Gotowe bibliografie tematyczne / Immunodeficiency disease

Gotowa bibliografia na temat „Immunodeficiency disease”

Autor: Grafiati
Data publikacji: 4 czerwca 2021
Data aktualizacji: 20 lutego 2023

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Artykuły w czasopismach na temat "Immunodeficiency disease"

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Burton, Janet, Elyse Murphy i Patty Riley. "Primary Immunodeficiency Disease". Professional Case Management 15, nr 1 (styczeń 2010): 5–14. http://dx.doi.org/10.1097/ncm.0b013e3181b5dec4.

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&NA;. "Primary Immunodeficiency Disease". Professional Case Management 15, nr 1 (styczeń 2010): 15–16. http://dx.doi.org/10.1097/ncm.0b013e3181d06874.

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Dinakar, Chitra. "Alleviating disease burden in primary immunodeficiency diseases". Annals of Allergy, Asthma & Immunology 96, nr 2 (luty 2006): 260–62. http://dx.doi.org/10.1016/s1081-1206(10)61234-3.

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Iritani, Brian M. "Metabolism meets immunodeficiency disease". Blood 137, nr 4 (28.01.2021): 436–37. http://dx.doi.org/10.1182/blood.2020008875.

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Yamamoto-Furusho, Jesus K. "Crohn’s disease: Innate immunodeficiency?" World Journal of Gastroenterology 12, nr 42 (2006): 6751. http://dx.doi.org/10.3748/wjg.v12.i42.6751.

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Jones, Kimmith M. "Human Immunodeficiency Virus Disease". Critical Care Nursing Clinics of North America 11, nr 4 (grudzień 1999): 455–64. http://dx.doi.org/10.1016/s0899-5885(18)30137-0.

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Shiraki, Mayuka, Saori Kadowaki, Tomonori Kadowaki, Norio Kawamoto i Hidenori Ohnishi. "Primary Immunodeficiency Disease Mimicking Pediatric Bechet’s Disease". Children 8, nr 2 (22.01.2021): 75. http://dx.doi.org/10.3390/children8020075.

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Behcet’s disease (BD) is a chronic inflammatory disease with multisystemic involvement. Its etiology is considered to involve complex environmental and genetic factors. Several susceptibility genes for BD, such as human leukocyte antigen (HLA)-A26, IL23R-IL12RB2, IL10 and ERAP1, in addition to the well-studied HLA-B51, were mainly identified by genome-wide association studies. A heterozygous mutation in TNFAIP3, which leads to A20 haploinsufficiency, was found to cause an early-onset autoinflammatory disease resembling BD in 2016. Several monogenic diseases associated with primary immunodeficiency disease and trisomy 8 have recently been reported to display BD-like phenotypes. Among the genes causing these diseases, TNFAIP3, NEMO, RELA, NFKB1 and TNFRSF1A are involved in the NF-κB (nuclear factor κ light-chain enhancer of activated B cells) signaling pathway, indicating that this pathway plays an important role in the pathogenesis of BD. Because appropriate treatment may vary depending on the disease, analyzing the genetic background of patients with such diseases is expected to help elucidate the etiology of pediatric BD and assist with its treatment. Here, we summarize recently emerging knowledge about genetic predisposition to BD.
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Sleasman, J. W. "The Association Between Immunodeficiency and the Development of Autoimmune Disease". Advances in Dental Research 10, nr 1 (kwiecień 1996): 57–61. http://dx.doi.org/10.1177/08959374960100011101.

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There is a paradoxical relationship between immunodeficiency diseases and autoimmunity. While not all individuals with immunodeficiency develop autoimmunity, nor are all individuals with autoimmunity immunodeficient, defects within certain components of the immune system carry a high risk for the development of autoimmune disease. Inherited deficiencies of the complement system have a high incidence of systemic lupus erythematosus (SLE), glomerulonephritis, and vasculitis. Carrier mothers of children with chronic granulomatous disease, an X-linked defect of phagocytosis, often develop discoid lupus. Several antibody deficiencies are associated with autoimmune disease. Autoimmune cytopenias are commonly observed in individuals with selective IgA deficiency and common variable immune deficiency. Polyarticular arthritis can be seen in children with X-linked agammaglobulinemia. Combined cellular and antibody deficiencies, such as Wiskott-Aldrich syndrome, carry an increased risk for juvenile rheumatoid arthritis and autoimmune hemolytic anemia. Several hypothetical mechanisms have been proposed to explain the associations between autoimmunity and immunodeficiency. Immunologic defects may result in a failure to exclude microbial antigens, resulting in chronic immunologic activation and autoimmune symptoms. There may be shared genetic factors, such as common HLA alleles, which predispose an individual to both autoimmunity and immunodeficiency. Defects within one component of the immune system may alter the way a pathogen induces an immune response and lead to an inflammatory response directed at self-antigens. An understanding of the immunologic defects that contribute to the development of autoimmunity will provide an insight into the pathogenesis of the autoimmune process.
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McShane, Pamela J. "Common Variable Immunodeficiency and Other Immunodeficiency Syndromes in Bronchiectasis". Seminars in Respiratory and Critical Care Medicine 42, nr 04 (14.07.2021): 525–36. http://dx.doi.org/10.1055/s-0041-1730893.

