Human T-lymphotropic virus type 4 and the human immunodeficiency virus in West Africa

A new human T-lymphotropic virus (HTLV-4) was recently described in healthy people from Senegal. This virus has many properties in common with members of the human T-lymphotropic viruses, particularly the human immunodeficiency virus or HIV, the etiologic agent of acquired immune deficiency syndrome (AIDS), but does not appear to be associated with immunodeficiency-related disorders. In the present study, serum samples were obtained from 4248 individuals from six West African countries, including Senegal, Guinea, Guinea Bissau, Mauritania, Burkina Faso, and Ivory Coast. These samples, collected during 1985-1987, were from people categorized as healthy control, sexually active risk, and disease populations. All samples were analyzed for reactivity to HTLV-4 and HIV by radioimmunoprecipitation-sodium dodecyl sulfate-polyacrylamide gel electrophoresis and immunoblotting. Evidence for HTLV-4 infection was found in five of the six countries. The seroprevalence varied markedly from country to country. Healthy sexually active individuals in the risk category had the highest levels of HTLV-4 infection compared to individuals in the healthy control category and the disease category, the latter including AIDS patients. The seroprevalence of HIV infection in most of these countries was quite low, although tightly associated with the rare cases of AIDS. The biology of HTLV-4 infection thus differs from that of HIV in Central Africa or the United States and Europe. The presence of these viruses and their different pathogenicities in several countries of West Africa indicate the necessity for serologic assays that will distinguish between them. Further studies of their origin and distribution as well as of their biology will be important in advancing our understanding of AIDS.     

Human chromosome 12 is required for elevated HIV-1 expression in human-hamster hybrid cells

Host cell factors act together with regulatory genes of the human immunodeficiency virus (HIV) to control virus production. Human-Chinese hamster ovary hybrid cell clones were used to probe for human chromosomes involved in regulating HIV gene expression. DNA transfection experiments showed that 4 of 18 clones had high levels of HIV gene expression measured by both extracellular virus production and transactivation of the HIV long terminal repeat in the presence of the trans-activator (tat) gene. Karyotype analyses revealed a 94% concordance (17/18) between human chromosome 12 and HIV gene expression. Other chromosomes had an 11 to 72% concordance with virus production.     

河南省动物狂犬病的诊断与防制研究

从河南病牛脑组织中分离到5株牛狂犬病病毒,用电镜、间接免疫荧光试验等方法鉴定分离病毒的生物学特性。通过微量免疫酶试验,对疫区牛、马、猪、羊、犬、猫、鸡、鼠和蝙蝠9种动物的1 138份血清标本进行检测,阳性率12.65%;其中,疫点内牛、猪、犬、猫和鼠的血清阳性率更高,为20%左右。     

复合型甘蓝夜蛾核型多角体病毒对三种夜蛾的室内毒杀试验

复合型甘蓝夜蛾核型多角体病毒是由甘蓝夜蛾核型多角体病毒(MbNPV)与苜蓿银纹夜蛾核型多角体病毒(ACNPV)按0.5∶1复合而成的。为了掌握其对甘蓝夜蛾的毒杀效果,用蒸馏水将其稀释成2.0×10~3、2.0×10~4、2.0×10~5、2.0×10~6、2.0×10~7PIB·mL~(-1)五个所需的浓度进行测试,并用方差分析和新复极差法测验。结果表明:复合型甘蓝夜蛾核型多角体病毒对斜纹夜蛾、甜菜夜蛾、甘蓝夜蛾毒杀效果差异显著。饲毒后第2天,甘蓝夜蛾对复合剂较敏感;饲毒后第3天对复合剂敏感性均增强;饲毒后第4天,甘蓝夜蛾、甜菜夜蛾死亡率均在80%以上,斜纹夜蛾死亡率在60%以上。     

The Fc and not CD4 receptor mediates antibody enhancement of HIV infection in human cells

