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Query: UMLS:C0021051 (immunodeficiency)
 71,517 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Recent advances in immunobiology have led to a greater understanding of the healthy immune system and the complex pathogenesis of human immunodeficiency virus (HIV) infection. Knowledge of the mechanisms underlying the decrease in CD4+ T cells is rapidly evolving as a result of new assays, genetic advances, and recombinant DNA technologies. Studying the immune responses of long-term non-progressors is also providing insight into the immunopathology of HIV. Trials using highly active antiretroviral therapy and immune modulators have shown that it may be possible to reverse damage to the immune system and increase CD4+ T-cell numbers. Current and future findings might provide the knowledge necessary to identify effective HIV drugs and vaccines with acceptable toxicity profiles and to determine whether it will be possible to fully restore immune system function in patients with HIV disease.
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PMID:Immune mechanisms in HIV infection. 1468 70

Among non-primate vertebrates, feline immunodeficiency virus (FIV) infection in the cat may be the closest model of human immunodeficiency virus (HIV) infection and acquired immunodeficiency syndrome (AIDS). Clinical evolution and immunological and virological relationships between human HIV/AIDS and disease produced by FIV infection in cats are very close. These similarities should facilitate progress in the understanding of mechanisms of viral infection and immunopathology, and make this model potentially very valuable in evaluation of experimental therapeutic approaches to AIDS in man. Development of feline immunodeficiency virus vectors bearing therapeutic genes targeting different human diseases is a promising strategy for gene therapy, despite some recent studies which suggest that despite lack of evidence of infection of man by FIV, additional epidemiological surveillance may be indicated to determine if transmission can occur from this close companion to humans in some circumstances.
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PMID:Feline immunodeficiency virus: a concise review. 1476 74

RSV is the primary cause of hospitalisation in the first year of life for children in most parts of the world, and nearly 100% of children in the USA are infected with the virus by 2 to 3 years of age. The agent is an enveloped RNA virus with a non-segmented single-stranded negative-sense genome. The viral genome encodes 8 structural and 2 non-structural proteins. Important structural proteins include the fusion (F) protein and the attachment (G) protein which are essential for viral penetration and attachment to the host cells. Both proteins are important in development of immune responses. The virus is estimated to cause 3000 to 4000 deaths annually. Primary infections are as a rule symptomatic. The spectrum of clinical manifestations ranges from mild upper tract illness, infection in middle ear which progresses to acute otitis media, croup, to apnoea in premature infants, pneumonia and bronchiolitis. Premature babies born at 30-35 weeks of gestation, infants with cyanotic congenital heart disease, HIV-infected subjects, and patients on intensive immunosuppressive therapy especially after bone marrow transplant are considered to be at risk for increased mortality and morbidity during RSV infection. The virus does not normally replicate outside of the bronchopulmonary tree and the infection is exquisitely restricted to the respiratory mucosa. However, development of extrapulmonary disease has been observed in certain T and B cell immunodeficiency states. The association of RSV with asthma and reversible reactive airway disease in early childhood has attracted significant attention. Recurrent wheezing for up to 5 to 7 years of age and established airway disease has been observed in a significant number of children with a strong family history of allergy, after primary infection or reinfection with RSV. Immune response to primary infection is relatively small but on reinfection, a significant booster effect with sustained immunologic reactivity is observed in serum and respiratory mucosa. Both CD(4)- and CD(8)-specific as well as Th(1)- and Th(2)-cell specific immune responses have been observed during human infection. In addition, proinflammatory as well as immunoregulatory cytokines and chemokines are induced in the respiratory tract after natural and induced (in vitro) infection. Significant progress has been made in understanding the role of Th(1) vs. Th(2), IgE, viral induced cytokines and chemokines in the mechanisms of pathogenesis of the disease, development of wheezing and in the prevention and treatment of the infection and its sequelae. Respiratory syncytial virus (RSV) is one of the commonest human viral infections, and virtually every child is infected by the third birthday. Because of its restricted mucosal immunopathology, and frequent association with bronchial hyperreactivity and development of wheezing, RSV has served as an important model to investigate mechanisms of mucosal immune responses and development of mucosal disease following infection. The importance of RSV in bronchopulmonary disease and development of bronchial hyperreactivity has been the focus of several recent symposia [Kimpen JL, Simoes EAF. Am J Respir Crit Care Med 2001; 163:S1-S6]. This brief report will only summarise, based on selected references, the historical landmarks of its discovery and current understanding of the mechanisms of immunity, and their possible role in the pathogenesis of bronchopulmonary disease.
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PMID:Respiratory syncytial virus: the virus, the disease and the immune response. 1498 Feb 56

The paper presents the results of a complex biochemical study of the health status of children from Moscow, the Moscow Region, Yaroslavl, Cherepovets, the Voronezh Region, etc. The presented results allowed the authors to detect renal protective dysfunction in children in relation to environmental pollution. The greatest deviations of the studied parameters were observed in Moscow (Garden Ring, Central Administration Okrug (CAO)) and in the industrial town of Cherepovets (the area in vicinity of the Severostal enterprise). The results of a complex biomedical examination of 486 children in the Moscow CAO were first analyzed. The spread of changes was established in the studied parameters over a time, which indicates the presence of immunodeficiency, immunopathology, renal detoxifying dysfunction, and nasal and oral mucosal changes.
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PMID:[Study of the influence of chemical pollution of the environment on the health status of children by noninvasive biochemical diagnosis]. 1514 16

