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Several viruses, including \u003Cjats:italic>Human immunodeficiency virus 1\u003C\u002Fjats:italic> (HIV-1), have developed strategies to evade the NK-cell response. This study was designed to evaluate whether HIV-1 could interfere with the expression of NK cell-activating ligands, specifically the human leukocyte antigen (HLA)-I-like MICA and ULBP molecules that bind NKG2D, an activating receptor expressed by all NK cells. Results show that the HIV-1 Nef protein downmodulates cell-surface expression of MICA, ULBP1 and ULBP2, with a stronger effect on the latter molecule. The activity on MICA and ULBP2 is well conserved in Nef protein variants derived from HIV-1-infected patients. In HIV-1-infected cells, cell-surface expression of NKG2D ligands increased to a higher extent with a Nef-deficient virus compared with wild-type virus. Mutational analysis of Nef showed that NKG2D ligand downmodulation has structural requirements that differ from those of other reported Nef activities, including HLA-I downmodulation. Finally, data demonstrate that Nef expression has functional consequences on NK-cell recognition, causing a decreased susceptibility to NK cell-mediated lysis. These findings provide a novel insight into the mechanisms evolved by HIV-1 to escape from the NK-cell response.\u003C\u002Fjats:p>","\u003Cjats:p>Các tế bào tự nhiên (NK) là thành phần chính trong hệ miễn dịch bẩm sinh của cơ thể chống lại nhiều loại tác nhân gây bệnh khác nhau. Một số virus, bao gồm \u003Cjats:italic>Virus gây suy giảm miễn dịch ở người loại 1\u003C\u002Fjats:italic> (HIV-1), đã phát triển các chiến lược để né tránh phản ứng của tế bào NK. Nghiên cứu này được thiết kế để đánh giá liệu HIV-1 có thể can thiệp vào sự biểu hiện của các ligand kích hoạt tế bào NK hay không, cụ thể là các phân tử human leukocyte antigen (HLA)-I-like MICA và ULBP, mà liên kết với NKG2D, một thụ thể kích hoạt được biểu hiện bởi tất cả các tế bào NK. Kết quả cho thấy rằng protein Nef của HIV-1 đã làm giảm sự biểu hiện trên bề mặt tế bào của MICA, ULBP1 và ULBP2, với tác động mạnh hơn đối với phân tử sau cùng. Hoạt động trên MICA và ULBP2 được bảo tồn tốt trong các biến thể protein Nef từ bệnh nhân nhiễm HIV-1. Ở các tế bào nhiễm HIV-1, sự biểu hiện trên bề mặt tế bào của các ligand NKG2D tăng lên nhiều hơn với virus thiếu Nef so với virus kiểu hoang dã. Phân tích đột biến của Nef cho thấy rằng sự hạ thấp ligand NKG2D có các yêu cầu cấu trúc khác với các hoạt động khác của Nef đã được báo cáo, bao gồm hạ thấp HLA-I. Cuối cùng, dữ liệu cho thấy rằng sự biểu hiện của Nef có những hậu quả chức năng đối với sự nhận diện của tế bào NK, dẫn đến sự giảm độ nhạy cảm với sự ly giải do tế bào NK gây ra. Những phát hiện này cung cấp cái nhìn mới về các cơ chế mà HIV-1 đã phát triển để thoát khỏi phản ứng của tế bào NK.\u003C\u002Fjats:p>",{"EN":1736,"VI":1737},"Human immunodeficiency virus 1 Nef protein downmodulates the ligands of the activating receptor NKG2D and inhibits natural killer cell-mediated cytotoxicity","Protein Nef của virus gây suy giảm miễn dịch ở người 1 hạ thấp các ligand của thụ thể kích hoạt NKG2D và ức chế sự tiêu diệt của tế bào tự nhiên (NK)",{"VOID":1739},"17170457",{"VOID":1741},"10.1099\u002Fvir.0.82125-0",[110],[1744],"VI","https:\u002F\u002Fwww.microbiologyresearch.org\u002Fcontent\u002Fjournal\u002Fjgv\u002F10.1099\u002Fvir.0.82125-0",[1747,1766,1785,1802,1819,1836,1861,1878],{"id":1748,"sortIndex":25,"researcher":24,"roles":1749,"affiliations":1750,"properties":1759,"displayName":1763,"givenName":24,"familyName":24},"b59fce20-baae-495f-ab45-696464130f6e",[],[1751],{"id":1752,"sortIndex":25,"affiliation":1753,"properties":24},"15f1c221-8851-433d-98c4-e0bd878e0c24",{"id":1752,"createTime":24,"updateTime":24,"relativeEntities":1754,"slug":24,"properties":1755,"entityType":24,"verifyStatus":24,"verifyTime":24,"verifyNote":24,"languages":24,"translateLanguages":24,"viewCount":24,"url":24,"parentIds":1758,"statistic":24},[],{"title":1756},{"EN":1757},"Department of Experimental Medicine and Pathology, Istituto Pasteur-Fondazione Cenci Bolognetti, University La Sapienza, 00161 Rome, Italy",[],{"orcid":1760,"title":1762,"openalex":1764},{"VOID":1761},"https:\u002F\u002Forcid.org\u002F0000-0002-0371-9534",{"EN":1763},"Cristina Cerboni",{"VOID":1765},"A5059669297",{"id":1767,"sortIndex":132,"researcher":24,"roles":1768,"affiliations":1769,"properties":1778,"displayName":1782,"givenName":24,"familyName":24},"794806a2-edd5-4022-b933-0674031121df",[],[1770],{"id":1771,"sortIndex":25,"affiliation":1772,"properties":24},"039bf545-6b5e-4fdb-9991-f5860b4b4fb9",{"id":1771,"createTime":24,"updateTime":24,"relativeEntities":1773,"slug":24,"properties":1774,"entityType":24,"verifyStatus":24,"verifyTime":24,"verifyNote":24,"languages":24,"translateLanguages":24,"viewCount":24,"url":24,"parentIds":1777,"statistic":24},[],{"title":1775},{"EN":1776},"Division of Immunology and Infectious Disease, Children's Hospital Bambino Gesù, Piazza S. 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10.1128\u002FJVI.77.21.11536-11545.2003",{"doi":1974},"10.1128\u002FJVI.77.21.11536-11545.2003",{"id":24,"text":1976,"url":24,"identifiers":1977},"Cerboni, 2001, Synergistic effect of IFN-gamma and human cytomegalovirus protein UL40 in the HLA-E-dependent protection from NK cell-mediated cytotoxicity, Eur J Immunol, 31, 2926, 10.1002\u002F1521-4141(2001010)31:10\u003C2926::AID-IMMU2926>3.0.CO;2-2",{"doi":1978},"10.1002\u002F1521-4141(2001010)31:10\u003C2926::AID-IMMU2926>3.0.CO;2-2",{"id":24,"text":1980,"url":24,"identifiers":1981},"Chalupny, 2003, ULBP4 is a novel ligand for human NKG2D, Biochem Biophys Res Commun, 305, 129, 10.1016\u002FS0006-291X(03)00714-9",{"doi":1982},"10.1016\u002FS0006-291X(03)00714-9",{"id":24,"text":1984,"url":24,"identifiers":1985},"Chowers, 1994, Optimal infectivity in vitro of human immunodeficiency virus type 1 requires an intact nef gene, J Virol, 68, 2906, 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structure of an attenuated quasi species of HIV-1 from a blood transfusion donor and recipients, Science, 270, 988, 10.1126\u002Fscience.270.5238.988",{"doi":2002},"10.1126\u002Fscience.270.5238.988",{"id":24,"text":2004,"url":24,"identifiers":2005},"Doms, 2000, The plasma membrane as a combat zone in the HIV battlefield, Genes Dev, 14, 2677, 10.1101\u002Fgad.833300",{"doi":2006},"10.1101\u002Fgad.833300",{"id":24,"text":2008,"url":24,"identifiers":2009},"Eger, 2004, Perturbation of natural killer cell function and receptors during HIV infection, Trends Microbiol, 12, 301, 10.1016\u002Fj.tim.2004.05.006",{"doi":2010},"10.1016\u002Fj.tim.2004.05.006",{"id":24,"text":2012,"url":24,"identifiers":2013},"Gasser, 2005, The DNA damage pathway regulates innate immune system