Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0023418 (leukemia)
 93,477 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Transmission of murine leukemia virus (MuLV) from parent to progeny C3H/St and C57BL/St mice was examined by four assay systems: 1) recovery of infectious NB-tropic MuLV from spleen cultures, 2) the radioimmunoassay for p30 antigenemia, 3) morphologic examination for lymphoma development, and 4) the indirect fluorescent antibody technique for antinuclear antibodies (ANA). Transmission of MuLV (Scripps) occurred in 90-100% of C3H/St and C57BL/St progeny nursed by mothers with p30 antigenemia. All assays except ANA were equally sensitive for the determination of MuLV transmission in C3H/St mice, but the incidence of transmission in C57BL/St mice was determined only by assays of their cultured spleens for MuLV. Incidences of ANA were increased in all generations of C57BL/St mice compared with controls; the route of transmission of MuLV (Scripps) was not a factor. Only C3H/St mice infected by virus transmitted from parent to progeny developed ANA. Infectious MuLV was invariably recovered from spleens cultured from mice with p30 antigenemia, which was present in all mice that developed lymphoma. NB-tropic MuLV was also recovered after prolonged cultivation from spleens of 75% of C57BL/St progeny mice that did not develop p30 antigenemia. These suggested that MuLV (Scripps) could exist either as a productive persistent or nonproductive latent infection in C57BL/St mice.
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PMID:Transmission of murine leukemia virus (Scripps) from parent to progeny mice: a comparison of assay systems. 18 73

Marrow stromal fibroblasts (FBs) likely play an important role in the regulation of hematopoiesis within the marrow microenvironment. Infection of these cells by feline leukemia virus (FeLV) might not only contribute to the pathogenesis of FeLV-induced hematologic diseases, but could provide a reservoir for virus in the infected cat. To determine the frequency of FeLV infection among marrow FB precursor cells (fibroblast colony-forming units, CFU-F) of cats viremic with FeLV-C/Sarma and FeLV-A/61E, marrow FBs and FB cell clones were isolated and assayed for expression of FeLV gag protein. From 30% to 86% and 64% to 88% of marrow FB precursors were infected with FeLV-C/Sarma and FeLV-A/61E, respectively. CFU-F from a cat viremic with FeLV-A/61E were not affected by exposure to antibody against FeLV envelope glycoprotein gp70 and heterologous complement, whereas similarly treated hematopoietic progenitors (erythroid colony-forming units, CFU-E; erythroid burst-forming units, BFU-E; and granulocyte-macrophage colony-forming units, CFU-GM) and culture-propagated, FeLV-infected marrow FBs were effectively lysed, suggesting that infected CFU-F within the marrow microenvironment do not express a significant amount of gp70 on their cell membranes. Thus, marrow FB precursor cells appear to be a major target for FeLV in vivo. Furthermore, the low level of gp70 antigen expression on the surface of these cells in vivo may allow them to escape immune surveillance and provide a reservoir of virus during active or latent infection.
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PMID:In vivo infection of marrow stromal fibroblasts by feline leukemia virus. 132 84

A genetically engineered herpes simplex virus variant was constructed for use as a stable gene vector for neurons. To inhibit replication, the agent possessed a deletion in the immediate early gene ICP4, and to minimize reactivation from the latent state, the gene encoding the latency-associated transcript was deleted. The E. coli beta-galactosidase gene under the control of the Maloney murine leukemia virus long terminal repeat promoter was inserted into the ICP4 region. When introduced into the peripheral nervous system, this virus established latent infections and stably expressed beta-galactosidase in primary sensory neurons. Expression of beta-galactosidase over a more limited time period was observed when the latent infection was established in motor neurons of the hypoglossal nucleus. Agents of this general design have considerable potential for use as gene vectors for studies of neuronal function and correction of genetic defects affecting neurons.
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PMID:A latent, nonpathogenic HSV-1-derived vector stably expresses beta-galactosidase in mouse neurons. 216 71