The simian immunodeficiency viruses are a diverse group of viruses that naturally infect a wide range of African primates, including chimpanzees, African green monkeys (AGM) and sooty mangabey monkeys (SM). Although natural infection is widespread in feral populations of AGMs and SMs, this infection does not result in immunodeficiency. However, experimental inoculation of Asian macaque species results in an immunodeficiency syndrome that is remarkably similar in pathogenesis to human AIDS. Thus, SIVsm infection of macaques results in AIDS, and similarly experimental inoculation of pigtailed macaques with at least one SIVagm isolate, SIVIhoest or SIVsun, results in AIDS. The extent of plasma viremia in pathogenic infection is an excellent prognostic indicator of clinical course, with higher viral load being predictive of shorter survival and low viremia being predictive of long-term non-progression. Based upon this paradigm, one would have expected naturally infected animals to exhibit low levels of viremia. In reality, AGMs, SMs, mandrills and chimpanzees infected naturally with their own unique viruses display moderate to high levels of plasma viremia. A significant reduction in CD4+ T-cells in infected versus uninfected SMs suggests that the virus may be cytopathic to some degree. These infected animals still maintain adequate CD4+ T-cells over their entire life in captivity. A distinct characteristic of natural infection is the lack of immunopathology as demonstrated by normal lymph node morphology, lower expression of activation and proliferation markers on CD4+ T-cells, and a generally muted immune response to the virus. Naturally infected SMs and AGMs clearly mount antiviral cellular and humoral immune responses. Therefore, models suggesting immune tolerance to SIV are far too simplistic to explain the lack of disease in these animals. It is probable that a unique balance between T-cell renewal and proliferation and loss through activation-induced apoptosis, and virus-induced cell death has been achieved in SMs and AGMs. The study of the dynamics of T-cell production, proliferation and cell death in asymptomatic natural infection should, therefore, yield insights into the pathogenesis of AIDS.
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PMID:What can natural infection of African monkeys with simian immunodeficiency virus tell us about the pathogenesis of AIDS? 1516 40

Immune Restoration Diseases (IRD) are a collection of atypical 'opportunistic infections' and inflammatory diseases seen in human immunodeficiency virus (HIV) patients after HIV viraemia is suppressed by highly active antiretroviral therapy (HAART). IRD probably reflect dysregulated immune responses against pre-existing infections by opportunistic pathogens, with different immunopathological mechanisms for different pathogens. For example, mycobacterial IRD are associated with delayed type hypersensitivity (DTH) responses to mycobacterial antigens, whereas patients who experience cytomegalovirus (CMV) IRD have elevated plasma levels of soluble CD30, a marker of a T2 cytokine environment expressed by activated CD8 T-cells. As IRD are often compartmentalised to organs, monitoring serological markers such as pathogen-specific IgG antibody, may be informative, as demonstrated for CMV and hepatitis C virus (HCV)-associated IRD. Genetic studies have provided evidence of distinct immunopathological mechanisms and inherited susceptibility to IRD associated with mycobacterial and herpesviridae infections. The expansion of HAART in the developing world where many HIV patients have low CD4+ T-cell counts and high rates of concomitant infections will place a large number of patients at-risk of developing IRD. It is therefore important to understand the immunopathology so that prevention, diagnosis and treatment can be improved.
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PMID:Immune restoration disease: a consequence of dysregulated immune responses after HAART. 1527 87

ELISA test systems were designed on the basis of synthetic peptides (SP) simulating the primary structure of functionally significant epitopes of the respiratory and cyncyntial virus (RCV) F-protein for the purpose of investigating the structure and age-related peculiarities of humoral immunity in respect to separate epitopes of RCV F-protein. One of them (221-232) simulates a part of RCV "virus-neutralizing domain" and another one (479-491) is highly important for the fusion mechanisms. New SP-based ELISA were used to examine pair sera in 159 patients with documented RCV infection including children, aged up to 3 years and 3 to 15, and adults. The activity of anti-RCV antibodies to SP was found to be significantly lower in children aged up to 3 years versus the older children and especially versus the adults. The virus neutralizing and, to a greater extent, fusion-inhibiting activities of antibodies were increasing with age, which collated with the results of detecting the antibodies to SP by immune-enzyme assay. The results testify to synchronism of formation of antibodies to different epitopes of the RCV F-protein. The shaping-up of antibodies with the above SP could denote the protective properties of humoral immunity, which justifies the use of the SP-based ELISA in its analysis, especially, in babies as well as in different-type immunodeficiency and immunopathology conditions.
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PMID:[The age-related specificity of site-oriented immunity in respiratory-syncytial virus infection]. 1529 8