ligands of the NKG2D receptor, Nature, 436, 1186, 10.1038\u002Fnature03884",{"doi":2014},"10.1038\u002Fnature03884",{"id":24,"text":2016,"url":24,"identifiers":2017},"Gervaix, 1997, A new reporter cell line to monitor HIV infection and drug susceptibility in vitro, Proc Natl Acad Sci U S A, 94, 4653, 10.1073\u002Fpnas.94.9.4653",{"doi":2018},"10.1073\u002Fpnas.94.9.4653",{"id":24,"text":2020,"url":24,"identifiers":2021},"Geyer, 2001, Structure–function relationships in HIV-1 Nef, EMBO Rep, 2, 580, 10.1093\u002Fembo-reports\u002Fkve141",{"doi":2022},"10.1093\u002Fembo-reports\u002Fkve141",{"id":24,"text":2024,"url":24,"identifiers":2025},"Groh, 2002, Tumour-derived soluble MIC ligands impair expression of NKG2D and T-cell activation, Nature, 419, 734, 10.1038\u002Fnature01112",{"doi":2026},"10.1038\u002Fnature01112",{"id":24,"text":2028,"url":24,"identifiers":2029},"Grzesiek, 1996, The CD4 determinant for downregulation by HIV-1 Nef directly binds to Nef. Mapping of the Nef binding surface by NMR, Biochemistry, 35, 10256, 10.1021\u002Fbi9611164",{"doi":2030},"10.1021\u002Fbi9611164",{"id":24,"text":2032,"url":24,"identifiers":2033},"Hanna, 1998, Nef harbors a major determinant of pathogenicity for an AIDS-like disease induced by HIV-1 in transgenic mice, Cell, 95, 163, 10.1016\u002FS0092-8674(00)81748-1",{"doi":2034},"10.1016\u002FS0092-8674(00)81748-1",{"id":24,"text":2036,"url":24,"identifiers":2037},"Kirchhoff, 1995, Brief report: absence of intact nef sequences in a long-term survivor with nonprogressive HIV-1 infection, N Engl J Med, 332, 228, 10.1056\u002FNEJM199501263320405",{"doi":2038},"10.1056\u002FNEJM199501263320405",{"id":24,"text":2040,"url":24,"identifiers":2041},"Lanier, 2005, NK cell recognition, Annu Rev Immunol, 23, 225, 10.1146\u002Fannurev.immunol.23.021704.115526",{"doi":2042},"10.1146\u002Fannurev.immunol.23.021704.115526",{"id":24,"text":2044,"url":24,"identifiers":2045},"Le Gall, 1998, Nef interacts with the mu subunit of clathrin adaptor complexes and reveals a cryptic sorting signal in MHC I molecules, Immunity, 8, 483, 10.1016\u002FS1074-7613(00)80553-1",{"doi":2046},"10.1016\u002FS1074-7613(00)80553-1",{"id":24,"text":2048,"url":24,"identifiers":2049},"Liu, 2001, HIV Nef-mediated cellular phenotypes are differentially expressed as a function of intracellular Nef concentrations, J Biol Chem, 276, 32763, 10.1074\u002Fjbc.M101025200",{"doi":2050},"10.1074\u002Fjbc.M101025200",{"id":24,"text":2052,"url":24,"identifiers":2053},"Lodoen, 2005, Viral modulation of NK cell immunity, Nat Rev Microbiol, 3, 59, 10.1038\u002Fnrmicro1066",{"doi":2054},"10.1038\u002Fnrmicro1066",{"id":24,"text":2056,"url":24,"identifiers":2057},"Maier, 2000, Kinetics of CXCR4 and CCR5 up-regulation and human immunodeficiency virus expansion after antigenic stimulation of primary CD4(+) T lymphocytes, Blood, 96, 1853, 10.1182\u002Fblood.V96.5.1853",{"doi":2058},"10.1182\u002Fblood.V96.5.1853",{"id":24,"text":2060,"url":24,"identifiers":2061},"McMichael, 1998, T cell responses and viral escape, Cell, 93, 673, 10.1016\u002FS0092-8674(00)81428-2",{"doi":2062},"10.1016\u002FS0092-8674(00)81428-2",{"id":24,"text":2064,"url":24,"identifiers":2065},"Pende, 2001, Role of NKG2D in tumor cell lysis mediated by human NK cells: cooperation with natural cytotoxicity receptors and capability of recognizing tumors of nonepithelial origin, Eur J Immunol, 31, 1076, 