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AbstractImmunodeficiency represents a vast number of diseases and syndromes. Both primary and secondary forms of immunodeficiency are important contributors to the development of bronchiectasis. Primary immune deficiencies, in particular, are increasingly identified and defined as contributors. Specific immune deficiencies that are closely associated with bronchiectasis and as discussed in this article are common variable immunodeficiency, specific antibody deficiency, immunodeficiencies involving immunoglobulin E, DOCK8 immunodeficiency, phosphoglucomutase 3 deficiency, activated phosphoinositide 3-kinase delta syndrome, and X-linked agammaglobulinemia. Each of these primary immune deficiencies has unique nuances. Vigilance for these unique signs and symptoms is likely to improve recognition of specific immunodeficiency in the idiopathic bronchiectasis patient. Secondary forms of immunodeficiency occur as a result of a separate disease process. Graft versus host disease, malignancy, and human immunodeficiency virus are three classic examples discussed in this article. An awareness of the potential for these disease settings to lead to bronchiectasis is necessary to optimize patient care. With understanding and mindfulness toward the intricate relationship between bronchiectasis and immunodeficiency, there is an opportunity to elucidate pathophysiologic underpinnings between these two syndromes.
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Bodemer, W. "Immunodeficiency viruses and prion disease". Primate Biology 2, nr 1 (24.08.2015): 65–69. http://dx.doi.org/10.5194/pb-2-65-2015.

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Abstract. Two threatening human diseases have emerged during the past 35 years. Human immunodeficiency virus (HIV) was transmitted from non-human primates – e.g., the chimpanzee to humans – and then spread into populations all over the world. To date, around 35 million people are infected and no vaccine is available because the virus undergoes rapid mutation, resulting in a swarm of virus strains. At best, therapeutical intervention is possible with antiviral drugs; however because of its capacity to rapidly mutate, resistant virus strains develop. Since non-human primates (NHPs) carry simian immunodeficiency virus (SIV), we could assess infection and immunity by SIV/HIV in rhesus monkeys (M. mulatta) as a model for acquired immunodeficiency syndrome (AIDS). Transmissible spongiform encephalopathy (TSE) emerged in ruminants in the 1980s and shortly thereafter appeared in humans, leading to variant Creutzfeldt–Jakob disease (vCJD). The vCJD is a terminal neurological disorder since it heavily and irreversibly damages the brain. No cure is at hand. The causative agents for TSE are prions. They are unusual pathogens and enigmatic since they lack nucleic acid as inheritable information. On the other hand, prions were suspected as infectious agents for years and suspected to be the etiological agent of scrapie in sheep. Molecular biology and medicine have clearly identified prions in recent years as the responsible agent for bovine spongiform encephalopathy in ruminants (BSE). BSE has been transmitted to humans, resulting in around 225 vCJD cases. Similar to the SIV/HIV model for Acquired Immunodeficiency Syndrome (AIDS), we could establish a prion infection model in rhesus monkeys. HIV/AIDS and vCJD are zoonoses since their original pathogens can be transmitted from animals to humans. Our experimental efforts to understand these intriguing pathogens and their corresponding diseases in rhesus monkeys as a valid model for both human diseases are summarized in this review.
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Rozprawy doktorskie na temat "Immunodeficiency disease"

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Tsang, Chiu-shun Peter. "Oral biology of human immunodeficiency virus-infected individuals in Hong Kong /". [Hong Kong : Faculty of Dentistry, University of Hong Kong], 1997. http://sunzi.lib.hku.hk/hkuto/record.jsp?B19900661.

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Cook, Scott C. "Human immunodeficiency virus : determining predictors of unsafe sexual behavior /". free to MU campus, to others for purchase, 1999. http://wwwlib.umi.com/cr/mo/fullcit?p9962514.

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Tsang, Chiu-shun Peter, i 曾昭舜. "Oral biology of human immunodeficiency virus-infected individuals in Hong Kong". Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 1997. http://hub.hku.hk/bib/B31237770.

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Yim, Chi-ho Howard. "Cytokine dysregulation by human immunodeficiency virus-1 transactivating protein". Click to view the E-thesis via HKUTO, 2006. http://sunzi.lib.hku.hk/hkuto/record/B36987700.

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Roscioli, Tony Clinical School Prince of Wales Hospital Faculty of Medicine UNSW. "The genetic basis of veno-occlusive disease with immunodeficiency syndrome". Awarded by:University of New South Wales. Clinical School - Prince of Wales Hospital, 2007. http://handle.unsw.edu.au/1959.4/40599.