Antibodies that enhance human immunodeficiency virus (HIV) infectivity have been found in the blood of infected individuals and in infected or immunized animals. These findings raise serious concern for the development of a safe vaccine against acquired immunodeficiency syndrome. To address the in vivo relevance and mechanism of this phenomenon, antibody-dependent enhancement of HIV infectivity in peripheral blood macrophages, lymphocytes, and human fibroblastoid cells was studied. Neither Leu3a, a monoclonal antibody directed against the CD4 receptor, nor soluble recombinant CD4 even at high concentrations prevented this enhancement. The addition of monoclonal antibody to the Fc receptor III (anti-FcRIII), but not of antibodies that react with FcRI or FcRII, inhibited HIV type 1 and HIV type 2 enhancement in peripheral blood macrophages. Although enhancement of HIV infection in CD4+ lymphocytes could not be blocked by anti-FcRIII, it was inhibited by the addition of human immunoglobulin G aggregates. The results indicate that the FcRIII receptor on human macrophages and possibly another Fc receptor on human CD4+ lymphocytes mediate antibody-dependent enhancement of HIV infectivity and that this phenomenon proceeds through a mechanism independent of the CD4 protein.     

CD8+ lymphocytes can control HIV infection in vitro by suppressing virus replication

Lymphocytes bearing the CD8 marker were shown to suppress replication of human immunodeficiency virus (HIV) in peripheral blood mononuclear cells. The effect was dose-dependent and most apparent with autologous lymphocytes; it did not appear to be mediated by a cytotoxic response. This suppression of HIV replication could be demonstrated by the addition of CD8+ cells at the initiation of virus production as well as after several weeks of virus replication by cultured cells. The observations suggest a potential approach to therapy in which autologous CD8 lymphocytes could be administered to individuals to inhibit HIV replication and perhaps progression of disease.     

猪伪狂犬病病毒FZ株的分离鉴定及gD基因序列分析

采集福州郊区病仔猪的鼻腔黏液、脑、脾脏、肾脏、淋巴结等组织病料,研磨上清接种到非洲绿猴肾(Vero)细胞和狗肾(MDCK)细胞进行病毒分离,通过对分离病毒株进行形态学、血清学、荧光抗体试验、动物接种试验、PCR试验等鉴定,确定所分离的病毒为猪伪狂犬病病毒(PRV),命名为PRV-FZ株.根据GenBank收录的PRVg...     

The human immunodeficiency virus: infectivity and mechanisms of pathogenesis

Infection with the human immunodeficiency virus (HIV) results in a profound immunosuppression due predominantly to a selective depletion of helper/inducer T lymphocytes that express the receptor for the virus (the CD4 molecule). HIV also has tropism for the brain leading to neuropsychiatric abnormalities. Besides inducing cell death, HIV can interfere with T4 cell function by various mechanisms. The monocyte serves as a reservoir for HIV and is relatively refractory to its cytopathic effects. HIV can exist in a latent or chronic form which can be converted to a productive infection by a variety of inductive signals.     

Dual infection of the central nervous system by AIDS viruses with distinct cellular tropisms

Human immunodeficiency virus (HIV) is the causative agent of the acquired immune deficiency syndrome (AIDS). A large number of AIDS patients show evidence of neurologic involvement, known as AIDS-related subacute encephalopathy, which has been correlated with the presence of HIV in the brain. In this study, two genetically distinct but related viruses were isolated from one patient from two different sources in the central nervous system: brain tissue and cerebrospinal fluid. Both viruses were found to replicate in peripheral blood lymphocytes, but only virus from brain tissue will efficiently infect macrophage/monocytes. The viruses also differ in their ability to infect a brain glioma explant culture. This infection of the brain-derived cells in vitro is generally nonproductive, and appears to be some form of persistent or latent infection. These results indicate that genetic variation of HIV in vivo may result in altered cell tropisms and possibly implicate strains of HIV with glial cell tropism in the pathogenesis of some neurologic disorders of AIDS.     

