两类SIV传染病模型的行波解（英文）

首先讨论了一个总人口为常数的扩散SIV传染病模型,用几何奇异扰动方法证明了其行波解的存在性.接着说明了另一个具有指数输入的SIV模型也具有类似的结果.     

接种和迁移的多斑块传染病模型生存性分析

研究一类具有接种和迁移的多斑块SIV传染病模型的动力学行为.在适当的条件下,证明该模型存在平稳的马尔可夫过程,也得到感染者数量趋于灭绝的结果.最后,数值模拟验证了主要结果.     

Estimation of Sediment Incipient Velocity Using B-Mode Ultrasound Imaging Technique

Sediment incipient velocity(SIV) is a vital parameter for sediment research and river dynamics. This paper describes a novel method of estimating SIV based on the known flow velocity in the movable-bed model experiment. In this method, we use B-mode ultrasound imaging technique to get video images of moving particles and topography under water. By statistical analysis of video images, the relationship between the average number of imaging particles and flow velocity is obtained. The relationship between the change rate of average number and flow velocity is analyzed in sediment incipient process. These relationships are used to estimate the SIV. Lastly, the changed topography verifies the estimated velocity. The results show there is a sudden change in these relationships which can be used to estimate the SIV with high resolution by using a B-mode ultrasound device. The estimated SIV of plastic sands(particle size is about 0.25 mm) is 3.64 cm · s–1 and the estimated SIV of natural sands(particle size is about 0.25 mm) is 5.47 cm · s–1 in the same condition.     

IL-21免疫调节HIV/SIV感染者T淋巴细胞的研究进展

白细胞介素21（IL-21）是一种新近发现的、具有免疫调节作用的细胞因子,可通过多途径影响CD4＋T细胞的应答,增强CD8＋T细胞介导的抗HIV/SIV作用,具有潜在的抗HIV/SIV的临床应用前景。血清IL-21水平测定有望作为确定HIV感染者AIDS病程以及HIV感染者抗病毒治疗反应的重要免疫学参数。近年来关于IL-21免疫调节HIV/SIV感染者T淋巴细胞的研究日益增多,并取得了一些成果。     

负载SIV抗原肽的中国恒河猴Mamu-B~* 1703可溶性单体及其四聚体的制备和鉴定

目的:制备负载SIV抗原肽的中国恒河猴Mamu-B*1703可溶性单体及其四聚体.方法:以含Mama-B*1703重链cDNA序列的pMD19-T克隆为模板,通过PCR的方法克隆Mama-B*1703重链基因,进而构建羧基端融合生物索化酶BirA底物肽(BSP)的Mamu-B*1703重链胞外域融合蛋白的表达载体,并在大肠杆菌中获得表达.β微球蛋白、SIV抗原肽共存时,通过稀释法复性可溶性Mamu-B*1703单体,经生物素化并纯化后与荧光素标记的链亲和素按4:1的比例混合形成四聚体.结果:ELISA检测显示获得具有正确构象的负载SIV抗原肽的Mamu-B-1703四聚体.结论:印度恒河猴Mamu.B}1701特异性抗原肽IW9,与中国恒河猴的Mamu-B*1703相结合形成可溶性Mamu-B*1703/IW9单体和四聚体.     

基于SSR子带信息融合的波达方向宽带估计算法

针对SIF方法在进行带宽DOA估计时,共同利用所有频点信息来弥补单个稀疏信号表示向量(SIV)的问题,基于多个频率测量向量的单稀疏表示信号,提出了一种新的子带信息融合算法(SIF).SIF方法属于稀疏信号表示域,它会受到代数混淆和空间混叠2个模糊性因素的影响.组合所有频率成分可以减小这2个模糊性因素的影响,通过SIV对SIF算法进行了弥补.通过大量的模拟仿真结果表明,与W-CMSR算法相比,基于稀疏信号SIF方法的波达方向宽带估计算法具有更加优越的性能.     

艾滋病病毒通过性接触、体液和母婴传播,那第一个艾滋病患者是如何感染的?

