Uncovering the Impact of B. miyamotoi Infection on Ixodes scapularis ER Homeostasis
Latoyia Downs and Shahid Karim
Department of Cell and Molecular Biology, The University of Southern Mississippi, Hattiesburg, MS
Tick-borne diseases are a public health issue and they affect people every day. A new tick-borne pathogen, Borrelia miyamotoi, has emerged. It is a relapsing fever spirochete that is considered a distant cousin to Lyme Disease agent and has recently been found to cause disease in humans. This pathogen has been found in Ixodid ticks such as Ixodes ricinus (Sheep Tick) and Ixodes scapularis (Black-legged Tick). In humans, Borrelia miyamotoi causes recurrent fever, flu-like symptoms, and can also cause more severe illnesses such as meningoencephalitis. Unlike other Borrelia spirochetes, this pathogen can be vertically transmitted, passed from mother to offspring, which allows for the survival of the pathogen for many generations. There is very little to no research on B. miyamotoi infection within the tick vector that contribute to the understanding of its molecular mechanism to survive within the tick host before transmission to the mammalian host. To study the molecular determinants of B. miyamotoi infection in Ixodes scapularis, we used an Ixodes scapularis embryonic cell line (ISE6) to study the gene expression of select genes involved in Endoplasmic Reticulum stress. Confluent ISE6 cells were infected with B. miyamotoi. The cells were harvested at 2, 4, and 6 days post infection (dpi). RNA was extracted and multiple ERAD genes were analyzed using qRT-PCR. Our results show that Borrelia miyamoti causes upregulation of endoplasmic reticulum-associated degradation (ERAD) and Unfolded Protein Response (UPR) genes. During B. miyamotoi infection there is significant upregulation of up to a 100-fold increase of ERAD component selenoprotein genes, SelenoK, SelenoM, SelenoN, and SelenoS, and UPR genes, IRE1 and Derlin. Studies are still ongoing.