Relevant bibliographies by topics / HIV; Immunology; Viral infections

Contents

  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers
  6. Reports

Academic literature on the topic 'HIV; Immunology; Viral infections'

Author: Grafiati
Published: 4 June 2021
Last updated: 5 February 2022

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Journal articles on the topic "HIV; Immunology; Viral infections"

1

Schmack, Ingo, Seda Ballikaya, Brigitte Erber, Irina Voehringer, Ulrich Burkhardt, Gerd U. Auffarth, and Paul Schnitzler. "Validation of Spiked Postmortem Blood Samples from Cornea Donors on the Abbott ARCHITECT and m2000 Systems for Viral Infections." Transfusion Medicine and Hemotherapy 47, no. 3 (September 24, 2019): 236–43. http://dx.doi.org/10.1159/000502866.

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Background: Transplantation of human corneal tissue is associated with the potential risk of transmittance of viral infections. In accordance with European directives and federal laws, in Germany each tissue donor has to be tested for infectious diseases such as hepatitis B and C virus (HBV and HCV) and human immunodeficiency virus (HIV) infection. However, most of the currently available CE-marked serologic and nucleic acid screening systems are only validated for antemortem blood. Methods: Twenty related and paired ante- and postmortem blood samples from cornea donors were obtained and subsequently analyzed for hepatitis B surface antigen (HBsAg), hepatitis B antibody (anti-HBc), anti-HCV, HCV RNA, anti-HIV-1/2, and HIV p24 Ag using Abbott test systems. The sera were also spiked with reference materials in concentrations giving low and high positivity for HBV, HCV, and HIV markers. Results: The spiked ante- and postmortem sera from related donors showed similar results for HBsAg, anti-HBc, anti-HCV, HCV RNA, anti-HIV, and HIV p24 Ag, indicating a high stability of viral markers in cadaveric specimens. Three cornea donors had a medical history of HBV infection and revealed anti-HBc at similar levels in the ante- and postmortem sera. In addition, there was a single postmortem sample demonstrating a weak signal of anti-HIV-1 and HIV-1 p24 Ag. False-positive or false-negative results were not detected. The results obtained with the Abbott ARCHITECT analyzer and Abbott RealTime HCV PCR showed no significant differences. Conclusion: The analyzed screening assays are suitable for the detection of infectious markers of HBV, HCV, and HIV at similar levels in spiked ante- and postmortem sera from cornea donors.
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2

Miller, M. D., M. T. Warmerdam, I. Gaston, W. C. Greene, and M. B. Feinberg. "The human immunodeficiency virus-1 nef gene product: a positive factor for viral infection and replication in primary lymphocytes and macrophages." Journal of Experimental Medicine 179, no. 1 (January 1, 1994): 101–13. http://dx.doi.org/10.1084/jem.179.1.101.

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Considerable controversy and uncertainty have surrounded the biological function of the Human Immunodeficiency Virus (HIV)-1 nef gene product. Initial studies suggested that this early, nonstructural viral protein functioned as a negative regulatory factor; thus, it was proposed to play a role in establishing or maintaining viral latency. In contrast, studies in Simian Immunodeficiency Virus (SIV)mac-infected rhesus monkeys have suggested that Nef is not a negative factor but rather plays a central role in promoting high-level viral replication and is required for viral pathogenesis in vivo. We sought to define a tissue culture system that would approximate the in vivo setting for virus infection in order to assess the role of HIV-1 Nef in viral replication. We show that infection of mitogen-activated peripheral blood mononuclear cells (PBMC) with Nef+ HIV results in enhanced replication as evidenced by earlier gag p24 expression when compared with infections performed with nef mutant viruses. Moreover, when unstimulated freshly isolated PBMC are infected with Nef+ and Nef- viruses and then subsequently activated with mitogen, the Nef-induced difference in viral replication kinetics is even more pronounced, with the Nef- viruses requiring much more time in culture for appreciable growth. A positive effect of Nef on viral replication was also observed in primary macrophages infected with a recombinant of YU-2, a patient-derived molecular clone with macrophage tropism. These positive effects of Nef on viral replication are dependent on the initial multiplicity of infection (MOI), in that infections of unstimulated PBMC at low MOI are most dependent upon intact nef for subsequent viral growth. We now provide evidence that the Nef+ HIV is more infectious than Nef- HIV from both a tissue culture infectious dose analysis, and a single-cell HIV infection assay. In the latter case, we demonstrate that infection with equivalent doses of HIV based on virion-associated gag p24 yields five- to sixfold more infected cells if Nef+ viral stocks were used. Furthermore, we find that the differential infectivity is not dependent on CD4 down-regulation as Nef+ virus produced from transfected COS cells lacking CD4 is also more infectious. However, normalization of PBMC infections to equivalent infectivity between that of the Nef+ and Nef- viruses continues to reveal delayed viral replication in the absence of Nef, suggesting that secondary viral spread in PBMC is also enhanced in Nef+ infections. We demonstrate this directly by showing a 13-15-fold increase in infectivity of PBMC-derived Nef+ HIC.(ABSTRACT TRUNCATED AT 400 WORDS)
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Swiecki, Melissa, Yaming Wang, William Vermi, Susan Gilfillan, Robert D. Schreiber, and Marco Colonna. "Type I interferon negatively controls plasmacytoid dendritic cell numbers in vivo." Journal of Experimental Medicine 208, no. 12 (November 14, 2011): 2367–74. http://dx.doi.org/10.1084/jem.20110654.

