Inhibition of antibodies to nuclear antigen and to DNA in New Zealand mice infected with lactate dehydrogenase virus

New Zealand mice developed antibodies to nuclear antigen leading to immune-complex nephritis. Humoral antibody was directed primarily against denatured DNA, although antibody to native DNA was also found. Persistent infection with lactate dehydrogenase virus significantly lowered antibodies both to nuclear antigen and to DNA in these mice. In addition, female (NZB x W)F(1) mice infected with lactate dehydrogenase virus were protected from the usual nephritic death occurring after the trapping of complexes of nuclear antigen and its antibody and of DNA and its antibody in the glomerular filter.     

Tolerance to polyinosinic-polycytidylic acid in NZB-NZW mice

Immunological tolerance to polyinosinic * polycytidylic acid was induced in NZB/ NZW mice. This is the first experimental induction of tolerance to a nucleic antigen.     

Neoplastic transformation of rat thymic cells induced in vitro by Gross leukemia virus

Cultures of embryonal rat thymus infected initially with Gross leukemia virus have, at the present time, abundantly replicated infectious virus particles for 20 months. Cells from these cultures, after 3 months in vitro, displayed morphological changes and induced formation of tumors upon isotransplantation. The tumors were serially transplantable, and subsequent transplants continue to carry the initial Gross leukemia virus.     

Xenotropic viruses: murine leukemia viruses associated with NIH Swiss, NZB, and other mouse strains

Murine leukemia virus activity is present in tissues from NIH Swiss and other mouse strains after cocultivation with nonvirus-yielding rat cells transformed by Harvey sarcoma virus. The resulting pseudotype sarcoma virus has the same type-specific coat as the virus previously isolated from New Zealand black (NZB) mice, and, like the NZB virus, it is unable to infect mouse cells. The results show that this NZB type virus is endogenous in other strains of mice and is xenotropic; that is, it grows only in cells foreign to the host. This is the first clear demonstration that NIH Swiss mice also carry indigenous infectious murine leukemia virus.     

Transmission of vesicular stomatitis virus from infected to noninfected black flies co-feeding on nonviremic deer mice

Vesicular stomatitis is an economically important arboviral disease of livestock. Viremia is absent in infected mammalian hosts, and the mechanism by which insects become infected with the causative agents, vesicular stomatitis viruses, remains unknown. Because infected and noninfected insects potentially feed on the same host in nature, infected and noninfected black flies were allowed to feed on the same host. Viremia was not detected in the host after infection by a black fly bite, but because noninfected black flies acquired the virus while co-feeding on the same host with infected black flies, it is concluded that a viremic host is not necessary for an insect to be infected with the virus. Thus co-feeding is a mechanism of infection for an insect-transmitted virus.     

Specific tropism of HIV-1 for microglial cells in primary human brain cultures

Human immunodeficiency virus (HIV) frequently causes neurological dysfunction and is abundantly expressed in the central nervous system (CNS) of acquired immunodeficiency syndrome (AIDS) patients with HIV encephalitis or myelopathy. The virus is found mostly in cells of the monocyte-macrophage lineage within the CNS, but the possibility of infection of other glial cells has been raised. Therefore, the effects of different HIV-1 and HIV-2 strains were studied in primary cultures of adult human brain containing microglial cells, the resident CNS macrophages, and astrocytes. These cultures could be productively infected with macrophage-adapted HIV-1 isolates but not with T lymphocyte-adapted HIV-1 isolates or two HIV-2 isolates. As determined with a triple-label procedure, primary astrocytes did not express HIV gag antigens and remained normal throughout the 3-week course of infection. In contrast, virus replicated in neighboring microglial cells, often leading to their cell fusion and death. The death of microglial cells, which normally serve immune functions in the CNS, may be a key factor in the pathogenesis of AIDS encephalitis or myelopathy.     

Functional properties of antigen-specific T cells infected by human T-cell leukemia-lymphoma virus (HTLV-I)

Tetanus-toxoid specific helper-inducer T-cell clones, which had been infected and transformed by human T-cell leukemia-lymphoma virus (HTLV-I), were obtained from an antigen-specific human T cell line by using a limiting dilution technique in the presence of the virus. These HTLV-I-infected T-cell clones proliferated specifically in response to soluble tetanus toxoid but, unlike normal T cells, they could do so in the absence of accessory cells. The HTLV-I-infected T-cell clones did not present the antigen to autologous antigen-specific T cells that were not infected with HTLV-I. The capacity of helper-inducer T cells to retain antigen-specific reactivity after infection by HTLV-I, while losing the normal T-cell requirement for accessory cells, has clinical and theoretical implications.     