<正>A:现在比较认可的观点是,人类免疫缺陷病毒HIV(Human Immunodeficiency Virus)起源于感染非洲狒狒(chimpanzee)和黑猩狸(gorillas)的类人猿免疫缺陷病毒SIV(Simian Immunodeficiency Virus)。SIV最初只在非人灵长类之间传播,到了20世纪,SIV侵入到人体并且发生基因突变和重组,成为HIV。     

<非洲绿猴和食蟹猴主要肠道细菌的实时定量 PCR 检测及分析

摘要:目的 非洲绿猴具有不同于食蟹猴和恒河猴等猕猴的生物学特征,如脂质代谢、自发性高血压、SIV 感染不引起获得性免疫缺陷综合症( AIDS)等,本研究拟对食蟹猴和非洲绿猴肠道细菌的相对含量进行比较研究。 方法随机选取 SIV 抗体阴性的成年食蟹猴和非洲绿猴各 12 只,排除肥胖和疾病个体,收集其新鲜粪便样本,按 200 mg每份等分后进行液氮速冻,-80 ℃ 保存。 其中 1 份进行肠道细菌的实时定量 PCR 分析。 结果 与食蟹猴相比,非洲绿猴双歧杆菌、乳酸菌以及肠杆菌相对含量显著偏低( P<0. 05) ,而普氏菌以及丁酸盐产生菌 ———普拉梭菌和真细菌相对含量更高( P<0. 05) 。 结论 非洲绿猴产丁酸盐的细菌相对含量更高,反映出其肠道免疫细胞稳态和黏膜完整性具有不同于食蟹猴的进化适应特征,为深入研究非洲绿猴对 SIV 感染不致病的相关机制奠定了基础。     

25株SIV/HIV的进化分析及意义

选取了16株SIV和9株HIV毒株,以人T细胞白血病病毒HTLV-1为outgroup,使用CLUSTAL X、PHYLIP及MEGA三种软件对它们的基因组序列及三个主要蛋白(Env,Gag,Pol)序列分别进行了比对分析,用Neighbor-Joining(N-J)方法和Maximum Likelihood(ML)方法分别构建出进化树.结果显示HIV起源于SIV,其中HIV-1的起源与SIVcpz的几种亚型高度相关,HIV-2的起源与SIVsm及SIVmm高度相关.     

流感传播的影响因素

以广东某地2015年4月至9月流感实际病例数据为例,通过易感者-感染者(susceptible-infected, SI)传染病模型以及改进的易感者-感染者-环境中病毒数(susceptible-infected-the number of viruses in the environment, SIV)传染病模型,考察环境中病毒数和温度等因素对流感传播的影响,并利用最小二乘法拟合得出相关参数.结果表明:流感传播与环境中病毒数、温度等因素有关,且此次广东地区流感传播的最适温度约为24.9℃.     

Sequence of simian immunodeficiency virus from macaque and its relationship to other human and simian retroviruses

Because of the growing incidence of AIDS (acquired immune deficiency syndrome), the need for studies on animal models is urgent. Infection of chimpanzees with the retroviral agent of human AIDS, the human immunodeficiency virus (HIV), will have only limited usefulness because chimpanzees are in short supply and do not develop the disease. Among non-human primates, both type D retroviruses and lentiviruses can be responsible for immune deficiencies. The D-type retroviruses, although important pathogens in macaque monkey colonies, are not satisfactory as a model because they differ in genetic structure and pathophysiological properties from the human AIDS viruses. The simian lentivirus, previously referred to as simian T-cell lymphotropic virus type III (STLV-III), now termed simian immunodeficiency virus (SIV) is related to HIV by the antigenicity of its proteins and in its main biological properties, such as cytopathic effect and tropism for CD4-bearing cells. Most importantly, SIV induces a disease with remarkable similarity to human AIDS in the common rhesus macaques, which therefore constitute the best animal model currently available. Natural or experimental infection of other monkeys such as African green monkeys or sooty mangabeys has not yet been associated with disease. Molecular approaches of the SIV system will be needed for biological studies and development of vaccines that could be tested in animals. We have cloned and sequenced the complete genome of SIV isolated from a naturally infected macaque that died of AIDS. This SIVMAC appears genetically close to the agent of AIDS in West Africa, HIV-2, but the divergence of the sequences of SIV and HIV-2 is greater than that previously observed between HIV-1 isolates.     

