The Impact of Powassan Virus and Borrelia burgdorferi Coinfection in Ixodes scapularis Ticks
Ticks (Order: Ixodida) are hematophagous arthropods that transmit a number of medically significant pathogens. Two of these include Powassan virus (POWV) and the spirochete Borrelia burgdorferi, both of which are transmitted by Ixodes scapularis in the northern parts of the United States. Powassan virus can lead to neuroinvasive illness with a high fatality rate. B. burgdorferi causes Lyme disease, a potentially long-term infection of the joints, heart and brain. B. burgdorferi is present in 20-70% of ticks, while POWV is present in less than 5%. This suggests the possibility that most ticks capable of transmitting POWV are coinfected with B. burgdorferi. The existence of negative or synergistic interactions between ticks are unknown, though, as are unique consequences of dual disease. Field surveillance was conducted in endemic areas to ascertain the baseline rates of both pathogens and the rate of coinfection, and to gain an insight into the environment where the pathogens are present. B. burgdorferi was common in New York and Connecticut, while POWV was detected at a low rate, primarily in the form of Deer Tick virus (POWV Lineage II) but also in I. scapularis as a non-Lineage II strain. Coinfection was limited by the rate of POWV. Laboratory analysis of the pathogen interaction was performed to assess possible inhibition or synergistic effects that could influence their shared sylvatic cycles and to assess the risk of human co-exposure. It was determined that ticks can harbor both pathogens, and that the presence of B. burgdorferi enhances viral replication in the midgut and accelerates dissemination to the salivary glands. Transcriptome analysis suggests this response is caused by enhancement of anti-Borrelia responses in the midgut and suppression of POWV-induced metabolic changes in the salivary glands. No change was noted in the microbiome. Dual infection was studied in a murine model. A lethal model of POWV infection was developed for C3H mice, the primary model of Lyme disease. Dual infection did not attenuate the response to POWV, although the expression of some cytokines was enhanced by dual infection. Additionally, Powassan virus replication was noted in the heart, suggesting a potential interaction role in Lyme carditis.