overlapping components, the cellular and humoral, and these are regulated through several signal transduction pathways. The signal pathways are initiated by the recognition of pathogen-associated molecular patterns by germline-encoded pattern recognition receptors leading to the production of different effector molecules that act against the pathogens. RNAi-mediated post-transcriptional gene silencing and microRNA regulation of immune response have also been found to be functional in shrimp. Similarly, apoptosis and apoptosis-related genes are also reported, besides interferon (IFN) system-like antiviral regulatory mechanism. Further, some form of immune memory, termed 'immune priming' or 'innate immunity with specificity' and 'quasi-immune response' is recorded in shrimp and these abilities have been exploited in verifying the immunoprotection against different pathogens. Antigens developed either directly from the pathogens or through recombinant proteins have been tested for immune-protective ability. RNAi-mediated protection has also been demonstrated against different shrimp viruses. This review summarizes the available scientific information on immune responses and the immunoprotection trials carried out in crustaceans with a focus on shrimp. The available research evidences indicate the potential of developing effective immunoprophylactic measures in shrimp.

DNA double-strand breaks (DSBs) are mostly repaired by nonhomologous end joining (NHEJ) and homologous recombination (HR) in higher eukaryotes. In contrast, HR-mediated DSB repair is the major double-strand break repair pathway in lower order organisms such as bacteria and yeast. Penaeus monodon, commonly known as black tiger shrimp, is one of the economically important crustaceans facing large-scale mortality due to exposure to infectious diseases. The animals can also get exposed to chemical mutagens under the culture conditions as well as in wild. Although DSB repair mechanisms have been described in mammals and some invertebrates, its mechanism is unknown in the shrimp species. In the present study, we show that HR-mediated DSB repair is the predominant mode of repair in P. monodon. Robust repair was observed at a temperature of 30 °C, when 2 µg of cell-free extract derived from hepatopancreas was used for the study. Although HR occurred through both reciprocal recombination and gene conversion, the latter was predominant when the bacterial colonies containing recombinants were evaluated. Unlike mammals, NHEJ-mediated DSB repair was undetectable in P. monodon. However, we could detect evidence for an alternative mode of NHEJ that uses microhomology, termed as microhomology-mediated end joining (MMEJ). Interestingly, unlike HR, MMEJ was predominant at lower temperatures. Therefore, the results suggest that, while HR is major DSB repair pathway in shrimp, MMEJ also plays a role in ensuring the continuity and stability of the genome.

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In shrimp, which rely largely on their innate immune system for defense against invading pathogens, the Toll-pathway has been extensively studied, as it plays a crucial role in innate immune responses. Different innate immune genes in the Toll-pathway of shrimp, Penaeus monodon viz., Toll-Like receptor (PmToll), Myeloid differentiation factor-88

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