nattrol ct/ng panel Archives - Gen9 Genetics
Autophagy is a cellular process that maintains cellular homeostasis through proteolytic recycling of the cytoplasm. Autophagy occurs at basal levels in almost all cells. It is positively regulated in cellular stress, including hunger, oxidative stress, or during infection. Several viruses, including the flavivirus, have developed strategies to subvert or utilize autophagy for efficient replication. Bovine viral diarrhea virus (BVDV) is a member of the Flaviviridae family and the pestivirus group of viruses. BVDV is responsible for significant economic losses in the livestock industry worldwide. A unique feature of BVDV is the well-characterized genetic changes that can result in two different phenotypes (biotypes) in cell culture: cytopathic (cp) or non-cytopathic (ncp) effects. The ncp viruses are the most prevalent and important for clinical disease. This study was carried out to determine the effect of different BVDV phenotypes using the virus pair, cp TGAC and ncp TGAN on the induction of autophagy, as well as to investigate the role of autophagy in the cytopathic effect induced by BVDV.
Results
demonstrated that both BVDV biotypes (cp and ncp) induced autophagy in the Madin-Darby immortal bovine kidney (MDBK) cell line as well as in primary bovine turbinate (Bt) cells after infection. There were no significant differences between BVDV cp or ncp strains in autophagosome formation (p <0.05) in MDBK or Bt cells. The autophagy inhibitor drug, 3-methyladenine (3MA) significantly reduced autophagy (p < 0.05) as well as viral replication. While rapamycin, an autophagy inducing drug, significantly improved autophagy and viral replication. Co-localization study using BVDV NS5A, Erns and E1 proteins with autophagy marker, light chain-3 (LC3) revealed that BVDV replication was associated with autophagosomes. This study revealed that BVDV strains cp and ncp induced autophagy at a similar level and used autophagy machinery for their replication.