Skip to main content
ARS Home » Research » Publications at this Location » Publication #175521
Title: EXPERIMENTAL VESICULAR STOMATITIS NEW JERSEY VIRUS (VSVNJV) INFECTION IN CATTLE: PATHOGENESIS, VIRUS DISTRIBUTION AND LOCALIZATION DETERMINED BY USING CONFOCAL MICROSCOPY

Author
item SCHERER, CHARLES - UNIV TEXAS MEDICAL BR
item O'DONNELL, VIVIAN - UNIV OF CONNECTICUT
item Gregg, Douglas
item ESTES, D - UNIV TEXAS MEDICAL BRANCH
item Rodriguez, Luis

Submitted to: Virology
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 9/26/2006
Publication Date: N/A
Citation: N/A

Interpretive Summary: Vesicular Stomatitis (VS) is a costly viral disease in cattle, horses and pigs. VS is included in the OIE list A of reportable diseases, and is clinically undistinguishable from foot-and-mouth disease, one of the most devastating disease of livestock. Little is known about the pathogenesis of this virus in livestock species. In order to better understand virus distribution and local immune response to VSV infection we developed a disease model in cattle utilizing a coronary-band scarification procedure that consistently resulted in vesicular lesions in the inoculation sites, with increase in virus titers. In contrast inoculation in the flank skin yielded no clinical disease and no increase in viral titer was observed. Virus was never found in blood. In postmortem examination virus was not found in muscle or in any major organ or tissue indicating that viral infection was restricted to the site of inoculation and draining lymph nodes. In the coronary band, primary cells containing virus were on the upper layers of the skin (keratinocytes). In contrast flank skin keratinocytes were not infected but virus was found in local immune cells. This work explains in part the location of vesicular lesions and might help in developing protection strategies in cattle.

Technical Abstract: Vesicular Stomatitis Virus (VSV) is a negative-sense RNA virus that causes vesicular disease in cattle, horses and pigs. Little is known about the pathogenesis of this virus in livestock species. In order to better understand virus distribution and local immune response to VSV infection we developed a disease model in cattle utilizing a coronary-band scarification procedure that consistently resulted in clinical disease. Over 72 hours, virus titers increased from 2 log10 TCID50 to >8 log10 TCID50 by in the inoculated coronary bands (cb), but virus was never found in blood, oral-pharyngeal fluid, nor in non-inoculated coronary bands. Inoculation in the flank skin yielded no clinical disease and no increase in viral titer was observed. Six of the cb-inoculated animals were euthanized at 72 hpi and virus was consistently found only in primary lymph nodes draining the inoculated cb (i.e. prescapular or popliteal) and occasionally in secondary draining lymph node and tonsil. Virus was not found in any major organ or tissue indicating that viral infection was restricted to the site of inoculation and draining lymph nodes. Viral antigens co-localized primarily with keratinocytes on the stratum spinosum of the coronary band, and in a few MHC-II-stained fusiform cells found in the basal layer, in the dermis and in the afferent and efferent sections of the regional lymph nodes. Fusiform cells containing VSNJV antigen were found in large numbers in the dermis of a flank-inoculated animal,suggesting they are skin dendritic cells. Results demonstrated that infection by scarification with VSNJV results in localized infection limited to the inoculation site and regional draining lymph nodes and suggest that skin dendritic cells might play a role in controlling the viral infection.