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This thesis addresses the genetic basis of a rare autosomal recessive primary immunodeficiency disorder with the characteristic additional feature of venoocclusive disease of the liver (VODI). The interest in this condition was stimulated both by the potential to identify the genetic basis of a rare immunodeficiency and the opportunity to gain an insight into the biological basis of hepatic veno-occlusive disease, a poorly understood condition that is encountered most frequently in Australia as a consequence of bone marrow transplantation. The gene responsible for VODI was identified by homozygosity mapping and DNA sequence analysis of positional candidates and was shown to be the PML Nuclear Body expressed protein Sp110. This is the first time a PML Nuclear Body protein has been shown to be involved in immunodeficiency disorder. Subsequent immunofluorescence studies of affected patient cell lines showed absence of Sp110 in patient B cells. The role of SP110 alleles in the susceptibility of bone marrow transplant patients to hepatic veno-occlusive disease was investigated using a cohort of patients from the Fred Hutchinson Cancer Center, Seattle. A SNP association study identified initial evidence for an association, but the study lacked sufficient power after correction for multiple testing. Contemporaneously, Dr Igor Kramnik published a report that the murine homologue of Sp110, Ifi75 (also termed Ipr1) was deleted in mice that were supersusceptible to infection with Mycobacterium tuberculosis. A further SNP association study was therefore performed utilising a NSW cohort of Mantouxpositive South East Asian migrants, which detected evidence that alleles of SP110 may be associated with progression of M. tuberculosis infection. Again, the limited size of this cohort precluded definitive findings.
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Yim, Chi-ho Howard, i 嚴志濠. "Cytokine dysregulation by human immunodeficiency virus-1 transactivating protein". Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2006. http://hub.hku.hk/bib/B36987700.

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Groves, Katherine Claire. "Disease progression in Human Immunodeficiency Virus type 1 infected viraemic controllers". Thesis, Queen Mary, University of London, 2012. http://qmro.qmul.ac.uk/xmlui/handle/123456789/3114.

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Background: The mechanism of CD4+ T-cell decline in Human Immunodeficiency Virus-1 (HIV-1) infection is unclear, but the association with plasma HIV-1 RNA-load suggests viral replication is involved. Viraemic controller patients with low HIV-1 RNA-loads (<2000 copies/ml) typically maintain good CD4+ T-cell counts (>450 CD4+ T-cells/mm3). However, within a cohort of 86 viraemic controllers, a subgroup (18 ‘discord controllers’) was identified with low CD4+ T-cell counts (<450 CD4+ T-cells/mm3) which present clinical uncertainty. The underlying mechanism accounting for CD4+ T-cell decline in the face of low or undetectable HIV-1 RNAloads is unknown. The objective of the work described in this thesis was to investigate the virological and host immune system dynamics in discord controllers compared with typical controllers. Method Epidemiological features, HIV-1 subtype, cellular HIV-1 DNA-load, T-cell populations (CD4+/CD8+ naïve/ central-memory/ effector-memory subsets; CD45RA/RO ± CD62L) and Tcell activation markers (CD38, HLA-DR) were examined for discord controllers and typical controllers as well as progressors with HIV-1 RNA-load >10000 copies/ml, <450 CD4+ Tcells/ mm3. Results Discord controllers and typical controllers were similar, based on epidemiological features and viral subtype distribution. They resembled progressors, showing high HIV-1 DNA-load, depletion of naïve CD4+ T-cells and higher activation in all CD4+ T-cell subsets. However, the CD8+ T-cell compartment in discord controllers was similar to typical controllers with preserved naïve CD8+ T-cells and low level CD8+ T-cells activation. Conclusion The data presented in this thesis is consistent with a relationship between CD4+ T-cell activation, HIV-1 DNA-load and disease progression but not HIV-1 RNA-load. This suggests that in viraemic controllers, HIV-1 DNA-load may be a better marker of viral replication and disease progression than HIV-1 RNA-load. Furthermore, low level CD8+ T-cell activation correlate with low plasma HIV-1 RNA-load but not with HIV-1 DNA-load.
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Burnett, Mary Susan. "Development of a live vaccine for human immunodeficiency virus /". Digital version accessible at:, 1997. http://wwwlib.umi.com/cr/utexas/main.

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Hashim, Ilie. "Mutation of Regnase-1 causes primary immunodeficiency associated with auto-inflammatory disease". Thesis, University of Cambridge, 2017. https://www.repository.cam.ac.uk/handle/1810/269453.