Several lines of evidence are compatible with the hypothesis that Epstein-Barr virus (EBV) nuclear antigen 2 (EBNA-2) or leader protein (EBNA-LP) affects expression of the EBV latent infection membrane protein LMP1. We now demonstrate the following. (i) Acute transfection and expression of EBNA-2 under control of simian virus 40 or Moloney murine leukemia virus promoters resulted in increased LMP1 expression in P3HR-1-infected Burkitt's lymphoma cells and the P3HR-1 or Daudi cell line. (ii) Transfection and expression of EBNA-LP alone had no effect on LMP1 expression and did not act synergistically with EBNA-2 to affect LMP1 expression. (iii) LMP1 expression in Daudi and P3HR-1-infected cells was controlled at the mRNA level, and EBNA-2 expression in Daudi cells increased LMP1 mRNA. (iv) No other EBV genes were required for EBNA-2 transactivation of LMP1 since cotransfection of recombinant EBNA-2 expression vectors and genomic LMP1 DNA fragments enhanced LMP1 expression in the EBV-negative B-lymphoma cell lines BJAB, Louckes, and BL30. (v) An EBNA-2-responsive element was found within the -512 to +40 LMP1 DNA since this DNA linked to a chloramphenicol acetyltransferase reporter gene was transactivated by cotransfection with an EBNA-2 expression vector. (vi) The EBV type 2 EBNA-2 transactivated LMP1 as well as the EBV type 1 EBNA-2. (vii) Two deletions within the EBNA-2 gene which rendered EBV transformation incompetent did not transactivate LMP1, whereas a transformation-competent EBNA-2 deletion mutant did transactivate LMP1. LMP1 is a potent effector of B-lymphocyte activation and can act synergistically with EBNA-2 to induce cellular CD23 gene expression. Thus, EBNA-2 transactivation of LMP1 amplifies the biological impact of EBNA-2 and underscores its central role in EBV-induced growth transformation.
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PMID:Epstein-Barr virus nuclear antigen 2 transactivates latent membrane protein LMP1. 235 28

Challenge of naive experimental animals with a retroviral inoculum may result in one of two broad sequelae. The first is the establishment of an appropriate humoral and cellular immune response leading to a condition of immunity to subsequent infection with the retrovirus. Alternatively, the host may fail to develop a successful immune response, resulting in a chronic viremia associated with immunosuppression and ultimately death due to secondary pathogens. An alternate disease course is the establishment of a latent infection characterized by the presence of neutralizing antibody and strong cellular immune reactivity. Recent data from the feline leukemia virus (FeLV) system suggest that cats infected with this virus may develop immunosuppression in the form of persistent neutrophil dysfunction. The potential effect of this cellular dysfunction is the possible susceptibility of the host to the same opportunistic pathogens which are responsible for the increased mortality noted in chronic FeLV infections. These data demonstrate that persistent retroviremia is not essential for the establishment of immunosuppression. This overview presents data accumulated from the feline model of the human acquired immunodeficiency syndrome (AIDS) and discusses its relationship to human retroviral infections.
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PMID:Immunodeficiency in latent feline leukemia virus infections. 254 92

Cats exposed to the feline leukemia virus (FeLV) may mount an effective immune response and eliminate the virus, develop a non-viremic, latent infection or become persistently infected and shed the virus. Persistently infected cats commonly die of secondary opportunistic infections that result from FeLV-induced immunosuppression. The acquired immunosuppression is the most frequent and most devastating consequence of FeLV infection in the cat. Immunosuppression is targeted primarily to the cell-mediated immune system and has been attributed to the viral p15e envelope protein. The decreased IgG response and proliferative response to T cell mitogens is thought to be due to a defect in the helper cell function. As a result of T helper cell immunosuppression, infected cats may also have defective cytotoxic lymphocyte and activated macrophage functions which are regulated by their lymphokines. Research has shown that the virus causes a general suppression in the production of T cell-derived lymphokines, including gamma interferon and interleukin 2. A decrease in the function of polymorphonuclear leukocytes has also been reported and may contribute to deaths due to opportunistic infections in FeLV-positive cats. There are numerous parallels between the acquired immunodeficiency syndrome (AIDS) in man and the FeLV-induced immunodeficiency syndrome in cats. Frequent deaths due to opportunistic infections, lymphopenia, depressed cell-mediated immune responses to T cell-dependent antigens despite hypergammaglobulinemia and the presence of a long period of time between infection and the onset of clinical signs are just a few of the syndromes that are similar between the 2 retroviral diseases. A new strain of FeLV, FeLV-FAIDS has been associated with a naturally occurring immunosuppressive syndrome that is strikingly similar to AIDS in man. In addition, a T-lymphotropic retrovirus has recently been identified from cats with an immunodeficiency-like syndrome; this feline lentivirus disease is morphologically similar, but antigenically distinct from the human immunodeficiency virus, the cause of AIDS. Treatment for FeLV immunosuppression is primarily supportive. The development of a soluble tumor cell antigen vaccine has been shown to be efficacious in preventing FeLV infections.
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PMID:Clinical and immunologic aspects of FeLV-induced immunosuppression. 284 93