Epitopes of the CD4 antigen and HIV infection

The CD4 (or T4) surface antigen of human T lymphocytes is an important part of the receptor for the human immunodeficiency virus (HIV). After binding to the receptor, the HIV may enter the T cell and induce the formation of syncytia. In an attempt to identify the receptor site more closely, monoclonal antibodies (Mab's) to CD4 were tested for their ability to block HIV infection in a syncytium formation assay, and the CD4 epitopes so identified were mapped by antibody cross-blocking. The antibodies that showed strong inhibition of HIV fell into two main families while a third group of Mab's blocked syncytia formation weakly or not at all. Several different isolates of HIV as well as the laboratory strain CBL1 grown in CEM cells were used to induce the syncytia. The data indicate that only some epitopes of CD4 are important for virus binding and imply that the virus-binding site for CD4 is conserved in different isolates of HIV with substantially divergent env gene sequences. Preliminary studies of patients suggest that polymorphism of these epitopes does not play a role in determining susceptibility to infection.     

Alterations in T4 (CD4) protein and mRNA synthesis in cells infected with HIV

Cells infected with the human immunodeficiency virus (HIV) show decreased expression of the 58-kilodalton T4 (CD4) antigen on their surface. In this study, the effect of HIV infection on the synthesis of T4 messenger RNA (mRNA) and protein products was evaluated in T-cell lines. Metabolically labeled lysates from the T4+ cell line Sup-T1 were immunoprecipitated with monoclonal antibodies to T4. Compared with uninfected cells, HIV-infected Sup-T1 cells showed decreased amounts of T4 that coprecipitated with both the 120-kilodalton viral envelope and the 150-kilodalton envelope precursor molecules. In four of five HIV-producing T-cell lines studied, the steady-state levels of T4 mRNA were also reduced. Thus, the decreased T4 antigen on HIV-infected cells is due to at least three factors: reduced steady-state levels of T4-specific mRNA, reduced amounts of immunoprecipitable T4 antigen, and the complexing of available T4 antigen with viral envelope gene products. The data suggested that the T4 protein produced after infection may be complexed with viral envelope gene products within infected cells. Retroviral envelope-receptor complexes may thus participate in a general mechanism by which receptors for retroviruses are down-modulated and alterations in cellular function develop after infection.     

Induction of CD4+ human cytolytic T cells specific for HIV-infected cells by a gp160 subunit vaccine

Cytolytic T lymphocyte (CTL) responses were evaluated in humans immunized with recombinant human immunodeficiency virus type 1 (HIV) envelope glycoprotein gp160. Some vaccinees had gp160-specific CTLs that were shown by cloning to be CD4+. Although induced by exogenous antigen, most gp160-specific CTL clones also recognized gp160 synthesized endogenously in target cells. These clones lysed autologous CD4+ T lymphoblasts infected with HIV. Of particular interest were certain vaccine-induced clones that lysed HIV-infected cells, recognized gp160 from diverse HIV isolates, and did not participate in "innocent bystander" killing of noninfected CD4+ T cells that had bound gp120.     

A quantitative bioassay for HIV-1 based on trans-activation

A bioassay that is based on trans-activation has been developed for the detection and quantitation of the human immunodeficiency virus type 1 (HIV-1). Indicator cell lines were constructed that contain the HIV-1 long terminal repeat ligated to the chloramphenicol acetyltransferase (CAT) gene. Infection of these cells by HIV activates the expression of CAT protein. Isolates of HIV-1 with divergent nucleotide sequences activated the indicator cell lines to a similar extent, approximately 500- to 1000-fold. Human T cell lymphotropic viruses types 1 and 2, equine infectious anemia virus, and herpes simplex virus 1 did not activate the indicator cell lines. Isolates of simian immunodeficiency virus and human T cell lymphotropic virus type 4 activated these cells to a much lesser extent, which suggests that these viruses contain similar, but distinct, trans-activators. This assay can be used for the detection, quantitation, and typing of HIV and for studying the effect of drugs on the replication of HIV in different cellular backgrounds.     