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Primary immunodeficiencies (PIDs) are a heterogeneous group of disorders causing immune dysfunction that manifest with increased susceptibility to infection. Some PID patients may also have autoimmune and autoinflammatory manifestations. In many cases, PIDs are monogenic disorders that follow Mendelian inheritance and mutations in more than 250 genes have been shown to cause PIDs. However, in the majority of PID patients the causative mutations remain unknown. Here I report a study of a patient from a consanguineous family who presented in infancy with colitis, autoimmune hepatitis, autoimmune anemia and thrombocytopenia. The patient also suffered recurrent respiratory infections leading to bronchiectasis and had several episodes of severe varicella zoster virus (VZV) infections, including pneumonia and meningitis. Immunologically, the patient had increased IgM and IgG levels, absent IgA, low specific antibodies and multiple auto-antibodies, including anti-Interferon- antibodies. Whole blood stimulation assays identified an increased production of the pro-inflammatory cytokine IL-6. Throughout his life the patient received immunosuppressive therapy. Whole exome sequencing of the patient discovered a homozygous frameshift mutation in the ZC3H12A gene that encodes the Regnase-1 protein also known as MCPIP1. Regnase-1 is a regulatory RNase that directly degrades mRNAs of several pro-inflammatory genes, e.g. mRNA of cytokine IL-6, thus curbing the immune activation. The presentation of the patient resembled the phenotype of the Regnase-1-knockout mice that developed spontaneous systemic inflammation, disorganisation of lymphoid organs, severe anaemia and hyperimmunoglobulinemia, with the increased production of IL-6. I studied expression of the mutant Regnase-1 protein using commercial antibodies; also a new custom-made antibody that detects the truncated mutant Regnase-1 protein was developed. Analysis of the patient-derived cells demonstrated absence of the full-length Regnase-1 protein. Cloning and forced expression of the truncated mutant protein showed that it is mislocalized inside the cells and is functionally impaired. Studies of the iPSC-derived macrophages, EBV-transformed B cells and primary fibroblasts of the patient demonstrated increased levels of the IL-6 mRNA in the resting cells. They also showed impaired regulation of the truncated mutant Regnase-1 protein and IL-6 mRNA levels after cell stimulation. Mutations in Regnase-1 have never been associated with human diseases previously. Therefore, this study describes a novel PID caused by the Regnase-1 deficiency.
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Jansson, Marianne. "HIV-1 variability in relation to host defence mechanisms and disease outcome /". Stockholm, 1998. http://diss.kib.ki.se/search/diss.se.cfm?19980608jans.

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Książki na temat "Immunodeficiency disease"

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Webster, A. D. B., red. Immunodeficiency and Disease. Dordrecht: Springer Netherlands, 1988. http://dx.doi.org/10.1007/978-94-009-1275-5.

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Marcus, Stephanie. Acquired immunodeficiency syndrome (AIDS). Washington, D.C. (10 First St., S.E., Washington 20540): Science Reference Section, Science and Technology Division, Library of Congress, 1991.

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Marcus, Stephanie. Acquired immunodeficiency syndrome (AIDS). Washington, D.C. (10 First St., S.E., Washington 20540): Science Reference Section, Science and Technology Division, Library of Congress, 1991.

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International, Conference on AIDS (2nd 1986 Paris France). Acquired immunodeficiency syndrome. Amsterdam: Elsevier, 1986.

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1956-, Gluckman Jennifer C., i Vilmer E, red. Acquired immunodeficiency syndrome. Amsterdam: Elsevier, 1986.

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Guiltinan, Jane. Naturopathic management of HIV disease and AIDS. Seattle, Wash: Bastyr University, 1995.

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Justice, Amy Caroline. An effective new prognostic staging system for acquired immunodeficiency syndrome (AIDS). [New Haven: s.n.], 1988.

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Ogden, Russel D. Euthanasia and assisted suicide in persons with acquired immunodeficiency syndrome (AIDS) or human immunodeficiency (HIV). New Westminster, B.C: Peroglyphics Publishing, 1994.

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Ogden, Russel D. Euthanasia and assisted suicide in persons with acquired immunodeficiency syndrome (AIDS) or human immunodeficiency virus (HIV). Pitt Meadows, B.C: Perreault Goedman, 1994.

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P, Kotler Donald, red. Gastrointestinal and nutritional manifestations of the acquired immunodeficiency syndrome. New York: Raven Press, 1991.

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Części książek na temat "Immunodeficiency disease"

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Gooch, Jan W. "Immunodeficiency Disease". W Encyclopedic Dictionary of Polymers, 900. New York, NY: Springer New York, 2011. http://dx.doi.org/10.1007/978-1-4419-6247-8_13991.

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Gallottini, Marina. "Immunodeficiency". W Infectious Disease and Parasites, 171–73. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-30009-2_1086.

