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Title: POTENTIATION OF VESICULAR STOMATITIS VIRUS INFECTION OF EQUINE DERMAL CELLS BY CULICOIDES SALIVARY GLAND HOMOGENATES

Authors
item Drolet, Barbara
item Lam, Vy - UNIV OF WISCONSIN

Submitted to: American Society for Virology Meeting
Publication Type: Abstract Only
Publication Acceptance Date: January 31, 2004
Publication Date: July 12, 2003
Citation: Drolet, B.S., Lam, V. 2003. Potentiation of vesicular stomatitis virus infection of equine dermal cells by culicoides salivary gland homogenates. American Society for Virology Meeting.

Interpretive Summary: The biting gnat, Culicoides sonorensis, is a potential biological vector for the transmission of vesicular stomatitis virus (VSV) in the western United States. When a virus-infected insect bites a susceptible host, numerous salivary proteins and virus are delivered to the tissues. In general, these salivary proteins facilitate feeding and inhibit host immune responses. To determine what effect Culicoides salivary gland proteins may have on VSV infection in horses, equine dermal cells were treated with salivary gland homogenates (SGH) simultaneously with, or prior to, infection with VSV. Treatment of cells with SGH resulted in a dose dependent increase in VSV infection. This viral potentiation likely facilitates the establishment of a localized infection from the minute inoculum at the site of the bite.

Technical Abstract: The biting gnat, Culicoides sonorensis, is a potential biological vector for the transmission of vesicular stomatitis virus (VSV) in the western United States. When a virus-infected insect bites a susceptible host, numerous salivary proteins and virus are delivered to the tissues. In general, these salivary proteins facilitate feeding and inhibit host immune responses. To determine what effect Culicoides salivary gland proteins may have on VSV infection in horses, equine dermal cells were treated with salivary gland homogenates (SGH) simultaneously with, or prior to, infection with VSV. Treatment of cells with SGH resulted in a dose dependent increase in VSV infection. This viral potentiation likely facilitates the establishment of a localized infection from the minute inoculum at the site of the bite.

   
 
 
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