医生你好，我想请问你“人免疫缺陷病毒抗体1+2型（HIV）”这个项目的检查_百度拇指医生
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问医生你好，我想请问你“人免疫缺陷病毒抗体1+2型（HIV）”这个项目的检查
病情描述(发病时间、主要症状等)：医生你好，我想请问你“人免疫缺陷病毒抗体1+2型（HIV）”这个项目的检查，包含了艾滋和梅毒了吗？梅毒还需要另外检查吗？
病情分析：意见建议：你好，这个只能化验艾滋，梅毒需要另外检查即可
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> 人类免疫缺陷病毒2型抗体（艾滋病病毒）
人类免疫缺陷病毒2型抗体（艾滋病病毒）
参考报价：
&1元 RMB (人民币)
&0.2ml/200μg
信息完整度：
英文名称：
&Anti-HIV2 gp36
供货周期：
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名　称： 上海基免实业有限公司
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人类免疫缺陷病毒2型抗体（艾滋病病毒）英文名称 &Anti-HIV2 gp36&中文名称 &人类免疫缺陷病毒2型抗体（艾滋病病毒）&别 & &名 &Gp36; HIV-2 gp36; HIV2 gp36; HIV2gp36; gp36; HIV 2; Human immunodeficiency virus 2; Human Immunodeficiency Virus Type 2; ENV_HV2RO.&浓 & &度 &1mg/1ml&规 格 &0.1ml/100μg &0.2ml/200μg & &&纯化的抗体可通过不同的途径获取，有些人类免疫缺陷病毒2型抗体（艾滋病病毒）可通过下述方法制备或从商家购买。从商家购买的抗体，通常附有正确的储存方法。1）工作液应在4℃下融化并存放，可能稳定达数月。2）如果没有特殊原因而避免使用叠氮钠，亦可加入叠氮钠，浓度为0．02％。将纯化的抗体样本分装成合适的体积，于-20℃保存。3）纯化的抗体溶液应以较高的浓度(如lmg／m1)在中性pH下保存。：常用的抗体储存浓度高达l0mg/ml。较低浓度的抗体冻存前应浓缩。所有标准的浓缩方法(如超滤法)，皆可使用。还有一个简单的方法是用蛋白A或蛋白G亲和柱来浓缩溶液。如果纯化的抗体不是用于标记，可将它们以较低浓度储存于加有1％BSA的溶液中。4）经纯化制备的抗体在常用的缓冲液中是稳定的。其DH应保持在中性左右。如果pH在7-8之间，即使保存多年，对抗体也无损害。多数情况下，盐浓度适于保持在0-150mmol/L之间，但在长期存放的抗体中，盐溶液浓度高达500mmol/L时，对人类免疫缺陷病毒2型抗体（艾滋病病毒）能有损害。如果没有其他说明．律议用PBS或50mmol/LTris(DH8．0)溶液长期存放抗体。 &抗体来源 &Rabbit &克隆类型 &polyclonal&交叉反应 &HIV2 &产品类型 &一抗 & &研究领域 &细胞生物 免疫学 细菌及病毒 &蛋白分子量 &predicted molecular weight: 43/92kDa&性 & &状 &Lyophilized or Liquid&免 疫 原 &KLH conjugated synthetic peptide derived from HIV2 gp36&亚 & &型 &IgG&纯化方法 &affinity purified by Protein A&储 存 液 &Preservative: 15mM Sodium Azide, Constituents: 1% BSA, 0.01M PBS, pH 7.4&产品应用 & WB=1:100-500 &ELISA=1:500-1000 &IP=1:20-100 &IHC-P=1:100-500 &IHC-F=1:100-500 &IF=1:100-500&（石蜡切片需做抗原修复）&&not yet tested in other applications.&optimal dilutions/concentrations should be determined by the end user. &保存条件 &Store at -20 °C for one year. Avoid repeated freeze/thaw cycles. The lyophilized antibody is stable at room temperature for at least one month and for greater than a year when kept at -20°C. When reconstituted in sterile pH 7.4 0.01M PBS or diluent of antibody the antibody is stable for at least two weeks at 2-4 °C.&Important Note &This product as supplied is intended for research use only, not for use in human, therapeutic or diagnostic applications.&人类免疫缺陷病毒2型抗体（艾滋病病毒）产品介绍 Human immunodeficiency virus type 2 (HIV2), orginally isolated from patients in West Africa, is the dominant form of HIV in West Africa capable of causing the acquired immunodeficiency syndrome (AIDS). HIV2 is closely related to simian immunodeficiency viruses (SIV). HIV1 and HIV2 share similarity in their genomes, transmission, clinical features, immunological effects, and in their action of binding to the same CD4 cellular receptor, but there are significant differences in the amino acid and nucleotide sequences of HIV1 and HIV2, especially within their envelope genes and proteins. Additionally, HIV2 may have a longer incubation period and may be less pathogenic than HIV1. HIV2 gp36 is a transmembrane protein located in the envelope of the virus specific to HIV2 that binds to the putative cellular receptor proteins P45 and P62.Function : The surface protein gp120 (SU) attaches the virus to the host lymphoid cell by binding to the primary receptor CD4. This interaction induces a structural rearrangement creating a high affinity binding site for a chemokine coreceptor like CXCR4 and/or CCR5. This peculiar 2 stage receptor-interaction strategy allows gp120 to maintain the