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Gartler, Stanley M., R. Scott Hansen, Vinzenz Oji, Heiko Traupe, Julia Horn, Bodo Grimbacher, Srijita Sen-Chowdhry i in. "Immunodeficiency". W Encyclopedia of Molecular Mechanisms of Disease, 1038–39. Berlin, Heidelberg: Springer Berlin Heidelberg, 2009. http://dx.doi.org/10.1007/978-3-540-29676-8_8927.

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Gooch, Jan W. "Primary Immunodeficiency Disease". W Encyclopedic Dictionary of Polymers, 917. New York, NY: Springer New York, 2011. http://dx.doi.org/10.1007/978-1-4419-6247-8_14560.

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Gooch, Jan W. "Secondary Immunodeficiency Disease". W Encyclopedic Dictionary of Polymers, 922. New York, NY: Springer New York, 2011. http://dx.doi.org/10.1007/978-1-4419-6247-8_14755.

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Dalgleish, A. G., i M. Malkovsky. "AIDS and the New Viruses". W Immunodeficiency and Disease, 1–24. Dordrecht: Springer Netherlands, 1988. http://dx.doi.org/10.1007/978-94-009-1275-5_1.

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Webster, A. D. B., i G. P. Spickett. "Hypogammaglobulinaemia: Recent Advances". W Immunodeficiency and Disease, 25–42. Dordrecht: Springer Netherlands, 1988. http://dx.doi.org/10.1007/978-94-009-1275-5_2.

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Cunningham-Rundles, C. "Immunoglobulin Replacement Therapy". W Immunodeficiency and Disease, 43–60. Dordrecht: Springer Netherlands, 1988. http://dx.doi.org/10.1007/978-94-009-1275-5_3.

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Crawford, D. H., i J. G. P. Sissons. "Chronic Herpes Virus Infections". W Immunodeficiency and Disease, 61–97. Dordrecht: Springer Netherlands, 1988. http://dx.doi.org/10.1007/978-94-009-1275-5_4.

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Hanson, L. Å., J. Björkander, R. Söderström i T. Söderstrom. "Clinical Significance of IgG Subclass and IgA Deficiency". W Immunodeficiency and Disease, 99–111. Dordrecht: Springer Netherlands, 1988. http://dx.doi.org/10.1007/978-94-009-1275-5_5.

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Streszczenia konferencji na temat "Immunodeficiency disease"

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Dzhuvalyakov, Pavel, Dmitry Bogomolov i Julia Zbrueva. "The relevance of the question of the study of a corpse with suspected HIV". W Issues of determining the severity of harm caused to human health as a result of the impact of a biological factor. ru: Publishing Center RIOR, 2020. http://dx.doi.org/10.29039/conferencearticle_5fdcb03a696517.02994233.

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HIV infection is a disease caused by the human immunodeficiency virus, characterized by acquired immunodeficiency syndrome, which contributes to the occurrence of secondary infections and malignant tumors due to deep inhibition of the body's protective properties. Today, the world is experiencing a pandemic of HIV infection, the incidence of the world's population, especially in Eastern Europe, is growing steadily.
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Shrestha, S., P. McKillion, A. Abdullah i J. P. Sugunaraj. "A Sarcoid Mimic - Granulomatous Lymphocytic Interstitial Lung Disease Due to Common Variable Immunodeficiency". W American Thoracic Society 2021 International Conference, May 14-19, 2021 - San Diego, CA. American Thoracic Society, 2021. http://dx.doi.org/10.1164/ajrccm-conference.2021.203.1_meetingabstracts.a2104.

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Tulio, Robertha, i Rômulo Machado Balmant. "Dental care for HIV positive patients - care and importance - case report". W II INTERNATIONAL SEVEN MULTIDISCIPLINARY CONGRESS. Seven Congress, 2023. http://dx.doi.org/10.56238/homeinternationalanais-087.

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Abstract Acquired immunodeficiency syndrome (AIDS) is caused by the "Lentivirus" family of retroviruses, called HIV-1. This syndrome is defined as an infectious disease of viral origin, with its manifestation interspersed in peaks and troughs, with a pathophysiology involving the compromising of the immune system, causing the defense system to not operate correctly, leaving the patient susceptible to the development of infections.
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Dewan, Pooja, Dhano Mardi, Sunil Gomber i Rumpa Saha. "IDDF2018-ABS-0044 Enteric pathogens and predictors for acute diarrhoea in children living with human immunodeficiency virus infection". W International Digestive Disease Forum (IDDF) 2018, Hong Kong, 9–10 June 2018. BMJ Publishing Group Ltd and British Society of Gastroenterology, 2018. http://dx.doi.org/10.1136/gutjnl-2018-iddfabstracts.80.

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Hance, B., i T. Wichman. "Recurrent Pneumonia in Pregnancy Unveils Common Variable Immunodeficiency and Associated Granulomatous Lymphocytic Interstitial Lung Disease". W American Thoracic Society 2019 International Conference, May 17-22, 2019 - Dallas, TX. American Thoracic Society, 2019. http://dx.doi.org/10.1164/ajrccm-conference.2019.199.1_meetingabstracts.a6289.

