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Query: UMLS:C0024312 (lymphopenia)
4,859 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Distemper virus is very similar antigenically to measles virus, and the disease produced in ferrets by distemper is a systemic illness quite similar to measles infection in humans. Using an attenuated strain of distemper virus, we produced a mild systemic illness in ferrets and were able to study the effects of the viral infection on cell-mediated immunity (CMI). Beginning on day 5 after viral inoculation and continuing to day 30, infected ferrets showed a marked lymphopenia, with a reduction in total numbers of all lymphocyte subpopulations studied. Transformation of circulating lymphocytes to the mitogens phytohemagglutinin, concanavalin A, and pokeweed mitogen was suppressed on day 5, reached a nadir by days 8 to 11, and returned toward normal by days 23 to 30 after viral inoculation. Production of macrophage migration inhibitory factor by splenic macrophages was diminished during distemper infection. In contrast to marked suppression of these in vitro assays for CMI, delayed hypersensitivity skin test responses were only slightly diminished in animals infected with distemper virus. This model should prove useful in exploring the mechanisms of measles induced immunosuppression.
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PMID:Distemper virus infection in ferrets: an animal model of measles-induced immunosuppression. 704 25

The effects of vaccination with RNA-free viral pseudoparticles, preinfection with non-pathogenic ecotropic virus, and induction of tolerance to viral proteins in newborns on the outcome of murine immunodeficiency syndrome (MAIDS) were studied. The parameters used to follow disease progression were: lymphopenia, circulating B and T8 cells, serum IgG and IgM levels, lymphoproliferation and skin graft rejection. Immunization with RNA-free viral pseudoparticles had no effect on any of these parameters. Preinfection of adults with ecotropic virus and the induction of tolerance in newborns to virus antigens both attenuated the early symptoms of viral infection and delayed the onset of immunodeficiency and lymphoproliferation in some mice, but did not significantly alter the number of deaths due to MAIDS. Failure of immune-based therapy to produce successful protection against MAIDS suggests that immune destruction caused by the persistent virus rather than hyperimmune activity is the main pathogenic factor in this disease.
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PMID:The significance of the pre-challenge immune status of mice for development of retrovirus-induced immunodeficiency syndrome (MAIDS). 814 68

Breast cancer chemotherapy and HIV-1 viral infection (AIDS) can result in respective transient or irreversible losses of up to 40-50% of circulating lymphocytes. The relationship of lymphopenia on tumor immunosurveillance and the control of opportunistic infections has yet to be established. The objective of this study was to characterize the changes in natural killer (NK) and lymphokine activated killer (LAK) cell function associated with cytotoxic drug therapy, breast cancer and HIV-1 infection. NK and LAK activities were measured at multiple effector to target ratios. Exponential regression analysis of target cell lysis determined the maximal % target kill and the lytic potential of effector cells. Flow cytometric analysis of lymphocyte subsets in seropositive populations was performed to determine the % of NK(CD56+) cells. Taken together, our findings indicate that cytotoxic NK pool sizes increased in breast cancer patients, diminish consequent to chemotherapy. The functional capacity of individual NK and LAK cells remains intact. In contrast, the diminution of NK and LAK functional responses in HIV-1 seropositive individuals is associated with reductions in cytotoxic NK and LAK pool sizes, as well as marked reductions in cytolytic function of individual cells. Zidovudine (AZT) treatment did not affect LAK activity in HIV+ subgroups. Our findings indicate that NK and activated LAK functions are affected both by chemotherapy and disease etiology.
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PMID:Different effects of breast cancer, HIV-1 infection and chemotherapy on inducible natural immunity. 815 88

We report a patient with systemic vasculitis who developed a Pneumocystis carinii pneumonia whilst he was on steroid n cyclophosphamide treatment. Severe lymphopenia was noted with a CD4 count of 0.023 x10(9)/1 with no evidence of Human Immunodeficiency virus infection. A literature review of recent reports about this particular topic reveals that the development of lymphopenia in patients under immunosuppressor treatment is a fact of a paramount importance. In that sense, a periodic monitorization of both the granulocyte and the lymphocyte count is widely recommended in patients under cytotoxic treatment. A dose adjustment or even suppression of drug administration would be necessary if severe lymphopenia was observed.
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PMID:[Pneumocystis carinii pneumonia. Complications of cytotoxic treatment in a systemic vasculitis]. 880 72

During measles virus (MV) infection, lymphopenia and immune suppression are observed in humans, yet the mechanisms underlying these effects remain unknown except that membrane cofactor protein (MCP, CD46) acts as a receptor for MV, accelerating entry of the virus into host cells. CD46 is a complement regulator, the role of which is to protect host cells from the autologous complement system. Thus, it encompasses complement-related and MV-mediated immune modulation. In this review, I discuss the structural and functional differences between CD46 on lymphocytes and on granulocytes, which partly explain the higher susceptibility of lymphocytes to MV than other blood cells to clarify the mechanisms of MV-mediated lymphopenia and immune suppression, and help resolve the T cell immunity dysfunction secondary to virus infection including HIV.
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PMID:CD46, a complement regulatory protein/measles virus receptor, and its relation to hematological disorders. 885 67

We present the unusual case of 16-year-old girl who developed intractable convulsions five days after the onset of a cold. Meningeal signs, lymphopenia, proteinuria, and lupus anticoagulant were also present. Treatment with anticonvulsants, antituberculous agents, and adenine arabinoside were ineffective. The initiation of methylprednisolone pulse therapy immediately resolved convulsions and fever. The diagnosis, suggested by the clinical course and the marked improvement of the meningoencephalitis by pulse therapy, was an encephalitic form of acute disseminated encephalomyelitis. Clinical and laboratory findings indicated that an immune disorder may have triggered an abnormal response to a viral infection leading to this patient's neurologic disorder.
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PMID:Patient with both lupus anticoagulant and acute disseminated encephalomyelitis. 889 67

