Background: The human leukocyte antigen (HLA) system represents the most polymorphic segment within human DNA sequences and constitutes a core component of immune defense responses and in understanding population genetics. This research investigates the distribution of HLA class I and II polymorphisms across different ethnic groups in Kazakhstan, offering valuable insights into the genetic diversity and demographic evolution within this region. Methods: We performed an in-depth examination of HLA class I and II polymorphisms across diverse ethnic communities living in Kazakhstan, including Kazakhs, Russians, Uzbeks, Ukrainians, Germans, Tatars, and Koreans. Utilizing data from high-resolution HLA typing studies allowed us to assess allele frequencies alongside haplotype distributions while analyzing genetic interrelations between these populations. Additionally, we performed comparative assessments with global HLA databases to determine the genetic affiliations between these groups and their relationships with neighboring and more distant populations. Results: Our study revealed over 200 HLA alleles within the analyzed populations, and significant variations were observed in their allele and haplotype frequencies. Notably, the Kazakh group exhibited strong genetic ties to Asian and Siberian demographics; conversely, other ethnicities showed associations reflective of their historical roots. Notable alleles included HLA-A*02:01, B*07:02, C*07:02, DRB1*07:01, and DQB1*03:01, commonly observed across various groups. Linkage disequilibrium analysis revealed the presence of population-specific haplotypes, highlighting distinct genetic structures within these communities. Conclusions: The findings highlight the significant genetic diversity in Kazakhstan, influenced by its geographical location at the crossroads of Europe and Asia. These results are pertinent to immunogenetics, transplantation medicine, and personalized healthcare within Kazakhstan and adjacent regions. Future research should expand the sample size and explore disease associations to enhance our comprehension of HLA genetics across Central Asia.

Plant viruses cause crop losses in agronomically and economically important crops, making global food security a challenge. Although traditional plant breeding has been effective in controlling plant viral diseases, it is unlikely to solve the problems associated with the frequent emergence of new and more virulent virus species or strains. As a result, there is an urgent need to develop alternative virus control strategies that can be used to more easily contain viral diseases. A better understanding of plant defence mechanisms will open up new avenues for research into plant- pathogen interactions and the development of broad-spectrum virus resistance. The scientific literature was evaluated and structured in this review, and the results of the reliability of the methods of analysis used were filtered. As a result, we described the molecular mechanisms by which viruses interact with host plant cells. To develop an effective strategy for the control of plant pathogens with a significant intensity on the agricultural market, clear and standardised recommendations are required. The current review will provide key insights into the molecular underpinnings underlying the coordination of plant disease resistance, such as main classes of resistance genes, RNA interference, and the RNA-mediated adaptive immune system of bacteria and archaea – clustered regularly interspaced short palindromic repeats (CRISPR) and CRISPR-associated Cas proteins – CRISPR/Cas. Future issues related to resistance to plant viral diseases will largely depend on integrated research to transfer fundamental knowledge to applied problems, bridging the gap between laboratory and field work.

Plant viral infections continue to pose a significant and ongoing threat to global food security, especially in the context of climatic instability and intensive agricultural practices. The CRISPR/Cas system has emerged as a powerful tool for developing virus-resistant crops by enabling precise modifications to viral genomes or plant susceptibility factors. Nonetheless, the efficacy and dependability of CRISPR-based antiviral approaches are limited by challenges in guide RNA design, off-target effects, insufficiently annotated datasets, and the intricate biological dynamics of plant–virus interactions. This paper summarizes the latest advancements in the incorporation of artificial intelligence (AI) methodologies, including machine learning and deep learning algorithms, into the CRISPR design and optimization framework. It examines how convolutional and recurrent neural networks, transformer architectures, and generative models like AlphaFold2, RoseTTAFold, and ESMFold can be used to predict protein structures, score sgRNAs, and model host–virus interactions. AI-enhanced methods have been proven to improve target specificity, Cas protein performance, and in silico validation. This paper aims to establish a foundation for next-generation genome editing strategies against plant viruses and promote the adoption of AI-powered CRISPR technologies in sustainable agriculture.

Global climate change is the impact of combined abiotic and biotic stresses negatively affecting plant health and productivity. This study investigated the molecular and cellular responses of Nicotiana benthamiana L. plants to wild-type tomato bushy stunt virus (wtTBSV) infection under conditions of pre-existing heat stress. The experiments were conducted under controlled temperature regimes of 30 °C and 37 °C in combination with virus challenge. Morphological and biochemical analyses in plants under the influence of combined stress showed the alleviation of disease symptoms, reduction in virus content and reduced expression levels of viral proteins P19 and P33. Under conditions of combined stress, accumulation of hydrogen peroxide and malondialdehyde, as well as activation of the antioxidant enzyme catalase, especially in root tissues, were observed. Notably, at 37 °C, virus infection was suppressed despite high levels of oxidative stress, whereas at 30 °C, a marked decrease in the expression of host factors was observed. The results indicate that thermal stress modulates virus–host interactions and activates defense mechanisms, including antioxidant and RNA interference pathways. Therefore, temperature adaptation can be considered as a promising strategy for enhancing plant resistance to viral pathogens under climate changes.

Agriculture is still at serious risk from viral infections, particularly in light of climate change and more intensive farming practices. Small non-coding RNAs (sRNAs), in particular microRNAs (miRNAs) and circular RNAs (circRNAs), have emerged as crucial post-transcriptional regulators of plant antiviral defense in this setting. These molecules provide an essential RNA-based immunity layer by regulating hormones, autophagy, redox balance, immunological signaling, and programmed cell death. In this work, we examine the molecular processes through which circRNAs and miRNAs function during viral infection, focusing on how they affect autophagy and systemic acquired resistance (SAR). Through thorough searches of PubMed, Web of Science, and Scopus, we combined findings from peer-reviewed experimental and transcriptomic studies. Our study covers important crops as well as model species (Arabidopsis thaliana, Nicotiana benthamiana), providing a thorough understanding of sRNA synthesis, target control, and antiviral signaling. By combining previously disparate data, this review provides a coherent framework for understanding how short RNAs affect plant immune responses to viral infections. We highlight key regulatory relationships that need further study and propose that these results can be used as a foundation for new RNA-based biotechnological approaches. By carefully altering RNA regulatory mechanisms, scientists can use this information to help them create more resistant crops.

Molecular chaperones HSP70 and HSP90 represent a critical, yet conflict-ridden, node in plant physiology, particularly under the dual impact of heat stress and viral infection. As key components of both thermotolerance (maintaining proteostasis) and innate immunity (stabilization of NLR receptors), they are simultaneously exploited by viruses to facilitate their own life cycle. This review critically analyzes this “trilemma,” focusing on the hypothesis of competition for a limited chaperone pool. We present mechanistic insights indicating that during heat stress, cellular priority shifts towards maintaining global proteostasis, thereby diverting chaperones from immune functions. This resource-based competition mechanism potentially explains the collapse of ETI-immunity, as NLR receptors, deprived of support from the HSP90-SGT1-RAR1 complex, are destabilized and targeted for degradation. We also integrate adjacent signaling pathways into this model, including hormonal cross-talk (SA, JA) and autophagy. Understanding this trade-off opens new perspectives for molecular breeding and the biotechnological engineering of stress-resilient crop varieties.