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Sidorova, A. P., i A. V. Bakunovich. "ANTIRETROVIRAL DRUGS AS POTENTIAL INHIBITORS OF SARS-COV-2 Mpro". W SAKHAROV READINGS 2022: ENVIRONMENTAL PROBLEMS OF THE XXI CENTURY. International Sakharov Environmental Institute of Belarusian State University, 2022. http://dx.doi.org/10.46646/sakh-2022-2-31-34.

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Ritonavir, nelfinavir and lopinavir are a group of protease inhibitors. These inhibitors are widely used in combination with other protease inhibitors in the therapy and prevention of human immunodeficiency virus. Also, the combination of these inhibitors seems to be an effective therapeutic agent that can affect the main protease of Mpro coronavirus and, thus, provide long-term suppression of viral load in the disease of severe acute respiratory syndrome caused by coronavirus 2 (SARS-CoV-2).
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Caulk, Alexander W., i Rudolph L. Gleason. "Treatment With Non-Nucleoside Reverse Transcriptase Inhibitor Efavirenz Leads to Increase of Carotid Intima-Media Thickness in Mice". W ASME 2013 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2013. http://dx.doi.org/10.1115/sbc2013-14744.

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Since the advent of highly active antiretroviral therapy (HAART), patients infected with human immunodeficiency virus-1 (HIV-1) are living longer lives. However, HIV-1-positive (HIV-1+) patients are now experiencing many non-AIDS related comorbidities including myocardial infarction, atherosclerotic lesions, and other preclinical markers of atherosclerosis including increased carotid intima-media thickness (cIMT), arterial stiffness, and impaired flow-mediated dilation (FMD). Studies have implicated the virus, the treatment, or both in the progression of these co-morbidities, causing the exact mechanisms of cardiovascular disease progression to remain unclear.
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8

Rubtcova, M. V., i A. M. Bolotnik. "THE DEGREE OF INFLUENCE OF SOCIO-ECONOMIC FACTORS ON THE INCIDENCE OF HIV IN THE RUSSIAN FEDERATION: THE RESULTS OF REGRESSION ANALYSIS". W Regional economy and territorial development. INSTITUTE OF PROBLEMS OF REGIONAL ECONOMICS OF THE RUSSIAN ACADEMY OF SCIENCES, 2021. http://dx.doi.org/10.52897/978-5-8088-1636-7-2021-15-1-85-93.

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The spread of the human immunodeficiency virus is one of the main global problems. In all countries of the world there are a number of programs aimed at combating this disease. We conducted a regression analysis to identify the most influencing factors of the population's life on the spread of HIV. The results showed that external socio-economic factors did not have a significant impact on the spread of the virus. It means that the health care system and its level of development directly affect the level of HIV prevalence in the country.
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9

Evers, Georg, Arik Bernard Schulze, Michael Thrull, Georg Lenz, Lars Henning Schmidt i Michael Mohr. "Alpha-1 antitrypsin deficiency and pulmonary morbidity in patients with primary immunodeficiency disease: A single center experience". W ERS International Congress 2018 abstracts. European Respiratory Society, 2018. http://dx.doi.org/10.1183/13993003.congress-2018.pa1141.

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Nosari, A. M., L. Barbarnano, T. M. Caimi, A. Strinchini, G. Muti, B. Branbo, F. decataldo i F. Baudo. "ANTIBODIES TO HUMAN IMMUNODEFICIENCY VIRUS (HIV) IN HAEMOPHILIA AND VON WILLEBRAND'S DISEASE AND IN THEIR HETEROSEXUAL PARTNERS". W XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644141.

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The prevalence of antibodies to HIV in Haemophiliacs varies in different series: the latest figures (19636) are 12-94%, the lower values referring to patients with the mild form or treated by blood bank products. Serum conversion dates back to 1978 in USA and to 1980 in Europe. Antibodies to HIV in heterosexual partners are reported in percentage from 0-24%. Our population of patients:ALL VON WILLEBRANND'disease-patients were treated by crycoprecipitates and are all antibodies to HIV negative lymphocyte subsets: CD4 × 109/1 (x) 863; CD4/CD8(x)1.148.10 hetrosexual partners of anti HIV positive heamophiliacs were tested:Stored samples of prozen plasam of 19 haemophiliacs were also tested:p patients were found anti HIV positive ;1 in 1980;2 in 1982;2 in 1994.
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Raporty organizacyjne na temat "Immunodeficiency disease"

1

Gardner, Murray B. Genetic Immunization for Lentiviral Immunodeficiency Virus Infection and Disease. Fort Belvoir, VA: Defense Technical Information Center, październik 1998. http://dx.doi.org/10.21236/ada361721.

