【文章內(nèi)容簡介】 改變 ? 信號途徑 ? DNA復制 ? 轉(zhuǎn)錄 ? 翻譯 ? 細胞膜改變 ? 包涵體 ? 細胞骨架改變 ? 細胞死亡 ? 細胞周期抑制 ? 細胞融合 ? 細胞轉(zhuǎn)化 ? 穩(wěn)定狀態(tài)感染 Cell structure changes ?病毒誘導的細胞膜結(jié)構(gòu)改變（ Virusinduced alterations in cellular membrances） ? 封閉和下調(diào)細胞表面的病毒受體 ? 調(diào)節(jié) MHC 的表達 ? 病毒蛋白質(zhì)發(fā)揮離子通道的功能 ? Vpu, Nef and Vpu prevent cell surface expression of CD4 by different mechanisms. The viral glycoprotein Env (gray) binds to the cellular receptor CD4 (green) during transport in the ER. Vpu also binds to CD4 in the ER and targets it for degradation (green fragments) by recruitment to the ubiquitinproteasome pathway through interactions with bTrCP and Skp1p. Nef removes preexisting CD4 from the cell surface by recruiting CD4 into clathrincoated pits, and ultimately into degradative lysosomes, through interactions with the AP2 adaptor plex. ? Science 1998,280:18801884. The MHC class I antigen presentation pathway. Immunology 2022,110:163169. ? Viral inhibition of the MHC class I antigen presentation pathway. Immunology 2022,110:163169. HCMV US2,3,6,10,11 HSV ICP47 Adenovirus E19 HHV7 U21 HHV8 K3, K5 HIV1 Nef Influenza A Virus M2 protein as proton transporter. M2TM exists in two conformational ensembles. In the OpenoutClosedin conformation the Val27 gate is open and the His37 gate is closed whereas the reverse is true for ClosedoutOpenin conformation. At high pH out, the OpenoutClosedin conformation is favored, because pH out decreases the His37 residues get protonated and channel is activated at Kact favoring the ClosedoutOpenin conformation. Release of protons into the viral interior and deprotonation of His37 stabilizes the OpenoutClosedin conformation and the cycle is repeated until equilibration. PNAS 2022, 106(4):106974. Cell structure changes ?包涵體（ Inclusion body） Inclusion bodies are nuclear or cytoplasmic aggregates of stainable substances, usually proteins. They typically represent sites of viral multiplication in a bacterium or a eukaryotic cell and usually consist of viral capsid proteins. Rabies: Negri bodies HSV, VZV： Cowdry bodies Cell structure changes ? 細胞骨架 The main cytoskeleton ponents participating to host cell/virus interaction。 in white, cytoskeletonperturbating agents able to interfere with viral infection, and, in green, the main viral proteins involved in HIV–host cell interaction. Cell Death Differ 2022,13(5):876. gp120induced polarization of T cells. After gp120 binding, CD4+ T cells undergo cytoskeletondriven polarization of CD95 and ezrin and CD95/ezrin molecular association (see boxed area showing ezrinCD95/Fas coimmunoprecipitation), resulting in an increased susceptibility to Fasmediated apoptosis. Cell Death Differ 2022,13(5):876. ? 分子水平變化 ? 細胞結(jié)構(gòu)改變 ? 細胞表型改變 ? 信號途徑 ? DNA復制 ? 轉(zhuǎn)錄 ? 翻譯 ? 細胞膜改變 ? 包涵體 ? 細胞骨架改變 ? 細胞死亡 ? 細胞周期抑制 ? 細胞融合 ? 細胞轉(zhuǎn)化 ? 穩(wěn)定狀態(tài)感染 Virusinduced cytopathology 病毒增殖性復制不一定摧毀宿主細胞 。 病毒復制沒有完成也可以引起細胞病變效應(yīng)。 ? 病毒誘導的細胞死亡 : ? 凋亡（ apoptosis） ? 壞死（ necrosis） Virusinduced cell death: apoptosis and necrosis ?Cells may die through two pathways, necrosis or apoptosis. ?Some viral proteins act directly to induce apoptosis while others act indirectly, by neutralizing the effect of a host cell protein that blocks apoptosis. ?Some virus proteins can block the apoptosis pathway, leading to prolonged cell life and increasing the yie