Caveolin-1-mediated endocytic pathway is involved in classical swine fever virus Shimen infection of porcine alveolar macrophages.

Macrophages are at the frontline of defense against pathogenic microorganisms. However, very little is known about the cell invasion mechanism of classical swine fever virus (CSFV) Shimen strain. To elucidate the infective mechanism of this important pathogen, we screened deep-sequencing data derived from macrophages infected with CSFV Shimen and uninfected macrophages, and identified a role of caveolin-1 (CAV1). Digital gene expression profiling showed that CAV1 was differentially expressed in CSFV Shimen-infected macrophages. Quantitative polymerase chain reaction and western blot analyses showed that the transcription and translation of CAV1 were significantly up-regulated in CSFV Shimen-infected macrophages. In addition, immunofluorescent confocal microscopy analysis suggested that CAV1 was temporally colocalized with CSFV E2 throughout the course of the infection. Through the overexpression of recombinant CAV1 or the silencing of CAV1 expression using small interfering RNA in macrophages, we demonstrated that CAV1 expression is beneficial for the replication of CSFV Shimen. However, RNA silencing of CAV1 did not prevent viral replication, which may indicate that CSFV can also enter macrophages by other mechanisms. Our findings suggest that CAV1-mediated endocytosis is advantageous for productive CSFV Shimen infection in macrophages, providing a new insight into the mechanisms of evasion of host immunity for successful viral infection.