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Gardner, Murray B. Genetic Immunization for Lentiviral Immunodeficiency Virus Infection and Disease. Fort Belvoir, VA: Defense Technical Information Center, listopad 1997. http://dx.doi.org/10.21236/ada338248.

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3

Zheng, Ruo-xiang, Xun Li, Jing Li, Zhen-wei Liu, Feng Jiang, Nicola Robinson i Jian-ping Liu. Does Chinese herbal remedy Tangcao tablet work for the treatment of HIV/AIDS：a systematic review of controlled clinical trials. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, czerwiec 2022. http://dx.doi.org/10.37766/inplasy2022.6.0042.

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Review question / Objective: This study aims to evaluate the effectiveness and safety of Tangcao tablet (Tangcao) for treating people with HIV/AIDS. Condition being studied: Acquired immunodeficiency syndrome (AIDS) is a chronic infectious disease characterized by severe immunodeficiency caused by the human immunodeficiency virus (HIV). The infection attacks specifically the white blood cells, CD4+T (CD4) cells, weakening the immunity of individuals against infections such as tuberculosis. Without treatment, patients with AIDS may survive up to 2 years. Pneumocystis pneumonia and infections of the central nervous system are two of the most common causes of death in people with AIDS. AIDS still remains a significant global public health problem, with an estimated 37.7 million people infected with HIV at the end of 2020.
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4

Haider, Huma. Malaria, HIV and TB in Nigeria: Epidemiology and Disease Control Challenges. Institute of Development Studies (IDS), grudzień 2021. http://dx.doi.org/10.19088/k4d.2022.040.

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Nigeria has the world’s highest number of people affected by malaria and the world’s second largest human immunodeficiency virus (HIV)/AIDS burden. There is a high occurrence of co-infection of malaria in HIV patients (Gumel et al., 2021). Nigeria is also ranked as one of the thirty high tuberculosis (TB) and TB-HIV co-infection burden countries in the world (Odume et al., 2020, 8). Co-infection can make each disease more severe and potentially more infectious (Gumel et al., 2021; Jemikalajah et al., 2021; Chukwuocha et al., 2019). This rapid literature review highlights key aspects of the epidemiology of malaria, HIV and TB in Nigeria, in addition to challenges in controlling the three diseases, in terms of prevention, detection and treatment. This is part of a series of reports looking into Epidemiology of Malaria, human immune deficiency virus (HIV) and tuberculosis (TB) across a set of African Nations.
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5

Booth-Kewley, Stephanie, Allyson M. Andrews, Richard A. Shaffer, Patricia Gilman i Rahn Y. Minagawa. One-Year Follow-Up Evaluation of the Sexually Transmitted Disease/Human Immunodeficiency Virus Intervention Program in a Marine Corps Sample. Fort Belvoir, VA: Defense Technical Information Center, styczeń 2000. http://dx.doi.org/10.21236/ada421106.

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Ozano, Kim. Integration of HIV, TB and malaria in Africa: A Reflection Workshop. Institute of Development Studies, lipiec 2022. http://dx.doi.org/10.19088/k4d.2022.095.

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Recognising the importance of integrated health service management and delivery to accelerate Universal Health Care (UHC) and tackle the Human Immunodeficiency Viruses (HIV), tuberculosis (TB), and malaria epidemics, the UK’s Foreign, Commonwealth and Development Office (FCDO) commissioned the Knowledge, Evidence and Learning for Development (K4D) Programme to undertake an evidence synthesis exercise of a set of BACKUP Health1 and K4D Helpdesk reports across six countries: Uganda, the Democratic Republic of Congo (DRC), Tanzania, Mozambique, Nigeria, and Zimbabwe (Ozano, 2022). The K4D reports highlight country-specific epidemiology, disease control programmes, and key interventions for each disease, including those likely to strengthen health systems and promote integration. The BACKUP reports focus more on integration and add country-specific details with recommendations.
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7

Ficht, Thomas, Gary Splitter, Menachem Banai i Menachem Davidson. Characterization of B. Melinensis REV 1 Attenuated Mutants. United States Department of Agriculture, grudzień 2000. http://dx.doi.org/10.32747/2000.7580667.bard.

