Pawan Kumar

Zika virus (ZIKV) remains a significant global public health threat due to its association with severe neurological and ocular abnormalities, including microcephaly and congenital glaucoma in infants. Viruses often exploit host metabolic programs, such as energy and lipid metabolism, to support their replication. However, how ZIKV-driven metabolic reprogramming affects the anterior segment of the eye, especially trabecular meshwork (TM) cells, remains poorly defined. In this study, we investigated the roles of AMP-activated protein kinase (AMPK) signaling, fatty acid (FA) metabolism, and lipid droplet (LD) biogenesis in ZIKV-induced ocular pathogenesis using primary human TM cells and an IFNAR1-deficient mouse model. ZIKV infection triggered time-dependent activation of the LKB1-AMPK-ACC signaling axis and significantly increased LD accumulation. Pharmacological activation of AMPK suppressed viral replication, whereas its inhibition enhanced infection, highlighting an antiviral role for AMPK signaling. In contrast, ZIKV promoted LD biogenesis, and inhibition of DGAT1 reduced both LD formation and viral replication, indicating a proviral role for LDs. Modulation of FA metabolism further revealed differential effects on ZIKV infection: saturated FA (palmitate) enhanced viral replication, whereas inhibition of FA oxidation with etomoxir reduced infection. Conversely, unsaturated FAs (oleate and linoleate) suppressed viral replication, in part by impairing viral binding and entry. Collectively, these findings show that ZIKV reshapes host metabolic pathways in TM by differentially engaging AMPK signaling, FA metabolism, and LD biogenesis to promote viral replication and spread in ocular tissue. Targeting these metabolic pathways may offer promising therapeutic avenues for preventing and/or treating ZIKV-associated ocular complications.

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Terminal heat stress is a major constraint to wheat production under global climate change, necessitating the identification of key adaptive traits and tolerant genotypes. This study evaluated 13 bread wheat (Triticum aestivum L.) genotypes under optimal and heat-stress conditions, focusing on morphological, physiological, and biochemical traits at the grain-filling stage. Significant genotypic variability was observed across all measured traits, indicating substantial diversity for heat adaptation. Based on the heat susceptibility index, genotypes TAW 119, DBW 187, and HD 2932 were identified as heat-tolerant. These genotypes exhibited minimal reductions in plant height, number of effective tillers, spike length, number of grains per spike, grain weight, and biological yield under stress, which was associated with enhanced scavenging of reactive oxygen species through increased enzymatic and non-enzymatic antioxidant activities. Physiologically, tolerant genotypes maintained higher chlorophyll and carotenoid content, leaf relative water content, membrane stability index, pollen viability, and canopy temperature depression, supporting sustained metabolic activity under heat stress. Biochemical analyses confirmed effective reactive oxygen species scavenging in tolerant genotypes, supported by elevated activities of catalase, ascorbate peroxidase, superoxide dismutase, and peroxidase, along with increased accumulation of proline and other osmoprotectants. Principal component analysis showed that the first two components explained 42.78% and 47.02% of the total variation under optimal and heat stress conditions, respectively, highlighting stronger trait divergence under stress. Biplot analysis identified catalase, ascorbate peroxidase, proline, grain filling rate, days to heading, superoxide dismutase, peroxidase, grain yield per plant, and grain filling duration as key traits contributing to heat tolerance. The identified tolerant genotypes and associated traits offer valuable resources for wheat breeding programs aimed at improving genetic gains and yield stability under high-temperature stress.

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