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SUMMARY
In this paper the authors briefly summarize the global and Hungarian history of
the Porcine reproductive and respiratory syndrome (PRRS) disease. They also
review the latest results targeting host virus interactions and explain the causes
of the broad spectrum of the pathology and pathogenesis of the disease. The
PRRSV emerged almost simultaneously in the USA and Europe at the end of the
1980s. Since then, the disease remained one of the biggest health threats to
the global swine industry. The virus was first detected in 1995 in Hungary, but it
has caused more significant economic losses only since 2002. As a consequence
of its economic impact, the virus has been intensively studied over the last two
decades. The PRRSV belongs to the Arteriviridae family, it contains a single stranded, positive-sense RNA genome with at least ten open reading frames
(ORFs). The PRRSV can be divided into two major genotypes: type 1 (European)
and type 2 (North American). Despite the distinct genetic and antigenic differ ences they cause very similar symptoms. In neonatal pigs the PRRSV infection
causes respiratory disease, while in sows the most frequent clinical signs are
reproductive failures. The primary cell targets of the virus are the alveolar mac rophages in the respiratory tract. The main reason of the abortion and stillbirth
is the damage of the maternal-foetal interface and infection of the foetus. One
of the major differences between the two genotypes is the cell tropism. Though
CD163 seems to be a main receptor for both genotypes, sialoadhesin receptor
is necessary only for the majority of type 1 viruses but the type 2 PRRSV and a
few type 1 strains can infect macrophages without sialoadhesin receptor. The
PRRSV is very often associated with other viral and bacterial pathogens (Pas teurella multicida, Mycoplasma hyopneumoniae and PCV-2) and to the porcine
respiratory disease complex (PRDC). Unfortunately, the genetic background of
the virulence and the pathogenicity is not completely clear yet. The available
vaccines against PRRSV do not give full protection, and the high genetic diver gence of the virus and its immune-evasive ability hinder the development of
effective vaccines.
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