Cellular membrane cholesterol is required for porcine reproductive and respiratory syndrome virus entry and release in MARC-145 cells

Sun, Ying; Xiao, ShaoBo; Wang, Dang; Luo, Rui; Li, Bin; Chen, HuanChun; Fang, LiuRong

Porcine reproductive and respiratory syndrome (PRRS), characterized by severe reproductive failure in sows and respiratory distress in piglets and growing pigs, is now considered one of the most economically important diseases in countries with intensive swine industries [13] . PRRS virus (PRRSV), the etiology of PRRS, is a positive-strand RNA virus that belongs to the genus Arterivirus, family Arteriviridae, along with Lactate-dehydrogenase-elevating virus (LDV) of mice, Equine arteritis virus (EAV) and Simian hemorrhagic fever virus (SHFV) [4] . It has been demonstrated that PRRSV has a strong tropism for cells of the monocyte/macrophage lineage in vivo, and for porcine al-veolar macrophages (PAM) and African green monkey kidney cells (MARC-145) in vitro [58] . Accumulating evidence has revealed that the replication of PRRSV in cultured cells partially depends on the composition of the host cellular plasma membrane [9, 10] . Cellular surface molecules, such as heparan sulfate and sialoadhesin, play an important role in PRRSV attachment and internalization [1113] . Moreover, simian vimentin and CD151 were considered to play a role in PRRSV infection of MARC-145 cells [14, 15] . However, some links within the detailed mechanism involved in PRRSV replication cycle remain poorly understood.