| dc.description.abstract | West Nile virus (WNV) is a single-stranded positive-sense RNA virus of the Flaviviri-
dae family within the Orthoflavivirus genus. It was first isolated in 1937 in Uganda
from a febrile woman and was considered a pathogen with minor significance
until the late 1990s. The outbreaks in 1996 in Romania, and 1999 in the United
States, respectively, have profoundly changed the perspectives around West Nile
virus. Today, the pathogen is endemic on all continents of the world, except for
Antarctica, and is considered one of the most important encephalitic arboviruses
worldwide. West Nile virus causes a significant number of human and equine neu-
rological cases every year by re-emerging in endemic areas and emerging in new
territories. In humans approximately 80% of the infections remain asymptomatic,
20% of the patients develop flu-like symptoms and less than 1% develop neuro-
logical signs. In horses, 80-90% of the infections are asymptomatic and 10-20%
of the infected animals develop neurological disease, ranging from mild ataxia
to recumbency. West Nile virus has become an important threat to the whole
world, but the clinical manifestation of the infection is still not understood. In
the past 20 years, many research have been made in the area of cellular immune
response to WNV infection. It is assumed that the cellular immune response
plays an important role in the manifestation of the clinical disease. Exacerbated
citotoxic T-cell response, as well as delayed regulatory T-cell response was shown
to play a role in the development of severe neurological form, however the regu-
latory mechanisms behind these pathways are still not clear. The first part of our
review provides a summary of the innate- and cellular immune response during
and following WNV infections in horses and humans. | en_US |
