CSFV, together with Bovine viral diarrhoea virus (BVDV) and sheep Border disease virus (BDV), belongs to the genus Pestivirus, the family Flaviviridae. CSFV is known to have high affinity to cells of the immune system, which seems to relate to its detrimental effects on the immune and hematopoietic systems
. Furthermore, CSFV can efficiently evade and compromise the host immune system, causing a severe disease of pigs characterized by fever, hemorrhage, thrombocytopenia, lymphoid organ atrophy and severe lymphopenia, particularly in B cells, due to the apoptosis of uninfected lymphocytes
[3, 4]. The lymphopenia can result in immunosuppression and serves as a hallmark of CSFV infections. Pestiviruses such as CSFV and BVDV can also cross the placenta to infect the developing fetus, resulting in the birth of persistently infected animals
[5, 6]. Recently, studies have found that CSFV evolves mechanisms for the inhibition of inflammation and type I interferon (IFN) production in infected cells, preventing double-stranded RNA-mediated apoptosis and giving rise to long-term infections
[7, 8]. Although a large number of works have been done, the mechanism of the CSFV infection in vivo and in vitro has not been fully elucidated.
Viruses have evolved sophisticated control mechanisms to redirect the cellular signal transduction pathway to its own advantage, and NF-κB pathway is a common target of many viruses
. The NF-κB pathway is recognized to be the central mediator of immune responses in mammals
, because several proteins encoded by target genes of NF-κB participate in the activation of immune and inflammatory responses. Therefore, NF-κB activation during viral infection has been interpreted as a protective response of the host to the viral pathogen
. Interestingly, certain viruses can utilize the activation of NF-κB as a strategy to increase viral replication and viral progeny production
. Whereas other reports indicate that some viruses inhibit the NF-κB pathway
[13–18]. The suppression of NF-κB activation represents a potential strategy of viral escape from the host immune system and contributes to virus pathogenesis in infected cells.
NF-κB is also a host nuclear transcription factor, activated by multiple stimuli including inflammatory cytokines, growth factors, bacterial and viral infections, and plays an important role in inflammation, innate immune responses, regulation of cell proliferation and survival
[11, 19, 20]. In non-stimulated cells, NF-κB is sequestered as a cytoplasmic complex, whose predominant form is a heterodimer consisting of p50 and p65 (RelA) subunits, bound to inhibitory IκB proteins
[21, 22]. Stimulation of cells by diverse agents causes phosphorylation of IκB and its degradation by the proteosome subsequently
. Liberated NF-κB is transported into the nucleus where it induces the transcription of target genes, including IκBα acting as the major feedback inhibitor of the NF-κB pathway
In the present study, we investigated NF-κB activity in vivo and in vitro in order to elucidate how CSFV carried out its infection in the host. The results demonstrate that CSFV does not activate the NF-κB signaling pathway which may represent a mechanism of CSFV-induced immunomodulation.