The effects of African swine fever (ASF) virus infection on bone marrow hematopoiesis and microenvironment were determined by studying the sequential development of ultrastructural lesions of bone marrow and blood cell changes. Eight pigs (two pigs/infected group) were inoculated by intramuscular route with 10(5) 50% hemadsorbing doses (HAD50) of the Malawi'83 ASF virus isolate. Two uninfected pigs were used as controls. Ultrastructural changes developed by day 3 postinoculation (PI), persisted through day 7 PI, and were characterized by activation of macrophages. From day 5 PI, viral replication was observed in monocytes/macrophages, reticular cells, immature neutrophils, and promonocytes. Also viral replication was detected in megakaryocytes, endothelial cells, and pericytes at day 7 PI. Vascular alterations consisted of activation of sinusoidal endothelial cells, intravascular coagulation, and fibrin strands interspersed among microenvironment and hematopoietic cells. No significant changes were observed in total white blood cells counts, percentage of monocytes, and platelet counts; however, severe lymphopenia and neutrophilia were detected from day 3 PI. Results of this experiment indicate that there is increased hematopoiesis in bone marrow during acute ASF, coinciding with macrophage activation. Neither vascular changes nor viral replication in different bone marrow cell populations gave rise to impaired bone marrow function. Increased hematopoiesis would exert a positive influence by preventing the early onset of thrombocytopenia and would exert a negative influence by stimulating the spread of the virus via neutrophils. Increased hematopoiesis would be unable to compensate for the lymphopenia.
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PMID:African swine fever virus infection of bone marrow: lesions and pathogenesis. 906 76

Infection of pigs with classical swine fever virus (CSFV), a member of the Flaviviridae family, causes a severe leukopenia, particularly notable with the lymphocytes. The goal of this study was to analyze mechanisms behind this CSFV-induced lymphopenia. To this end, the kinetics of leukocyte depletion, the appearance of apoptotic cells, and virus infection of leukocytes after infection of pigs with the virulent CSFV strain Brescia were analyzed. Depletion of B and T lymphocytes was noted as early as 1 day postinfection (p.i.). Circulating viable lymphocytes with reduced mitochondrial transmembrane potential--a particular early marker for apoptosis--were also detectable as early as 1 day p.i. When isolated peripheral blood mononuclear cells were cultured for 6 h, significantly more sub-G1 cells with reduced DNA content were detected among the lymphocytes from CSFV-infected animals, again as early as 1 to 3 days p.i. The first time virus was first found in the plasma, as well as infection of leukocytes, was 3 days p.i. However, throughout the observation time of 1 week, <3% of the circulating leukocytes and no lymphocytes contained virus or viral antigen. Further analysis of the T lymphocytes from infected animals demonstrated an increase in CD49d, major histocompatibility complex class II, and Fas expression. An increased susceptibility to apoptosis in vitro was also observed, particularly after addition of concanavalin A as well as apoptosis-inducing anti-Fas antibody to the cultures. Taken together, these results imply that activation-induced programmed cell death was the mechanism behind lymphopenia during classical swine fever.
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PMID:Lymphocyte apoptosis during classical swine fever: implication of activation-induced cell death. 949 36

HIV-1 disease is often associated with CD4+ T lymphopenia as well as quantitative reductions in naive CD8+ T cells and cytopenias involving nonlymphoid hemopoietic lineages. Studies in HIV-1-infected humans as well as in animal models of lenti-virus disease indicate that these effects may be secondary to infection and destruction of multilineage and lineage-restricted hemopoietic progenitor cells. To define the stages of T cell differentiation that might be susceptible to HIV-1, we performed flow cytometric analysis of the surface expression of CXCR4 and CCR5 on T cells and their progenitors from fetal tissue, cord blood, SCID-hu Thy/Liv mice, and adult peripheral blood. We found that CXCR4 is expressed at low levels on hemopoietic progenitors in the bone marrow, is highly expressed on immature (CD3-CD4+CD8-) T cell progenitors in the thymus, and then is down-regulated during thymocyte differentiation. As thymocytes leave the thymus and enter the peripheral circulation, the expression of CXCR4 is again up-regulated. In contrast, CCR5 is undetectable on most hemopoietic progenitors in the bone marrow and on intrathymic T progenitor cells. It is up-regulated when thymocytes coexpress CD4 and CD8, then down-regulated either in the thymus (CD4+ cells) or during exit from the thymus (CD8+ cells). These results indicate that discrete, lineage-related populations of T cell progenitors may vary widely in their potential to respond to chemokines and to be infected by HIV-1, and that T lymphoid differentiation is particularly vulnerable to CXCR4-using viruses.
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PMID:CXCR4 and CCR5 expression delineates targets for HIV-1 disruption of T cell differentiation. 975 95

A boy with ocular type myasthenia gravis was reported. The therapeutic effect of pyridostigmine bromide and corticosteroid was insufficient. However, clinical symptoms disappeared rapidly after an influenza A virus infection. On a peripheral lymphocytes subsets analysis, the CD 3, CD 4 and CD 4/CD 45 RA positive lymphocytes increased with the therapy and decreased after the infection. By contrast, CD 19 positive lymphocytes decreased with the therapy and increased after the infection. These results suggested that influenza A may improve the clinical signs of myasthenia gravis, as is the improved case with measles.
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PMID:[A case of myasthenia gravis with transient remission after influenza A virus infection]. 1002 39


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