An African primate lentivirus (SIVsm) closely related to HIV-2

The ancestors of the human immunodeficiency viruses (HIV-1 and HIV-2) may have evolved from a reservoir of African nonhuman primate lentiviruses, termed simian immunodeficiency viruses (SIV). None of the SIV strains characterized so far are closely related to HIV-1. HIV-2, however, is closely related to SIV (SIVmac) isolated from captive rhesus macaques (Macaca mulatta). SIV infection of feral Asian macaques has not been demonstrated by serological surveys. Thus, macaques may have acquired SIV in captivity by cross-species transmission from an SIV-infected African primate. Sooty mangabeys (Cercocebus atys), an African primate species indigenous to West Africa, however, are infected with SIV (SIVsm) both in captivity and in the wild (P. Fultz, personal communication). We have molecularly cloned and sequenced SIVsm and report here that it is closely related to SIVmac and HIV-2. These results suggest that SIVsm has infected macaques in captivity and humans in West Africa and evolved as SIVmac and HIV-2, respectively.     

Profound early control of highly pathogenic SIV by an effector memory T-cell vaccine

The acquired immunodeficiency syndrome (AIDS)-causing lentiviruses human immunodeficiency virus (HIV) and simian immunodeficiency virus (SIV) effectively evade host immunity and, once established, infections with these viruses are only rarely controlled by immunological mechanisms. However, the initial establishment of infection in the first few days after mucosal exposure, before viral dissemination and massive replication, may be more vulnerable to immune control. Here we report that SIV vaccines that include rhesus cytomegalovirus (RhCMV) vectors establish indefinitely persistent, high-frequency, SIV-specific effector memory T-cell (T(EM)) responses at potential sites of SIV replication in rhesus macaques and stringently control highly pathogenic SIV(MAC239) infection early after mucosal challenge. Thirteen of twenty-four rhesus macaques receiving either RhCMV vectors alone or RhCMV vectors followed by adenovirus 5 (Ad5) vectors (versus 0 of 9 DNA/Ad5-vaccinated rhesus macaques) manifested early complete control of SIV (undetectable plasma virus), and in twelve of these thirteen animals we observed long-term (≥1 year) protection. This was characterized by: occasional blips of plasma viraemia that ultimately waned; predominantly undetectable cell-associated viral load in blood and lymph node mononuclear cells; no depletion of effector-site CD4(+) memory T cells; no induction or boosting of SIV Env-specific antibodies; and induction and then loss of T-cell responses to an SIV protein (Vif) not included in the RhCMV vectors. Protection correlated with the magnitude of the peak SIV-specific CD8(+) T-cell responses in the vaccine phase, and occurred without anamnestic T-cell responses. Remarkably, long-term RhCMV vector-associated SIV control was insensitive to either CD8(+) or CD4(+) lymphocyte depletion and, at necropsy, cell-associated SIV was only occasionally measurable at the limit of detection with ultrasensitive assays, observations that indicate the possibility of eventual viral clearance. Thus, persistent vectors such as CMV and their associated T(EM) responses might significantly contribute to an efficacious HIV/AIDS vaccine.     

Peak SIV replication in resting memory CD4+ T cells depletes gut lamina propria CD4+ T cells

In early simian immunodeficiency virus (SIV) and human immunodeficiency virus-1 (HIV-1) infections, gut-associated lymphatic tissue (GALT), the largest component of the lymphoid organ system, is a principal site of both virus production and depletion of primarily lamina propria memory CD4+ T cells; that is, CD4-expressing T cells that previously encountered antigens and microbes and homed to the lamina propria of GALT. Here, we show that peak virus production in gut tissues of SIV-infected rhesus macaques coincides with peak numbers of infected memory CD4+ T cells. Surprisingly, most of the initially infected memory cells were not, as expected, activated but were instead immunophenotypically 'resting' cells that, unlike truly resting cells, but like the first cells mainly infected at other mucosal sites and peripheral lymph nodes, are capable of supporting virus production. In addition to inducing immune activation and thereby providing activated CD4+ T-cell targets to sustain infection, virus production also triggered an immunopathologically limiting Fas-Fas-ligand-mediated apoptotic pathway in lamina propria CD4+ T cells, resulting in their preferential ablation. Thus, SIV exploits a large, resident population of resting memory CD4+ T cells in GALT to produce peak levels of virus that directly (through lytic infection) and indirectly (through apoptosis of infected and uninfected cells) deplete CD4+ T cells in the effector arm of GALT. The scale of this CD4+ T-cell depletion has adverse effects on the immune system of the host, underscoring the importance of developing countermeasures to SIV that are effective before infection of GALT.     