Mycophenolate mofetil (MMF), the bioavailable form of mycophenolic acid (MPA), has been proposed as adjuvant therapy for human immunodeficiency virus type 1 (HIV-1) infection. MPA can inhibit viral replication and might blunt virus-induced immunopathology. However, other effects of this inhibitor might be detrimental in an HIV-infected patient. We therefore studied the effect of MPA on selected cellular processes of relevance to HIV infection. We found that MPA did not alter the expression of the primary HIV coreceptor CCR5 on primary resting lymphocytes, but modestly increased CCR5 expression after activation. Conversely, MPA modestly decreased the secretion of the CCR5 ligand RANTES in resting lymphocytes, but had no effect after activation. It has been suggested that the use of inhibitors of host nucleoside metabolism may enhance clinical toxicities induced by HIV-1 nucleoside reverse transcriptase inhibitors (NRTIs). We found no evidence that MPA induced mitochondrial dysfunction or enhanced dysfunction induced by NRTIs in an HepG2 cell line model of mitochondrial toxicity. Further, MPA did not selectively enhance apoptosis in HIV-1-infected lymphocytes. Our findings support the testing of MMF to augment suppression of viral replication. However, careful study will be required to demonstrate that MMF is beneficial when used without antiretroviral therapy, to inhibit residual replication, or to deplete the pool of latently infected nonactivated cells.
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PMID:Ex vivo modeling of the effects of mycophenolic acid on HIV infection: considerations for antiviral therapy. 1572 50

Experimental evidence from animal models has provided a framework for our current understanding of autoimmune disease pathogenesis and supports the importance of genetic predisposition, molecular mimicry, and immune dysregulation. However, only recently has evidence emerged to support the role of immune dysregulation in human organ-specific autoimmune disease. In the current study of the "late" manifestation of autoimmune thyroid disease (AITD) in a cohort of human immunodeficiency virus (HIV)-positive patients following highly active antiretroviral therapy (HAART), we discuss how immune dysregulation and factors associated with the immunopathology of HIV infection fit the current understanding of autoimmunity and provide a plausible basis for our clinical observations. De novo diagnoses of thyroid disease were identified between 1996 and 2002 in 7 HIV treatment centers (5/7 centers completed the study). Patients were diagnosed as clinical case entities and not discovered through thyroid function test screening. Paired plasma specimens were used to demonstrate sequential rise in thyroid antibodies. Seventeen patients were diagnosed with AITD (median age, 38 yr; 65% were of black African or black Caribbean ethnicity; and 82% were female). The median duration of immune reconstitution was 17 months. Graves disease (GD) was diagnosed in 15 of 17 patients. One patient developed hashithyrotoxicosis with atypically raised C-reactive protein, and another developed hypothyroidism. One GD patient had associated secondary hypoadrenalism. The estimated combined prevalence of GD for 4 treatment centers for female patients was 7/234 and for males was 2/1289. The denominator numbers were matched controls, from 4 centers able to provide data, who commenced HAART during the same time (January 1996 to July 2002) and who did not develop clinical AITD. The mean baseline pre-HAART CD4 count was 67 cells/mL, and the mean increase from nadir to AITD presentation was 355 cells/mL. AITD patients were more likely than controls (95% confidence interval, chi-square test) to be severely compromised at baseline (as defined by a CD4 count < 200 cells/mL or the presence of an acquired immunodeficiency syndrome [AIDS]-defining diagnosis), and to experience greater CD4 increments following HAART. AITD may be a late manifestation of immune reconstitution in HIV-positive patients taking HAART, and immune dysregulation may be an important factor.
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PMID:Characteristics of autoimmune thyroid disease occurring as a late complication of immune reconstitution in patients with advanced human immunodeficiency virus (HIV) disease. 1575 39

Human immunodeficiency virus (HIV) infection is the most powerful known risk factor for progression from latent infection with Mycobacterium tuberculosis to active tuberculosis (TB) disease. The worldwide HIV epidemic has affected TB in every aspect: immunopathology, epidemiology, diagnosis, treatment, and prevention. Of the 42 million people infected with HIV worldwide, more than a quarter of them are also infected with TB, and most live in countries with limited resources for health care in Africa and Asia. This chapter emphasizes HIV-associated TB in resource-limited settings. TB-infected persons with HIV-associated immunosuppression progress to TB disease at a rate of up to 10% per year. Standard TB diagnostic tools have diminished sensitivity in HIV co-infected cases. Standard TB treatment regimens may be less effective, particularly those that do not use a rifamycin throughout. Treatment is further complicated by toxicity, malabsorption, drug-drug interactions and immune reconstitution paradoxical reactions. TB control in the United States was destabilized in part by the HIV epidemic in the early 1990s; massive political will and resources were required to rebuild the public health infrastructure. Africa, Asia, and potentially the former Soviet Union are facing even greater destabilization of TB control due to the dual burden of disease and limited resources. An international response has been initiated but will require even greater political will and resources.
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PMID:Tuberculosis and HIV/AIDS: epidemiological and clinical aspects (world perspective). 1608 74


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