title: Persistent infection of SARS coronavirus in colonic cells in vitro.
abstract: Severe acute respiratory syndrome coronavirus (SARS-CoV) can produce gastrointestinal symptoms. The intestinal tract is the only extrapulmonary site where viable viruses have been detected. This study examined seven established human intestinal cell lines, DLD-1, HCT-116, HT-29, LoVo, LS-180, SW-480 and SW-620, for their permissiveness to SARS-CoV infection. The results showed that only LoVo cells were permissive to SARS-CoV infection as evident by positive findings from indirect immunofluorescence staining for intracellular viral antigens, in situ hybridization for intracellular viral RNA, and electron microscopy for intracellular viral particles. In contrast to Vero cells, SARS-CoV did not produce cytopathic effects on LoVo cells. However, LoVo cells were found to be highly permissive for productive infection with a high viral titre (>3 x 10(7) viral copies/ml) produced in culture supernatant following a few days of incubation. SARS-CoV established a stable persistent chronic infection that could be maintained after multiple passages. Being a cell line of human origin, LoVo cells could be a useful in vitro model for studying the biology and persistent infection of SARS-CoV. Our results on the expression of angiotensin-converting enzyme 2 (ACE2), a recently identified cellular receptor for SARS-CoV, in these cell lines indicated that it might not be the sole determinant for cells to be susceptible to SARS-CoV infection.
authors.affiliation: Centre for Emerging Infectious Diseases, and Department of Microbiology, The Chinese University of Hong Kong, Prince of Wales Hospital, Shatin, New Territories, Hong Kong SAR, China. paulkschan@cuhk.edu.hk
authors.forename: Paul K S
authors.initials: PK
authors.lastname: Chan
authors.forename: Ka-Fai
authors.initials: KF
authors.lastname: To
authors.forename: Anthony W I
authors.initials: AW
authors.lastname: Lo
authors.forename: Jo L K
authors.initials: JL
authors.lastname: Cheung
authors.forename: Ida
authors.initials: I
authors.lastname: Chu
authors.forename: Florence W L
authors.initials: FW
authors.lastname: Au
authors.forename: Joanna H M
authors.initials: JH
authors.lastname: Tong
authors.forename: John S
authors.initials: JS
authors.lastname: Tam
authors.forename: Joseph J Y
authors.initials: JJ
authors.lastname: Sung
authors.forename: Ho-Keung
authors.initials: HK
authors.lastname: Ng
mesh_terms: D000085962:Angiotensin-Converting Enzyme 2; D000956:Antigens, Viral / Q000032:analysis / Q000276:immunology; D002268:Carboxypeptidases / Q000096:biosynthesis / Q000378:metabolism; D045744:Cell Line, Tumor; D003106:Colon / Q000166:cytology / Q000821:virology*; D015179:Colorectal Neoplasms; D003588:Cytopathogenic Effect, Viral; D003593:Cytoplasm / Q000737:chemistry / Q000821:virology; D019084:Fluorescent Antibody Technique, Indirect; D006801:Humans; D017403:In Situ Hybridization; D008854:Microscopy, Electron; D007703:Peptidyl-Dipeptidase A; D012367:RNA, Viral / Q000032:analysis; D011991:Receptors, Virus; D020133:Reverse Transcriptase Polymerase Chain Reaction; D045473:Severe acute respiratory syndrome-related coronavirus / Q000254:growth & development* / Q000276:immunology
chemical_list: D000956:Antigens, Viral; D012367:RNA, Viral; D011991:Receptors, Virus; D002268:Carboxypeptidases; D007703:Peptidyl-Dipeptidase A; C000705307:ACE2 protein, human; D000085962:Angiotensin-Converting Enzyme 2