Lability of host-cell DNA in growing cell cultures due to Mycoplasma

In HeLa-cell cultures chronically infected with Mycoplasma, (PPLO) host-cell DNA is unstable as detected by incorporation of H(3)-or C1 i-thymidine into DNA and subsequent release into the medium as acidsoluble radioactivity. This characteristic can be transmitted to PPLO-free cultures of strain L cells by inoculation with preparations of PPLO from the HeLa cells, although chronically infected cultures of L cells continue to multiply. In addition, virus preparations also may carry PPLO contamination through numerous passages.     

猪CD151重组抗原表达及其免疫血清的PRRSV感染抑制作用

用RT-PCR从猪巨噬细胞中扩增CD151胞外区编码序列,将其插入含细胞毒性T细胞相关抗原4胞外区序列的表达载体,重组载体转化大肠杆菌,SDS-PAGE检测重组蛋白表达;用包涵体纯化和尿素变性与复性法获得可溶性蛋白,纯化蛋白免疫小鼠,ELISA测定免疫血清抗体效价,Western-blot验证免疫血清特异性;以处理细胞或处理病毒方式,用免疫血清进行猪繁殖与呼吸综合征病毒(PRRSV)感染抑制试验。结果表明:重组菌表达预期的32ku重组蛋白,获得的可溶性重组蛋白纯度较高;免疫血清抗体效价达1∶170 000,在猪巨噬细胞中能检测到预期的29ku蛋白,能抑制PRRSV感染MARC-145细胞,但有毒株差异性,处理病毒的感染抑制作用较强。结果提示猪CD151免疫血清能以结合细胞和结合病毒方式抑制PRRSV感染。     

Oxygen radicals in influenza-induced pathogenesis and treatment with pyran polymer-conjugated SOD

The pathogenicity of influenza virus infection in the mice involves, at least in part, overreaction of the immune responses of the host rather than a direct effect of virus multiplication. Xanthine oxidase, which is responsible for the generation of oxygen free radicals, was elevated in serum and lung tissue of mice infected with influenza virus. To test the theory that oxygen-free radicals are involved in pathogenesis, free radicals were removed by injecting superoxide dismutase (SOD), a specific superoxide radical scavenger, which was conjugated with a pyran copolymer. The conjugate protected mice against a potentially lethal influenza virus infection if administered 5 to 8 days after infection. These findings indicate that oxygen radicals are important in the pathogenesis of influenza virus infection, and that a polymer-conjugated SOD has therapeutic potential for this virus infection and other diseases associated with free radicals.     

Infection of normal human epithelial cells by Epstein-Barr virus

Primary cultures of epithelial cells were grown from the tonsils and adenoids of patients with diseases not related to Epstein-Barr virus. The cells could not be infected by Epstein-Barr virus. Fluorescein-labeled Epstein-Barr virus and a cytofluorograph were then used to show that the epithelial cells do not have detectable receptors for the virus. However, implantation with Epstein-Barr virus receptors gave the cells the ability to bind the labeled virus. One to 5 percent of receptor-implanted cells exposed to the transforming B95-8 substrain of the virus expressed Epstein-Barr nuclear antigen. The early and viral capsid Epstein-Barr virus-determined antigens were not detected in the virus-infected cultures. The results show that normal human epithelial cells from the nasopharynx become susceptible to infection by Epstein-Barr virus when the membrane barrier resulting from the lack of viral receptors is overcome by receptor implantation.     