10.1002\u002F1521-4141(200104)31:4\u003C1076::AID-IMMU1076>3.0.CO;2-Y",{"doi":2066},"10.1002\u002F1521-4141(200104)31:4\u003C1076::AID-IMMU1076>3.0.CO;2-Y",{"id":24,"text":2068,"url":24,"identifiers":2069},"Peterlin, 2003, Hide, shield and strike back: how HIV-infected cells avoid immune eradication, Nat Rev Immunol, 3, 97, 10.1038\u002Fnri998",{"doi":2070},"10.1038\u002Fnri998",{"id":24,"text":2072,"url":24,"identifiers":2073},"Pross, 1986, Assay for NK cell cytotoxicity – their values and pitfalls, In Immunobiology of Natural Killer Cells, 2",{},{"id":24,"text":2075,"url":24,"identifiers":2076},"Raulet, 2003, Roles of the NKG2D immunoreceptor and its ligands, Nat Rev Immunol, 3, 781, 10.1038\u002Fnri1199",{"doi":2077},"10.1038\u002Fnri1199",{"id":24,"text":2079,"url":24,"identifiers":2080},"Robertson, 1996, Characterization of a cell line, NKL, derived from an aggressive human natural killer cell leukemia, Exp Hematol, 24, 406",{},{"id":24,"text":2082,"url":24,"identifiers":2083},"Rölle, 2003, Effects of human cytomegalovirus infection on ligands for the activating NKG2D receptor of NK cells: up-regulation of UL16-binding protein (ULBP)1 and ULBP2 is counteracted by the viral UL16 protein, J Immunol, 171, 902, 10.4049\u002Fjimmunol.171.2.902",{"doi":2084},"10.4049\u002Fjimmunol.171.2.902",{"id":24,"text":2086,"url":24,"identifiers":2087},"Salih, 2003, Functional expression and release of ligands for the activating immunoreceptor NKG2D in leukemia, Blood, 102, 1389, 10.1182\u002Fblood-2003-01-0019",{"doi":2088},"10.1182\u002Fblood-2003-01-0019",{"id":24,"text":2090,"url":24,"identifiers":2091},"Schrager, 1999, HIV-1 Nef increases T cell activation in a stimulus-dependent manner, Proc Natl Acad Sci U S A, 96, 8167, 10.1073\u002Fpnas.96.14.8167",{"doi":2092},"10.1073\u002Fpnas.96.14.8167",{"id":24,"text":2094,"url":24,"identifiers":2095},"Schwartz, 1993, Reduced cell surface expression of processed human immunodeficiency virus type 1 envelope glycoprotein in the presence of Nef, J Virol, 67, 3274, 10.1128\u002FJVI.67.6.3274-3280.1993",{"doi":2096},"10.1128\u002FJVI.67.6.3274-3280.1993",{"id":24,"text":2098,"url":24,"identifiers":2099},"Welte, 2003, Selective intracellular retention of virally induced NKG2D ligands by the human cytomegalovirus UL16 glycoprotein, Eur J Immunol, 33, 194, 10.1002\u002Fimmu.200390022",{"doi":2100},"10.1002\u002Fimmu.200390022",{"id":2102,"createTime":2103,"updateTime":2104,"relativeEntities":2105,"slug":2106,"properties":2107,"entityType":106,"verifyStatus":107,"verifyTime":2103,"verifyNote":108,"languages":2124,"translateLanguages":2125,"viewCount":25,"primaryUrl":2126,"fullTextUrl":24,"authors":2127,"publicationType":182,"publisherRelationship":2315,"citationCount":2360,"citationInfo":2361,"publishDate":2365,"publishYear":608,"citationAnalyzeStatus":23,"lastCitationAnalyze":24,"indexDatabases":2366,"openAccess":24,"references":2367,"isForceReanalyzing":243},"2a914678-48e3-408d-b05a-5adda8de6508","2025-02-02T07:11:01.688+00:00","2025-02-09T17:12:24.313+00:00",[],"Analysis-of-ACE2-in-polarized-epithelial-cells-surface-expression-and-function-as-receptor-for-severe-acute-respiratory-syndrome-associated-coronavirus",{"mag":2108,"keywords":2110,"openalex":2112,"abstract":2114,"title":2117,"pm":2120,"doi":2122},{"VOID":2109},"2111334411",{"VI":2111},"SARS-CoV, ACE2, tế bào biểu mô phân cực, đường hô hấp, nhiễm