Skip to main content
ARS Home » Research » Publications at this Location » Publication #192776

Title: INFECTIVITY AND PERSISTENCE OF VESICULAR STOMATITIS VIRUS IN CULICOIDES CELLS

Author
item Drolet, Barbara
item Pavelko, Carol
item Bennett, Kristine

Submitted to: American Society for Virology Meeting
Publication Type: Abstract Only
Publication Acceptance Date: 2/10/2006
Publication Date: 7/15/2006
Citation: Drolet, B.S., Pavelko, C.M., Bennett, K.E. 2006. Infectivity and persistence of vesicular stomatitis virus in culicoides cells. American Society for Virology Meeting, P 10-5.

Interpretive Summary: The biting midge, Culicoides sonorensis, was recently shown to be a biologically competent vector for the arbovirus, vesicular stomatitis virus (VSV). While arboviruses can be extremely pathogenic to mammalian cells, they typically do not exert deleterious effects on their insect vectors. To better understand VSV infection in the cells of these insects, we examined the virus growth, the types of cells the virus grows in, how much virus is produced by infected cells, whether the virus kills the cells and how long the virus can cause an infection in insect cells. Virus produced during long term infections were examined for changes in specific genes. What we learn about long term insect infections may give us information about if and how arboviruses persistent in insects in nature between disease outbreaks.

Technical Abstract: The biting midge, Culicoides sonorensis, was recently shown to be a biologically competent vector for the arbovirus, vesicular stomatitis virus (VSV). While arboviruses can be extremely pathogenic to mammalian cells, they typically do not exert deleterious effects on their insect vectors. Infection of VSV in Culicoides cells was characterized by growth kinetics, cell tropism, virus release, cytopathology, apoptosis, and persistence. VSV established a productive persistent infection and were monitored for more than 250 days. At 37 days post infection (dpi), a microplaque phenotype was observed in released virus. By 51 dpi, 90% of plaques in released virus were of the microplaque phenotype. Microplaque mutants were triple plaque purified and were shown to have no temperature sensitivity. The matrix (M) and phosphoprotein (P) genes were sequenced and compared with wild type sequences. The role of persistent insect cell infections in overwintering of arboviruses is discussed.