highly conserved coreceptor-binding site in a cryptic conformation, protected from neutralizing antibodies. Since CD4 also displays a binding site for the disulfide-isomerase P4HB/PDI, a P4HB/PDI-CD4-CXCR4-gp120 complex may form. In that complex, P4HB/PDI could reach and reduce gp120 disulfide bonds, causing major conformational changes in gp120. TXN, another PDI family member could also be involved in disulfide rearrangements in Env during fusion. These changes are transmitted to the transmembrane protein gp41 and are thought to activate its fusogenic potential by unmasking its fusion peptide.&The surface protein gp120 is a ligand for CD209/DC-SIGN and CLEC4M/DC-SIGNR, which are respectively found on dendritic cells (DCs), and on endothelial cells of liver sinusoids and lymph node sinuses. These interactions allow capture of viral particles at mucosal surfaces by these cells and subsequent transmission to permissive cells. DCs are professional antigen presenting cells, critical for host immunity by inducing specific immune responses against a broad variety of pathogens. They act as sentinels in various tissues where they take up antigen, process it, and present it to T-cells following migration to lymphoid organs. HIV subverts the migration properties of dendritic cells to gain access to CD4+ T-cells in lymph nodes. Virus transmission to permissive T-cells occurs either in trans (without DCs infection, through viral capture and transmission), or in cis (following DCs productive infection, through the usual CD4-gp120 interaction), thereby inducing a robust infection. In trans infection, bound virions remain infectious over days and it is proposed that they are not degraded, but protected in non-lysosomal acidic organelles within the DCs close to the cell membrane thus contributing to the viral infectious potential during DCs' migration from the periphery to the lymphoid tissues. On arrival at lymphoid tissues, intact virions recycle back to DCs' cell surface allowing virus transmission to CD4+ T-cells. Virion capture also seems to lead to MHC-II-restricted viral antigen presentation, and probably to the activation of HIV-specific CD4+ cells.&The transmembrane protein gp41 (TM) acts as a class I viral fusion protein. Under the current model, the protein has at least 3 conformational states: pre-fusion native state, pre-hairpin intermediate state, and post-fusion hairpin state. During fusion of viral and target intracellular membranes, the coiled coil regions (heptad repeats) assume a trimer-of-hairpins structure, positioning the fusion peptide in close proximity to the C-terminal region of the ectodomain. The formation of this structure appears to drive apposition and subsequent fusion of viral and target cell membranes. Complete fusion occurs in host cell endosomes and is dynamin-dependent, however some lipid transfer might occur at the plasma membrane. The virus undergoes clathrin-dependent internalization long before endosomal fusion, thus minimizing the surface exposure of conserved viral epitopes during fusion and reducing the efficacy of inhibitors targeting these epitopes. Membranes fusion leads to delivery of the nucleocapsid into the cytoplasm.&The envelope glyprotein gp160 precursor down-modulates cell surface CD4 antigen by interacting with it in the endoplasmic reticulum and blocking its transport to the cell surface.