尖孢镰刀菌侵染下香蕉幼苗抗病生理响应研究

香蕉枯萎病由土传病菌尖孢镰刀菌侵染引起,为探究病原菌侵染过程中香蕉植株的抗病生理响应,本研究利用温室培养植株接种病原菌的方法,测定病原菌侵染之后叶绿素含量、抗病防御酶活性、总酚含量、木质素含量、可溶性糖含量和氨基酸含量。结果表明:(1)随着病原菌的侵染,叶绿素含量显著降低。在侵染第16天时,发病植株叶绿素含量相对于健康植株降低44%;(2)病原菌侵染之后,植株各部位抗病防御酶苯基丙氨酸解氨酶(PAL)、过氧化物酶(POD)和多酚氧化酶(PPO)活性显著提高;(3)随着病情的加剧,酚类物质和木质素逐渐在植株体内累积;(4)病原菌侵染之后,香蕉植株叶片和假茎可溶性糖含量显著增加,但根系可溶性糖含量显著降低。当植株发病等级为I级时,叶片和假茎可溶性糖含量增加至未侵染植株的1.53和1.62倍,根系可溶性糖含量降低至未侵染植株的67%;(5)当植株发病等级为II级时,叶片和假茎氨基酸含量分别增加至未侵染植株的的3.01、5.38和1.99倍。综上所述,病原菌侵染之后,香蕉植株会通过提高抗病防御酶活性,合成抗病物质酚类和木质素,同时,也会主动累积可溶性糖和氨基酸,来缓解由于病原菌侵染之后所造成的渗透胁迫。     

Proteolytic self-cleavage of hepatitis B virus core protein may generate serum e antigen

A model is proposed to explain the presence of the e antigen (HBeAg) of hepatitis B virus (HBV) in the serum of individuals infected with this virus. The e antigen, which has only recently been characterized, is a fragment of the virus core, or nucleocapsid, protein. Serum HBeAg is a valuable clinical marker for active HBV infection because its appearance correlates both with virus replication in the liver and with the presence of circulating virions. In this study a protease-like amino acid sequence was identified at the amino terminus of the core protein sequence. Experimental evidence indicates that HBeAg may be produced by proteolytic self-cleavage of the core protein.     

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.     

狂犬病病毒免疫组织化学定位方法的建立

应用抗狂犬病病毒的特异性抗体及免疫组织化学方法检测接种了狂犬病病毒SRV-9毒株感染的小鼠脑组织,并对狂犬病病毒抗原进行了组织定位分析。结果表明:在小鼠的小脑分子层蒲肯野氏细胞胞浆出现明显的局灶型阳性颗粒。说明免疫组织化学方法检测狂犬病病毒敏感度高、直观,可作为诊断狂犬病病毒的辅助性方法,对研究狂犬病病毒在脑组织神经细胞及其他组织器官内的分布具有一定的意义。     

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.     

Production of hemadsorption-negative areas by serums containing Australia antigen

Exposure of human Wi-38 cells to human serums containing Australia antigen, and presumably serum hepatitis virus, renders the cells refractory to infection by Newcastle disease virus as detected by the hemadsorption-negative plaque test for intrinsic interference. Induction of the Newcastle disease virus refractory state could be passed in cell culture with up to a 1 : 100,000 dilution of material obtained from cells "infected" with serums containing Australia antigen after filtration (0.45-microm pores) and heating to 60 degrees C for 1 hour. Human antiserums to the Australia antigen prevented induction of the Newcastle disease virus refractory state.     

Thymus-dependent lymphocytes: destruction by lymphocytic choriomeningitis virus

Selective destruction of small lymphocytes in the thymusdependent areas of lymph nodes and thymocytes was observed in mice infected with lymphocytic choriomeningitis virus. These changes were clearly evident in lymphoid and splenic tissue 3 days after infection and in the thymus by day 7. The destructive changes paralleled growth of the virus in these organs. The findings show that infection with lymphocytic choriomeningitis virus can temporarily cause the equivalent effect of neonatal thymectomy, that is, a "viral thymectomy," which appears to be related to the ability of this virus to cause persistent infection.     

中药复方制剂抗猪流感病毒作用的研究

[目的]探讨中药复方制剂(金银花、连翘、薄荷、牛蒡子、桔梗、甘草、淡竹叶、淡豆豉)对感染猪流感病毒小鼠的保护作用。[方法]猪流感病毒感染小鼠4 h后给药,以死亡率、平均存活时间、肺指数、肺指数抑制率、血凝滴度、脾脏指数、胸腺指数为评价指标,观察中药复方制剂在小鼠体内的抗流感病毒作用。[结果]中药复方制剂能降低流感病毒感染小鼠的死亡率(P0.01),延长小鼠的存活时间(P0.01),降低肺指数(P0.01),降低血凝滴度(P0.01),增加胸腺指数(P0.01)。[结论]该中药复方制剂具有良好的抗猪流感病毒作用。