TY - JOUR
T1 - Genome-wide CRISPR screen for HSV-1 host factors reveals PAPSS1 contributes to heparan sulfate synthesis
AU - Suzuki, Takeshi
AU - Sato, Yoshitaka
AU - Okuno, Yusuke
AU - Goshima, Fumi
AU - Mikami, Tadahisa
AU - Umeda, Miki
AU - Murata, Takayuki
AU - Watanabe, Takahiro
AU - Watashi, Koichi
AU - Wakita, Takaji
AU - Kitagawa, Hiroshi
AU - Kimura, Hiroshi
N1 - Funding Information:
The authors thank Christoph Seeger (Fox Chase Cancer Center, USA) for HepAD38 cells; Hiroyuki Miyoshi (RIKEN, Japan), Feng Zhang (Broad Institute, USA), Dider Trono (Ecole Polytechnique Federale de Lausanne, Switzerland), Yasuo Ariumi (Kumamoto University, Japan), and Bob Weinberg (Whitehead Institute for Biomedical Research, USA) for plasmids; Tetsuya Okajima and Yasuyuki Miyake (Nagoya University Graduate School of Medicine, Japan) for valuable discussion; Ken Sago, Daisuke Sasaki, Sho Suzuki, and Tomoko Kunogi (Nagoya University Graduate School of Medicine, Japan) for technical assistance; and the Division for Medical Research Engineering at the Nagoya University Graduate School of Medicine for FACS analysis. This work was supported in part by grants from the Japan Society for the Promotion of Science (JSPS) KAKENHI ( https://www.jsps.go.jp ) (Grant Numbers JP16H06231 to Y.S., JP19H04829 to Y.S., JP21K15448 to Y.S., JP20K06551 to T.Mikami, JP20H03386 to H.Kitagawa; and JP20H03493 to H.Kimura); the JST ( https://www.jst.go.jp ) PRESTO (Grant Number JPMJPR19H5) to Y.S.; the Japan Agency for Medical Research and Development (AMED, https://www.amed.go.jp ) (JP19jk0210023 to Y.S., JP21wm035042 to Y.S., JP19ck0106517 to Y.O., and JP20wm0325012 to T.Murata); the Takeda Science Foundation ( https://www.takeda-sci.or.jp ) to Y.S., Y.O., and T.Murata; the Hori Sciences and Arts Foundation ( https://www.hori-foundation.or.jp ) to Y.S., T.Murata, and H.Kimura; the MSD Life Science Foundation ( https://www.msd-life-science-foundation.or.jp ) to Y.S.; the Aichi Health Promotion Foundation ( https://ahpf.or.jp ) to T.S.; and the Uehara Memorial Foundation ( https://www.ueharazaidan.or.jp/ ) to H. Kimura; and the Chemo-Sero-Therapeutic Research Institute ( https://www.kaketsuken.org ) to H.Kimura. TS is supported by the Takeda Science Foundation scholarship. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.
Funding Information:
The authors thank Christoph Seeger (Fox Chase Cancer Center, USA) for HepAD38 cells; Hiroyuki Miyoshi (RIKEN, Japan), Feng Zhang (Broad Institute, USA), Dider Trono (Ecole Polytechnique Federale de Lausanne, Switzerland), Yasuo Ariumi (Kumamoto University, Japan), and Bob Weinberg (Whitehead Institute for Biomedical Research, USA) for plasmids; Tetsuya Okajima and Yasuyuki Miyake (Nagoya University Graduate School of Medicine, Japan) for valuable discussion; Ken Sago, Daisuke Sasaki, Sho Suzuki, and Tomoko Kunogi (Nagoya University Graduate School of Medicine, Japan) for technical assistance; and the Division for Medical Research Engineering at the Nagoya University Graduate School of Medicine for FACS analysis. This work was supported in part by grants from the Japan Society for the Promotion of Science (JSPS) KAKENHI (https://www.jsps.go.jp) (Grant Numbers JP16H06231 to Y.S., JP19H04829 to Y.S., JP21K15448 to Y.S., JP20K06551 to T.Mikami, JP20H03386 to H.Kitagawa; and JP20H03493 to H.Kimura); the JST (https://www.jst.go.jp) PRESTO (Grant Number JPMJPR19H5) to Y.S.; the Japan Agency for Medical Research and Development (AMED, https://www.amed.go.jp) (JP19jk0210023 to Y.S., JP21wm035042 to Y.S., JP19ck0106517 to Y.O., and JP20wm0325012 to T.Murata); the Takeda Science Foundation (https://www.takeda-sci.or.jp) to Y.S., Y.O., and T.Murata; the Hori Sciences and Arts Foundation (https://www.hori-foundation.or.jp) to Y.S., T.Murata, and H.Kimura; the MSD Life Science Foundation (https://www.msd-life-science-foundation.or.jp) to Y.S.; the Aichi Health Promotion Foundation (https://ahpf.or.jp) to T.S.; and the Uehara Memorial Foundation (https://www.ueharazaidan.or.jp/) to H. Kimura; and the Chemo-Sero-Therapeutic Research Institute (https://www.kaketsuken.org) to H.Kimura. TS is supported by the Takeda Science Foundation scholarship. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.
Publisher Copyright:
© 2022, The Author(s).
PY - 2022/12
Y1 - 2022/12
N2 - Herpes simplex virus type 1 (HSV-1) is a ubiquitous pathogen that causes various diseases in humans, ranging from common mucocutaneous lesions to severe life-threatening encephalitis. However, our understanding of the interaction between HSV-1 and human host factors remains incomplete. Here, to identify the host factors for HSV-1 infection, we performed a human genome-wide CRISPR screen using near-haploid HAP1 cells, in which gene knockout (KO) could be efficiently achieved. Along with several already known host factors, we identified 3′-phosphoadenosine 5′-phosphosulfate synthase 1 (PAPSS1) as a host factor for HSV-1 infection. The KO of PAPSS1 in HAP1 cells reduced heparan sulfate (HepS) expression, consequently diminishing the binding of HSV-1 and several other HepS-dependent viruses (such as HSV-2, hepatitis B virus, and a human seasonal coronavirus). Hence, our findings provide further insights into the host factor requirements for HSV-1 infection and HepS biosynthesis.
AB - Herpes simplex virus type 1 (HSV-1) is a ubiquitous pathogen that causes various diseases in humans, ranging from common mucocutaneous lesions to severe life-threatening encephalitis. However, our understanding of the interaction between HSV-1 and human host factors remains incomplete. Here, to identify the host factors for HSV-1 infection, we performed a human genome-wide CRISPR screen using near-haploid HAP1 cells, in which gene knockout (KO) could be efficiently achieved. Along with several already known host factors, we identified 3′-phosphoadenosine 5′-phosphosulfate synthase 1 (PAPSS1) as a host factor for HSV-1 infection. The KO of PAPSS1 in HAP1 cells reduced heparan sulfate (HepS) expression, consequently diminishing the binding of HSV-1 and several other HepS-dependent viruses (such as HSV-2, hepatitis B virus, and a human seasonal coronavirus). Hence, our findings provide further insights into the host factor requirements for HSV-1 infection and HepS biosynthesis.
UR - http://www.scopus.com/inward/record.url?scp=85134362271&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=85134362271&partnerID=8YFLogxK
U2 - 10.1038/s42003-022-03581-9
DO - 10.1038/s42003-022-03581-9
M3 - Article
C2 - 35854076
AN - SCOPUS:85134362271
VL - 5
JO - Communications Biology
JF - Communications Biology
SN - 2399-3642
IS - 1
M1 - 694
ER -