Virus research最新文献

Celiac disease (CeD) is a disorder due to abnormal immune response to gluten protein in individuals with predisposing genotypes. Its origin is not fully understood. Human endogenous retroviruses (HERVs) derive from ancestral infections of germinal cells and represent 8 % of the human DNA. They are mostly inactive, but some can be activated. Their aberrant expressions are associated with inflammatory and immune-mediated diseases. HERV transcription is modulated by TRIM28 and SETDB1, which are also directly implicated in epigenetic processes and modulation of the immune response. We reported HERV overexpressions in CeD children at diagnosis. In the current prospective study, using a PCR real-time Taqman amplification assay, we explored the transcription levels of HERV-H-pol, -HERV-K-pol, and HERV-W-pol, of syncytin 1 (SYN1), SYN2, and HERV-W-env, as well as of TRIM28 and SETDB1 in the whole blood from 51 adults with CeD after years of good compliance with gluten-free diet (GFD) as compared to healthy controls (HC) of similar age. The transcriptional levels of every HERV and of TRIM28/SETDB1 were significantly higher in CeD patients than in HC (constantly with p < 0.0001). Positive correlations were found between the RNA levels of TRIM28 or SETDB1 and HERVs in CeD patients. The upregulation of HERVs, TRIM28, and SETDB1 and their positive correlations are suggestive clues of their contribution to the pathophysiology of CeD and might justify the persistent risk of developing, despite GFD, autoimmune diseases, neuropsychiatric disturbances, and cancers, all disorders characterized by enhanced HERV expressions and epigenetic alterations.

Helicoverpa armigera nucleopolyhedrovirus (HearNPV1) shows considerable potential as a sustainable biological control agent against insect pests. Enhancing its efficacy through formulation with appropriate carrier materials is critical for improving pest management strategies. This study evaluated the potential of chitosan and zeolite nanoparticles as delivery vehicles for HearNPV1, assessing their effects on mortality and lethal time in second-instar Spodoptera litura larvae. A single-factor randomized block design with three replications was used. The treatments consisted of HearNPV1 formulated with various concentrations (0.125 % to 0.5 %) of either chitosan or zeolite nanoparticles. Larval mortality and lethal time (LT) were recorded and analyzed using one-way ANOVA, with significant differences further assessed by Duncan's multiple range test (α=0.05). Results showed that formulating HearNPV1 with either chitosan or zeolite nanoparticles significantly increased larval mortality. Notably, even the lowest concentration tested (0.125 %) of both chitosan and zeolite nanoparticles achieved 66.67 % larval mortality within seven days post-infection. However, no significant differences in lethal time were observed among treatments, regardless of nanoparticle type or concentration. Larvae exposed to virus-nanoparticle formulations exhibited lethal times ranging from 3.0 to 4.67 days on average-similar to the duration observed in larvae infected with HearNPV1 alone. In conclusion, both chitosan and zeolite nanoparticles at 0.125 % concentrations effectively enhanced HearNPV1-induced mortality in S. litura larvae, although they did not shorten the time to death. These findings underscore the potential for nanoparticle-based HearNPV1 formulations to improve biological pest control, warranting further investigation into their practical application and mechanisms of action.

Non-apoptotic programmed cell death (NAPCD) represents a diverse set of cell death mechanisms that differ from classical apoptosis and have recently gained attention in the context of viral infections. This review focuses on four key NAPCD types, including ferroptosis, cuproptosis, NETosis (neutrophil extracellular trap formation), and PANoptosis (a combination of pyroptosis, apoptosis, and necroptosis), and summarizes their distinct molecular pathways and roles during viral infections. We emphasize their functional relevance in SARS-CoV-2 infection, revealing how they significantly impact viral replication, host immune responses, and tissue damage. Furthermore, we explore the interaction between NAPCDs and specific immune responses. Specifically, ferroptosis influences macrophage polarization. Cuproptosis activates innate immunity via the cGAS-STING pathway. NETosis contributes to Th17 responses, and PANoptosis interacts with Th1, Th22, and Thαβ pathways. Understanding the interplay among these cell death pathways provides new insights into host-virus dynamics and uncovers potential therapeutic targets for viral diseases.