Skip to main content
. 2022 May 3;13:842453. doi: 10.3389/fimmu.2022.842453

Table 2.

Roles of pulmonary surfactant components in viral infection.

Name Function
SP-A SP-A prevents influenza infection by occupying the HA binding site (38). SP-A limits RSV infection by binding the F and G protein (39). SP-A limits coronavirus infection by binding HCoV-229E virions (40). SP-A can neutralize SARS-CoV-2 through interaction with the S protein (41). SP-A mediates the phagocytosis of human papillomavirus 16 (HPV16) pseudovirions (42) and herpes simplex virus (HSV) in the host.
SP-D SP-D can neutralize influenza virus through occupying the HA binding site (43). SP-D limits RSV infection by interacting with virus through attachment to the F and G proteins (44). SP-D limits coronavirus infection by binding HCoV-229E virions (40). SP-D limits SARS coronavirus by binding to the heavily glycosylated S protein (45). SP-D can neutralize SARS-CoV-2 through interaction with the S protein (41). rfhSP-D can compete with ACE-2 for binding to the S1 spike protein subunit of SARS-CoV-2 (16). SP-A can restrict HIV infection via binding to glycoprotein (gp)120 (46).
PC DPPC can promote adenoviral entry into epithelial cells by binding the virus (47).
PS PS can promote poxvirus infectivity (48), through apoptotic cell mimicry (49).
PG 1-Palmitoyl-2-oleoyl-sn-glycero-3-phosphatidylglycerol (POPG) can suppress RSV infection by binding to RSV with high affinity (50, 51). POPG can block influenza virus replication through inhibiting the attachment of influenza (52).
PI PI can prevent RSV infection by preventing virus attachment to epithelial cells (53, 54). PI can reduce influenza propagation by binding to the virus with high affinity (54, 55).1-stearoyl-2-arachidonoyl-PI can defend against dengue virus infection (47).
PE PE was required for the replication of a (+)RNA virus, such as tomato bushy stunt virus, hepatitis C virus, dengue virus, and West Nile virus (WNV) (56). RNA virus replication depends on PE enrichment at replication sites in subcellular membranes (57).
Cholesterol Cholesterol promotes entry of many viruses into host cells (58), such as SARS-CoV (59), murine coronavirus (60), porcine deltacoronavirus (61), infectious bronchitis virus (62), Hepatitis C virus (63), Ebola virus (64), influenza (65), and so on.