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lung: HveC ( PVRL1 ), PVRL3 , HveD ( PVR , CD155 ), HS3ST4 , and HS3ST5 [23, 24].
Finally, a number of members of the TNF receptor family, usually involved in apopto-
sis, were identifi ed ( TNFRSF10 , 21 , 25 , 9 , 17 , 8 , ). This apoptotic pathway was also
described in the study of HSV infection of glial cell types [25]. However, the result is
interesting as the family member TNFRSF14 has been shown to be involved in some
cases of viral entry, but we do not know whether these other family members are in-
volved in viral entry and cell fusion, or only have a downstream role.
Numerous other genes involved in cellular proliferation ( YWHAB , BUB1 ,
PCNA , GADD45 , MCM7 , CDK4 , CDK7 ) and apoptosis ( PRKACA , PDCD8 , AKT1 ,
PPP3CA ), were identifi ed. These pathways were previously described following
PRV and HSV infection in several models [5, 25] and might refl ect the proliferation
of immune cells. A number of other genes differentially expressed in the lung, such
as HSPD1 , HSPB2 , SERPINE-1 , are in common with human and mouse models
infected by HSV-1 [5, 26].
Recently, Flori et al. [27] have published a time course transcription profi ling
study (based on the Qiagen 8,541 gene porcine oligonucleotide array and a 1,789
porcine and PRV cDNA array) investigating both the PRV transcriptome and the host
transcriptome responses of PK15 (porcine kidney) cells in culture. This study reports
the early down-regulation of many cellular genes in contrast to the data in this chapter.
This difference most probably arises from the artifi cial cell culture study where there
is a homogeneous cell population, whereas our present study is an in vivo investigation
of complex tissues. It is entirely possible that minor tissue cell types exhibit down-
regulation of many of the same genes, however, their contribution to the overall signal
renders these changes undetectable. This may also explain the differences in gene ex-
pression changes for shared genes between lung and brain. In general, fold changes are
lower in brain which probably refl ects the complexity of cell types in the tissue, not all
of which may respond equally to infection. Nevertheless, it is clear that the Flori et al.
study has also observed changes in gene expression in the main categories of cellular
functions described in this chapter; most notably genes involved in immune responses
and cell proliferation and apoptosis.
Genetic differences have been reported in the susceptibility to PRV between Eu-
ropean Large White and Chinese Meishan pigs, with differences in cell-mediated and
humoral immunity, as well as the outward clinical signs in young pigs [28]. In this
study we identifi ed several differentially expressed genes located at or close to the
QTL regions previously reported. Two genes ( CD36 and NPL ) up-regulated in the
infected brain and lung are located near the SW749 marker, which is associated with
changes in body temperature and neurological signs. The ETA1 (alias SPP1 ), which
is involved in the recruitment of T-lymphocytes [29, 30], was up-regulated in both
tissues after natural PRV infection, and is linked to the QTL region of chromosome
8. One of the PRV receptors, PVRL3, which is differentially expressed in infected
lung, is linked to a QTL on chromosome 13. The CLDN7, which is involved with cell
communication, was down-regulated in the infected brain and is linked to a QTL on
chromosome 13 associated with neurological signs.
 
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