Popovici, IvonaHorhogea, Cristina-ElenaRîmbu, Cristina Mihaela2026-06-082026-06-0820251454-7406https://repository.iuls.ro/handle/20.500.12811/6553Coronaviruses have developed complex strategies to manipulate host cell pathways, in this way facilitating viral replication and enabling immune evasion. This review focuses on the interactions between coronaviruses and host cellular processes, especially on the modulation of autophagy, apoptosis, and additional regulatory pathways, including endoplasmic reticulum (ER) stress responses, interferon signaling, and lipid metabolism. Studies have shown that coronaviruses promote both the initiation of autophagy and inhibition of autophagic flux, resulting in the formation of non-degradative membrane compartments that support viral replication and limit immune detection of viral components. Furthermore, coronaviruses have a dual control over apoptotic signaling by both inducing and suppressing programmed cell death through mitochondrial pathways, caspase activation, and death receptor–mediated mechanisms. Clarification of these virus–host interactions provide important insights into coronavirus pathogenesis and identifies potential therapeutic targets, including autophagy modulators, kinase inhibitors, and agents targeting ER stress pathways and mitochondrial dysfunction.EnglishAttribution-NonCommercial-ShareAlike 4.0 International (CC BY-NC-SA 4.0)http://creativecommons.org/licenses/by-nc-sa/4.0/cellular pathwayscoronavirusapoptosisautophagyArticle2393-4603https://doi.org/10.61900/SPJVS.2025.03.19