virus",{"VOID":2113},"W2111334411",{"EN":2115,"VI":2116},"\u003Cjats:p>The primary target of severe acute respiratory syndrome-associated coronavirus (SARS-CoV) is epithelial cells in the respiratory and intestinal tract. The cellular receptor for SARS-CoV, angiotensin-converting enzyme 2 (ACE2), has been shown to be localized on the apical plasma membrane of polarized respiratory epithelial cells and to mediate infection from the apical side of these cells. Here, these results were confirmed and extended by including a colon carcinoma cell line (Caco-2), a lung carcinoma cell line (Calu-3) and Vero E6 cells in our analysis. All three cell types expressed human ACE2 on the apical membrane domain and were infected via this route, as determined with vesicular stomatitis virus pseudotypes containing the S protein of SARS-CoV. In a histological analysis of the respiratory tract, ACE2 was detected in the trachea, main bronchus and alveoli, and occasionally also in the small bronchi. These data will help us to understand the pathogenesis of SARS-CoV infection.\u003C\u002Fjats:p>","\u003Cjats:p>Đích chính của virus corona gây hội chứng hô hấp cấp tính nặng (SARS-CoV) là các tế bào biểu mô trong đường hô hấp và đường ruột. Thụ thể tế bào cho SARS-CoV, enzyme chuyển đổi angiotensin 2 (ACE2), đã được chứng minh là nằm trên màng tế bào bề mặt của các tế bào biểu mô hô hấp phân cực và có vai trò trung gian trong nhiễm trùng từ phía bề mặt của các tế bào này. Tại đây, các kết quả này đã được xác nhận và mở rộng bằng cách bao gồm một dòng tế bào ung thư đại tràng (Caco-2), một dòng tế bào ung thư phổi (Calu-3) và tế bào Vero E6 trong phân tích của chúng tôi. Cả ba loại tế bào đều biểu hiện ACE2 của người trên miền màng bề mặt và bị nhiễm qua con đường này, như đã được xác định với các kiểu virus giả thể viêm miệng có chứa protein S của SARS-CoV. Trong một phân tích mô học của đường hô hấp, ACE2 được phát hiện trong khí quản, phế quản chính và phế nang, và thỉnh thoảng cũng thấy trong các phế quản nhỏ. Dữ liệu này sẽ giúp chúng tôi hiểu rõ hơn về cách phát sinh bệnh của nhiễm SARS-CoV.\u003C\u002Fjats:p>",{"EN":2118,"VI":2119},"Analysis of ACE2 in polarized epithelial cells: surface expression and function as receptor for severe acute respiratory syndrome-associated coronavirus","Phân tích ACE2 trong các tế bào biểu mô phân cực: sự biểu hiện bề mặt và chức năng như là thụ thể cho virus corona gây hội chứng hô hấp cấp tính nặng",{"VOID":2121},"16690935",{"VOID":2123},"10.1099\u002Fvir.0.81749-0",[110],[1744],"https:\u002F\u002Fwww.microbiologyresearch.org\u002Fcontent\u002Fjournal\u002Fjgv\u002F10.1099\u002Fvir.0.81749-0",[2128,2147,2162,2179,2196,2211,2230,2247,2264,2281,2298],{"id":2129,"sortIndex":25,"researcher":24,"roles":2130,"affiliations":2131,"properties":2140,"displayName":2144,"givenName":24,"familyName":24},"b43a255c-b1f1-464d-90e4-042f96975825",[],[2132],{"id":2133,"sortIndex":25,"affiliation":2134,"properties":24},"e30e4a9e-4793-42d1-890e-3de845eac088",{"id":2133,"createTime":24,"updateTime":24,"relativeEntities":2135,"slug":24,"properties":2136,"entityType":24,"verifyStatus":24,"verifyTime":24,"verifyNote":24,"languages":24,"translateLanguages":24,"viewCount":24,"url":24,"parentIds":2139,"statistic":24},[],{"title":2137},{"VI":2138},"Institut für Virologie, Tierärztliche Hochschule Hannover, Bünteweg 17, D-30559 Hannover, 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