TY - JOUR
T1 - Proteomic Identification of Potential Target Proteins of Cathepsin W for Its Development as a Drug Target for Influenza
AU - Günther, Sira C.
AU - Martínez-Romero, Carles
AU - Borau, Milagros Sempere
AU - Pham, Christine T.N.
AU - García-Sastre, Adolfo
AU - Stertz, Silke
N1 - Publisher Copyright:
© 2022 Günther et al.
PY - 2022/8
Y1 - 2022/8
N2 - Influenza A virus (IAV) coopts numerous host factors for efficient replication. The cysteine protease cathepsin W (CTSW) has been identified as one host factor required for IAV entry, specifically for the escape of IAVs from late endosomes. However, the substrate specificity of CTSW and the proviral mechanism are thus far unknown. Here, we show that intracellular but not secreted CTSW promotes viral entry. We reveal 79 potential direct and 31 potential indirect cellular target proteins of CTSW using the high-throughput proteomic approach terminal amine isotopic labeling of substrates (TAILS) and determine the cleavage motif shared by the substrates of CTSW. Subsequent integration with data from RNA interference (RNAi) screens for IAV host factors uncovers first insights into the proviral function of CTSW. Notably, CTSW-deficient mice display a 25% increase in survival and a delay in mortality compared to wild-type mice upon IAV infection. Altogether, these findings support the development of drugs targeting CTSW as novel host-directed antiviral therapies.
AB - Influenza A virus (IAV) coopts numerous host factors for efficient replication. The cysteine protease cathepsin W (CTSW) has been identified as one host factor required for IAV entry, specifically for the escape of IAVs from late endosomes. However, the substrate specificity of CTSW and the proviral mechanism are thus far unknown. Here, we show that intracellular but not secreted CTSW promotes viral entry. We reveal 79 potential direct and 31 potential indirect cellular target proteins of CTSW using the high-throughput proteomic approach terminal amine isotopic labeling of substrates (TAILS) and determine the cleavage motif shared by the substrates of CTSW. Subsequent integration with data from RNA interference (RNAi) screens for IAV host factors uncovers first insights into the proviral function of CTSW. Notably, CTSW-deficient mice display a 25% increase in survival and a delay in mortality compared to wild-type mice upon IAV infection. Altogether, these findings support the development of drugs targeting CTSW as novel host-directed antiviral therapies.
KW - CTSW
KW - EPN2
KW - TAILS
KW - cathepsin W
KW - cysteine protease cathepsin W
KW - epsin 2
KW - host-directed antivirals
KW - influenza A virus
KW - influenza virus
KW - terminal amine isotopic labeling of substrates
KW - virus entry
UR - http://www.scopus.com/inward/record.url?scp=85137136403&partnerID=8YFLogxK
U2 - 10.1128/spectrum.00921-22
DO - 10.1128/spectrum.00921-22
M3 - Article
C2 - 35867415
AN - SCOPUS:85137136403
SN - 2165-0497
VL - 10
JO - Microbiology spectrum
JF - Microbiology spectrum
IS - 4
ER -