ARS | Publication request: VESICULAR STOMATITIS NEW JERSEY VIRUS IN CATTLE: PATHOGENESIS, VIRUS DISTRIBUTION AND LOCAL IMMUNE RESPONSE

Submitted to: Meeting Abstract
Publication Type: Abstract Only
Publication Acceptance Date: September 6, 2004
Publication Date: October 3, 2004
Citation: Scherer, C.F., Golde, W.T., Gregg, D.A., Estes, D.M., Drolet, B.S., Rodriguez, L.L. 2004. Vesicular Stomatitis New Jersey Virus in Cattle: Pathogenesis, Virus Distribution and Local Immune Response. Conference of Research Workers in Animal Disease Annual Meeting. P. 198.

Technical Abstract: Vesicular Stomatitis Virus (VSV) is a negative-sense RNA virus that causes vesicular disease in cattle, horses and pigs. To date, little is known about the pathogenesis of this virus in livestock species. In order to better understand the pathogenesis, virus distribution and local immune response to VSV infection we developed a disease model in cattle and determined that virus distribution is primarily restricted to the site of inoculation and the corresponding regional draining lymph nodes. Inoculation of the coronary band resulted in productive infection with 6-8 log10 increase in infectious virus titer detected at the inoculation site. Characterization of infected cells using VSV-specific antibodies by immunoshistochemistry and confocal microscopy, showed viral antigens predominantly in keratinocytes of the stratum spinosum of the coronary band, and in a few distinct cells of the basal layer. Target cells in lymph nodes were morphologically consistent with monocytes. Characterization of these monocytic cells using a double staining procedure with VSNJ and MHC-II/MAC 387 markers suggested that these cells were interdigitating dendritic cells. In contrast to the coronary band inoculation, inoculation of the flank skin resulted in non-productive infection (< 2logs). Results demonstrate that infection by scarification with VSV-NJ is restricted to the inoculation site (coronary band) and regional draining lymph node and this restriction might be mediated by innate immune responses.