Three patients developed acute toxoplasmosis after allogeneic marrow transplantation for treatment of leukemia. In each case, Toxoplasma gondii was isolated from peripheral blood buffy-coat cells inoculated into fibroblast tissue culture after 10 to 39 days of incubation. Serologic studies did not suggest acute toxoplasmosis, but complete autopsies done in two patients showed active invasive disease. Serologic tests done before the transplants showed that these cases resulted from reactivation of latent infection rather than primary disease. Parasitemia is a feature of reactivation toxoplasmosis in immunosuppressed patients that may be identified by recovery of T. gondii from peripheral blood buffy-coat cells in tissue culture.
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PMID:Toxoplasma gondii reactivation identified by detection of parasitemia in tissue culture. 389 54

The persistence of virus in the bone marrow of cats which had ostensibly recovered from feline leukaemia virus (FeLV) infection was investigated. Nineteen cats were exposed to FeLV by natural, contact infection and 36 weeks later three were found to be persistently viraemic while the remainder were non-viraemic and had virus neutralising serum antibodies. Virus was isolated in bone marrow cultures established from nine of the 16 non-viraemic cats which were considered, therefore, to have latent infections. Cats infected soon after exposure to FeLV carrier cats were more likely to become persistently viraemic or develop a latent infection than those infected later, which tended to recover. There was no difference in serum antibody levels between the latently infected and recovered cats. Whether cats with latent infections spread virus or develop FeLV-negative haemopoietic tumours was considered. Six kittens housed together for eight months with a cat with a latent infection showed no signs of having been exposed to FeLV. Virus was not isolated from bone marrow cultures of two cats with FeLV-free lymphosarcoma or myelomonocytic leukaemia.
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PMID:Recovery of feline leukaemia virus from non-viraemic cats. 630 86

The ability to direct foreign gene expression from the herpes simplex virus type 1 (HSV-1) genome during an acute or latent infection is a subject of increasing importance in the utilization of HSV vectors for gene therapy. Little is known about the types of transcription factors present in neurons or about whether different neuronal populations within a ganglion vary in their complement of these factors. With respect to HSV-1 latency, it is not known how or why the latency-associated transcript (LAT) promoter is able to function continually during latency while all other viral promoters are inactive. To further studies of these two phenomena, we constructed seven recombinant viruses with various promoter constructs driving expression of the lacZ reporter gene. Each construct was inserted into HSV-1 at the glycoprotein C locus, and recombinant viruses were evaluated for the ability to express beta-galactosidase during acute and latent viral infections in murine dorsal root ganglia. During acute infection of murine dorsal root ganglia, the activities of the promoters varied over a wide range. Constructs containing the murine metallothionein promoter (MT1), the phosphoglycerate kinase promoter, the Moloney murine leukemia virus long terminal repeat (LTR), or the region upstream of and including the HSV LAT core promoter (LAT) were active during the acute but not the latent phase of infection. The addition of transcription factor binding sites present in the upstream LAT region to the MT1 and LTR promoters (LAT-MT1 and LAT-LTR, respectively) significantly increased acute-phase expression. Despite these high initial rates of transcription, of all the promoter constructs only LAT-LTR was able to remain transcriptionally active after the establishment of a latent state. Thus, the Moloney murine leukemia virus LTR provides a DNA element which functions to prevent promoter inactivation during latency. An analogous HSV long-term-expression element is evidently not present in the upstream LAT promoter, indicating that the HSV long-term-expression function is provided by a region outside of that which gives high-level neuronal expression during the acute phase of infection.
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PMID:Long-term promoter activity during herpes simplex virus latency. 793 97

The presence of the HTLV-I gene in peripheral blood mononuclear cells was studied by polymerase chain reaction in 42 patients including 16 with lung cancer, 12 with diffuse panbronchiolitis (DPB), 11 with idiopathic interstitial pneumonia (IIP), and 3 with pneumoconiosis and hematological malignancy. Sequences equal to a part of the pX gene were found in 44% of the lung cancer cases, 50% of the DPB cases, 55% of the IIP cases, and 100% of the cases of pneumoconiosis and leukemia. In the lung cancer cases, detection of the pX gene was frequently associated with the existence of diffuse interstitial pulmonary shadows. The pX gene was detected in 100% of patients with anti-HTLV-I antibody, 50% of patients with HTLV-I-related reaction and 14% of patients who tested seronegative. It may be inferred from the results that respiratory diseases that produce diffuse interstitial pulmonary shadows are closely associated with HTLV-I infection and that the HTLV-I-related reaction to the immunofluorescent test might reflect the latent infection state of HTLV-I.
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PMID:Detection of the pX gene of human T-lymphotropic virus type I in respiratory diseases with diffuse interstitial pulmonary shadows and lung cancer. 812 9


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