Cellular stress is triggered by tick-borne encephalitis virus and limits the virus replication in PMJ2-R mouse macrophage cell line

• DOI: 10.1016/j.ttbdis.2023.102269
• Publication Date: 2023-10-09T11:00:07Z
• Authors: Zuzana Beránková; Ritesh Khanna; Markéta Spěváková; Helena Langhansová; Jan Kopecký; Jaroslava Lieskovská
• Keywords: Oxidative stress; Flavivirus; Tick-borne encephalitis virus; Cellular stress; Mitochondrial homeostasis; Infectious and parasitic diseases; RC109-216; Stress on endoplasmic reticulum; 3. Good health

Viral infection may represent a stress condition to the host cell. Cells react it by triggering defence programme restore homeostasis and these events in turn impact viral replication. The knowledge about tick-borne encephalitis virus (TBEV) infection-associated is limited. Here we investigated interplay between TBEV pathways PMJ2-R mouse macrophage cell line, as macrophages are target cells early phases of infection. First, determine how influences replication, effect inducers H2O2 tunicamycin (TM) was tested. multiplication decreased presence both suggesting that cellular responses restrict Second, induction oxidative endoplasmic reticulum (ER) upon level interrogated measuring reactive oxygen species (ROS). ROS were intermittently increased infected at 12 hpi 72 hpi. As mitochondrial dysfunction result level, evaluated membrane potential (MMP) found induced hyperpolarization MMP. Moreover, transient increase gene expression stress-induced antioxidative enzymes, like p62, Gclm Hmox1, detected. Next, ER analysing unfolded protein (UPR). We two general sensors BiP CHOP activated IRE1 pathway UPR. Finally, since natural transmission route from its tick vector mediated via saliva, saliva Ixodes ricinus on TBEV-infected observed only marginal potentiation UPR pathway. In conclusion, elicits changes redox balance triggers defences, including antioxidant Importantly, our results revealed negative stress-evoked replication pathways.