A naturally immunogenic virion-associated protein specific for HIV-2 and SIV

The genomic organization of HIV-1 and the family of HIV-2 and SIV viruses is similar. However, there is an open reading frame, orf-x, that is present in HIV-2 and SIV, but not in HIV-1. The extent of protein sequence conservation in orf-x between HIV-2ROD and SIVMAC suggests that this open reading frame encodes a gene that may be important for infectivity or replication. Here, we show that the orf-x products of SIVMAC and HIV-2SBL-6669 are virion-associated and that the introduction of a premature stop codon into orf-x, did not abrogate virus infectivity and replication in vitro. Antibody reactivity to the orf-x product was detected in 35 of 42 HIV-2 positive serum samples and 11 of 52 SIV seropositive monkeys. No such antibodies were detected in HIV-1 positive donors, blood donors seronegative for both HIV-2 and HIV-1, or SIV seronegative monkeys. This suggests that orf-x is dispensable for in vitro replication of SIVMAC and that the orf-x gene product of HIV-2 or its antibody can be used to distinguish HIV-2 from HIV-1 infection.     

H3N2SIV河南株非结构蛋白1(NS1)重组的纯化及Dot-ELISA的建立

为建立鉴别猪流感病毒感染猪和灭活疫苗免疫猪的诊断方法,利用pET-28a载体在大肠杆菌BL21中表达H3N2 SIV河南株NS1,并通过Ni2+-NTA亲和色谱法纯化His-NS1融合蛋白.用SDS-PAGE,Western blotting和Dot-ELISA分析纯化蛋白,表明重组NS1能与猪流感病毒感染猪血清进行特异性反应,而不与灭活疫苗免疫猪血清反应.结果表明重组蛋白能作为区别猪流感病毒感染猪和灭活疫苗免疫猪的诊断抗原,为控制猪群中的流感病毒奠定了基础.     

Immune control of an SIV challenge by a T-cell-based vaccine in rhesus monkeys

A recombinant adenovirus serotype 5 (rAd5) vector-based vaccine for HIV-1 has recently failed in a phase 2b efficacy study in humans. Consistent with these results, preclinical studies have demonstrated that rAd5 vectors expressing simian immunodeficiency virus (SIV) Gag failed to reduce peak or setpoint viral loads after SIV challenge of rhesus monkeys (Macaca mulatta) that lacked the protective MHC class I allele Mamu-A*01 (ref. 3). Here we show that an improved T-cell-based vaccine regimen using two serologically distinct adenovirus vectors afforded substantially improved protective efficacy in this challenge model. In particular, a heterologous rAd26 prime/rAd5 boost vaccine regimen expressing SIV Gag elicited cellular immune responses with augmented magnitude, breadth and polyfunctionality as compared with the homologous rAd5 regimen. After SIV(MAC251) challenge, monkeys vaccinated with the rAd26/rAd5 regimen showed a 1.4 log reduction of peak and a 2.4 log reduction of setpoint viral loads as well as decreased AIDS-related mortality as compared with control animals. These data demonstrate that durable partial immune control of a pathogenic SIV challenge for more than 500 days can be achieved by a T-cell-based vaccine in Mamu-A*01-negative rhesus monkeys in the absence of a homologous Env antigen. These findings have important implications for the development of next-generation T-cell-based vaccine candidates for HIV-1.     

Soluble CD4 blocks the infectivity of diverse strains of HIV and SIV for T cells and monocytes but not for brain and muscle cells

The CD4 antigen has been subverted as a receptor by the human and simian immunodeficiency viruses (HIV-1, HIV-2 and SIV). Several groups have reported that recombinant, soluble forms of the CD4 molecule (sCD4) block the infection of T lymphocytes by HIV-1, as CD4 binds the HIV envelope glycoprotein, gp120, with high affinity. We now report that sCD4 blocks diverse strains of HIV-1, HIV-2 and SIV, but is less effective for HIV-2. The blocking effect is apparent even after adsorption of virions to CD4 cells. Soluble CD4 prevents HIV infection of T-lymphocytic and myelomonocytic cell lines, but neither sCD4 nor anti-CD4 antibodies inhibit infection of glioma and rhabdomyosarcoma cell lines.