&The gp120-gp41 heterodimer seems to contribute to T-cell depletion during HIV-1 infection. The envelope glycoproteins expressed on the surface of infected cells induce apoptosis through an interaction with uninfected cells expressing the receptor (CD4) and the coreceptors CXCR4 or CCR5. This type of bystander killing may be obtained by at least three distinct mechanisms. First, the interaction between the 2 cells can induce cellular fusion followed by nuclear fusion within the syncytium. Syncytia are condemned to die from apoptosis. Second, the 2 interacting cells may not fuse entirely and simply exchange plasma membrane lipids, after a sort of hemifusion process, followed by rapid death. Third, it is possible that virus-infected cells, on the point of undergoing apoptosis, fuse with CD4-expressing cells, in which case apoptosis is rapidly transmitted from one cell to the other and thus occurs in a sort of contagious fashion.&The gp120-gp41 heterodimer allows rapid transcytosis of the virus through CD4 negative cells such as simple epithelial monolayers of the intestinal, rectal and endocervical epithelial barriers. Both gp120 and gp41 specifically recognize glycosphingolipids galactosyl-ceramide (GalCer) or 3' sulfo-galactosyl-ceramide (GalS) present in the lipid rafts structures of epithelial cells. Binding to these alternative receptors allows the rapid transcytosis of the virus through the epithelial cells. This transcytotic vesicle-mediated transport of virions from the apical side to the basolateral side of the epithelial cells does not involve infection of the cells themselves.Subunit : The mature envelope protein (Env) consists of a homotrimer of non-covalently associated gp120-gp41 heterodimers. The resulting complex protrudes from the virus surface as a spike. There seems to be as few as 10 spikes on the average virion. Surface protein gp120 interacts with human CD4, CCR5 and CXCR4, to form a P4HB/PDI-CD4-CXCR4-gp120 complex. Gp120 also interacts with the C-type lectins CD209/DC-SIGN and CLEC4M/DC-SIGNR (collectively referred to as DC-SIGN(R)). Gp120 and gp41 interact with GalCer.Subcellular Location : Transmembrane protein gp41: V Single-pass type I membrane protein. H Single-pass type I membrane protein. Ho Single-pass type I membrane protein (Potential). Note=It is probably concentrated at the site of budding and incorporated into the virions possibly by contacts between the cytoplasmic tail of Env and the N-terminus of Gag.&Surface protein gp120: V Peripheral membrane protein. H Peripheral membrane protein. Ho Peripheral membrane protein (Potential). Note=The surface protein is not anchored to the viral envelope, but associates with the extravirion surface through its binding to TM. It is probably concentrated at the site of budding and incorporated into the virions possibly by contacts between the cytoplasmic tail of Env and the N-terminus of Gag.Post-translational modifications : Specific enzymatic cleavages in vivo yield mature proteins. Envelope glycoproteins are synthesized as a inactive precursor that is heavily N-glycosylated and processed likely by host cell furin in the Golgi to yield the mature SU and TM proteins. The cleavage site between SU and TM requires the minimal sequence [KR]-X-[KR]-R.&Palmitoylation of the transmembrane protein and of Env polyprotein (prior to its proteolytic cleavage) is essential for their association with host cell membrane lipid rafts. Palmitoylation is therefore required for envelope trafficking to classical lipid rafts, but not for viral replication.Database links : UniProtKB/Swiss-Prot: P04577南京森贝伽生物科技有限公司
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