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Brucella Mutagenesis (TAMU) The working hypothesis for this study was that survival of Brucella vaccines was directly related to their persistence in the host. This premise is based on previously published work detailing the survival of the currently employed vaccine strains S19 and Rev 1. The approach employed signature-tagged mutagenesis to construct mutants interrupted in individual genes, and the mouse model to identify mutants with attenuated virulence/survival. Intracellular survival in macrophages is the key to both reproductive disease in ruminants and reticuloendothelial disease observed in most other species. Therefore, the mouse model permitted selection of mutants of reduced intracellular survival that would limit their ability to cause reproductive disease in ruminants. Several classes of mutants were expected. Colonization/invasion requires gene products that enhance host-agent interaction or increase resistance to antibacterial activity in macrophages. The establishment of chronic infection requires gene products necessary for intracellular bacterial growth. Maintenance of chronic infection requires gene products that sustain a low-level metabolism during periods characterized little or no growth (1, 2). Of these mutants, the latter group was of greatest interest with regard to our originally stated premise. However, the results obtained do not necessarily support a simplistic model of vaccine efficacy, i.e., long-survival of vaccine strains provides better immunity. Our conclusion can only be that optimal vaccines will only be developed with a thorough understanding of host agent interaction, and will be preferable to the use of fortuitous isolates of unknown genetic background. Each mutant could be distinguished from among a group of mutants by PCR amplification of the signature tag (5). This approach permitted infection of mice with pools of different mutants (including the parental wild-type as a control) and identified 40 mutants with apparently defective survival characteristics that were tentatively assigned to three distinct classes or groups. Group I (n=13) contained organisms that exhibited reduced survival at two weeks post-infection. Organisms in this group were recovered at normal levels by eight weeks and were not studied further, since they may persist in the host. Group II (n=11) contained organisms that were reduced by 2 weeks post infection and remained at reduced levels at eight weeks post-infection. Group III (n=16) contained mutants that were normal at two weeks, but recovered at reduced levels at eight weeks. A subset of these mutants (n= 15) was confirmed to be attenuated in mixed infections (1:1) with the parental wild-type. One of these mutants was eliminated from consideration due to a reduced growth rate in vitro that may account for its apparent growth defect in the mouse model. Although the original plan involved construction of the mutant bank in B. melitensis Rev 1 the low transformability of this strain, prevented accumulation of the necessary number of mutants. In addition, the probability that Rev 1 already carries one genetic defect increases the likelihood that a second defect will severely compromise the survival of this organism. Once key genes have been identified, it is relatively easy to prepare the appropriate genetic constructs (knockouts) lacking these genes in B. melitensis Rev 1 or any other genetic background. The construction of "designer" vaccines is expected to improve immune protection resulting from minor sequence variation corresponding to geographically distinct isolates or to design vaccines for use in specific hosts. A.2 Mouse Model of Brucella Infection (UWISC) Interferon regulatory factor-1-deficient (IRF-1-/- mice have diverse immunodeficient phenotypes that are necessary for conferring proper immune protection to intracellular bacterial infection, such as a 90% reduction of CD8+ T cells, functionally impaired NK cells, as well as a deficiency in iNOS and IL-12p40 induction. Interestingly, IRF-1-/- mice infected with diverse Brucella abortus strains reacted differently in a death and survival manner depending on the dose of injection and the level of virulence. Notably, 50% of IRF-1-/- mice intraperitoneally infected with a sublethal dose in C57BL/6 mice, i.e., 5 x 105 CFU of virulent S2308 or the attenuated vaccine S19, died at 10 and 20 days post-infection, respectively. Interestingly, the same dose of RB51, an attenuated new vaccine strain, did not induce the death of IRF-1-/- mice for the 4 weeks of infection. IRF-1-/- mice infected with four more other genetically manipulated S2308 mutants at 5 x 105 CFU also reacted in a death or survival manner depending on the level of virulence. Splenic CFU from C57BL/6 mice infected with 5 x 105 CFU of S2308, S19, or RB51, as well as four different S2308 mutants supports the finding that reduced virulence correlates with survival Of IRF-1-/- mice. Therefore, these results suggest that IRF-1 regulation of multi-gene transcription plays a crucial role in controlling B. abortus infection, and IRF-1 mice could be used as an animal model to determine the degree of B. abortus virulence by examining death or survival. A3 Diagnostic Tests for Detection of B. melitensis Rev 1 (Kimron) In this project we developed an effective PCR tool that can distinguish between Rev1 field isolates and B. melitensis virulent field strains. This has allowed, for the first time, to monitor epidemiological outbreaks of Rev1 infection in vaccinated flocks and to clearly demonstrate horizontal transfer of the strain from vaccinated ewes to unvaccinated ones. Moreover, two human isolates were characterized as Rev1 isolates implying the risk of use of improperly controlled lots of the vaccine in the national campaign. Since atypical B. melitensis biotype 1 strains have been characterized in Israel, the PCR technique has unequivocally demonstrated that strain Rev1 has not diverted into a virulent mutant. In addition, we could demonstrate that very likely a new prototype biotype 1 strain has evolved in the Middle East compared to the classical strain 16M. All the Israeli field strains have been shown to differ from strain 16M in the PstI digestion profile of the omp2a gene sequence suggesting that the local strains were possibly developed as a separate branch of B. melitensis. Should this be confirmed these data suggest that the Rev1 vaccine may not be an optimal vaccine strain for the Israeli flocks as it shares the same omp2 PstI digestion profile as strain 16M.
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