Second conserved domain of gp120 is important for HIV infectivity and antibody neutralization

Rabbit antisera were raised against three overlapping synthetic peptides with sequence homology to the second conserved domain of the external envelope glycoprotein (gp120) of the human immunodeficiency virus (HIV). All of the antisera immunoprecipitated the envelope glycoprotein. In particular, an antiserum directed against amino acids 254 to 274 of env was efficient in neutralizing three different isolates of HIV in vitro, without affecting the binding of the virus to CD4-positive cells. Therefore, this conserved region of gp120 appears to be critical in a postbinding event during virus penetration and may represent a target for antibody neutralization of HIV. These findings may be applicable in the design of a vaccine for the acquired immunodeficiency syndrome.     

Functional regions of the envelope glycoprotein of human immunodeficiency virus type 1

The envelope of the human immunodeficiency virus type 1 (HIV-1) plays a central role in the process of virus entry into the host cell and in the cytopathicity of the virus for lymphocytes bearing the CD4 molecule. Mutations that affect the ability of the envelope glycoprotein to form syncytia in CD4+ cells can be divided into five groups: those that decrease the binding of the envelope protein to the CD4 molecule, those that prevent a post-binding fusion reaction, those that disrupt the anchorage of the envelope glycoprotein in the membrane, those that affect the association of the two subunits of the envelope glycoprotein, and those that affect post-translational proteolytic processing of the envelope precursor protein. These findings provide a functional model of the HIV envelope glycoprotein.     

Anti-HIV and anti-anti-MHC antibodies in alloimmune and autoimmune mice

Alloimmune mice (mice that have been exposed to cells from another murine strain) were shown to make antibodies against gp120 and p24 of human immunodeficiency virus (HIV), and mice of the autoimmune strains MRL-lpr/lpr and MRL-(+)/+ made antibodies against gp120. This is surprising because the mice were not exposed to HIV. Furthermore, anti-anti-MHC antibodies (molecules that have shapes similar to those of major histocompatibility complex molecules) were detected in both alloimmune sera and MRL mice. These results are discussed in the context of a possible role for allogeneic stimuli in the pathogenesis of acquired immunodeficiency syndrome, as suggested by an idiotypic network model.     

Preventing AIDS but not HIV-1 infection with a DNA vaccine

Although there has been some success in treating human immunodeficiency virus (HIV) patients with triple drug therapy (highly active antiretroviral therapy or HAART), the best hope for combating AIDS (the disease caused by HIV) could be a combination of drug therapy and vaccination, according to Shen and Siliciano in their Perspective. A new study in rhesus monkeys treated with a DNA vaccine (Barouch et al.) demonstrates that a powerful vaccine-induced CD8(+) cytolytic T cell response reduces the amount of virus in the blood to very low levels preventing the drastic decrease in CD4(+) T helper cells and subsequent immunodeficiency. As the Perspective authors explain, vaccinating HIV patients that are receiving HAART may enable HIV levels to be permanently brought under control such that the drug treatment can eventually be stopped.     

鸡传染性喉气管炎病毒gD基因在重组痘病毒中表达及其免疫效力

将鸡传染性喉气管炎病毒(ILTV) 河南长葛株gD基因重组到鸡痘病毒基因组中,获得了能高效表达糖蛋白D的重组鸡痘病毒(rFPV-gD) .将rFPV-gD经皮下刺种途径接种30日龄的固始鸡,用ILTV商品弱毒疫苗经滴鼻、点眼途径免疫试验鸡,同时设非免疫对照鸡群.分别于免疫后7、14、21、28、35和42 d采血分离血清,用微量血清中和试验测定ILTV抗体效价,并于免疫后42 d用ILTV强毒攻击所有试验鸡只.血清中和抗体检测结果表明:疫苗对照组与重组病毒组差异不显著(P>0.05) ,而重绀病毒组和疫苗对照组与空白对照组相比筹异均显著(P<0.05) .免疫42 d攻毒后鸡的发病情况表明,重组病毒组和疫苗对照组对ILTV强毒攻击的保护率均为96.67%,而空白对照组为6.67%,说明该重组病毒作为弱毒疫苗能够抵抗ILTV强毒的攻击,对免疫鸡群有较好的保护作用.