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Plasmacytoid dendritic cells (pDCs) specialize in the secretion of type I interferons (IFN-I) and thus are considered critical mediators of antiviral responses. We recently reported that pDCs have a very early but limited and transient capacity to curtail viral infections. Additionally, pDC numbers are not sustained in human infections caused by Hepatitis B or C viruses (HBV and HCV) and HIV. Thus, the numbers and/or function of pDCs appear to be regulated during the course of viral infection. In this study, we show that splenic pDCs are reduced in vivo during several systemic viral infections and after administration of synthetic toll-like receptor ligands. We demonstrate that IFN-I, regardless of the source, contributes to this decline and mediates pDC death via the intrinsic apoptosis pathway. These findings demonstrate a feedback control mechanism by which IFN-I modulates pDC numbers, thus fine-tuning systemic IFN-I response to viruses. IFN-I–mediated control of pDCs may explain the loss of pDCs during human infections caused by HBV, HCV, or HIV and has important therapeutic implications for settings in which IFN-I is used to treat infections and autoimmune diseases.
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Yokozaki, Shouichi, Junki Takamatsu, Isao Nakano, Yoshiaki Katano, Hidenori Toyoda, Kazuhiko Hayashi, Tetsuo Hayakawa, and Yoshihide Fukuda. "Immunologic dynamics in hemophiliac patients infected with hepatitis C virus and human immunodeficiency virus: influence of antiretroviral therapy." Blood 96, no. 13 (December 15, 2000): 4293–99. http://dx.doi.org/10.1182/blood.v96.13.4293.

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Abstract Infection with hepatitis C virus (HCV) or human immunodeficiency virus (HIV) or both is common in hemophiliac patients due to putative transmission through clotting factor concentrates. Recently, highly active antiretroviral therapy (HAART) has been found to markedly improve viremia and immunologic parameters in patients infected with HIV. This report considers interactions between these viral infections, the immune system, and antiretroviral therapy. A total of 130 male hemophiliac patients were grouped according to type of viremia (HCV, HIV, both, or neither). Along with 30 healthy men age-matched to viremic patients, these groups were compared with respect to viral load and immunologic parameters. Thirty-five patients treated as above for HIV were serially followed up. HCV infection was associated with reduced peripheral B-cell and CD4+-cell counts and with increased serum IgG and IgM levels, whereas HIV infection was associated with reduced peripheral CD4+-cell counts and increased serum IgG and IgA levels. In patients with both viruses, HCV and HIV RNA load correlated inversely with peripheral B-cell and CD4+-cell counts, respectively. HAART reduced levels of both viruses in the blood. Of the 25 patients with both viruses, HAART eliminated HCV in 2. In conclusion, immunologic dynamics differed between hemophiliac patients infected with HCV, HIV, or both. The relative dynamics of HCV viral load, peripheral B-cell count, and serum IgM level were similar to those of HIV viral load, CD4+-cell count, and serum IgA.
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Yokozaki, Shouichi, Junki Takamatsu, Isao Nakano, Yoshiaki Katano, Hidenori Toyoda, Kazuhiko Hayashi, Tetsuo Hayakawa, and Yoshihide Fukuda. "Immunologic dynamics in hemophiliac patients infected with hepatitis C virus and human immunodeficiency virus: influence of antiretroviral therapy." Blood 96, no. 13 (December 15, 2000): 4293–99. http://dx.doi.org/10.1182/blood.v96.13.4293.h8004293_4293_4299.

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Infection with hepatitis C virus (HCV) or human immunodeficiency virus (HIV) or both is common in hemophiliac patients due to putative transmission through clotting factor concentrates. Recently, highly active antiretroviral therapy (HAART) has been found to markedly improve viremia and immunologic parameters in patients infected with HIV. This report considers interactions between these viral infections, the immune system, and antiretroviral therapy. A total of 130 male hemophiliac patients were grouped according to type of viremia (HCV, HIV, both, or neither). Along with 30 healthy men age-matched to viremic patients, these groups were compared with respect to viral load and immunologic parameters. Thirty-five patients treated as above for HIV were serially followed up. HCV infection was associated with reduced peripheral B-cell and CD4+-cell counts and with increased serum IgG and IgM levels, whereas HIV infection was associated with reduced peripheral CD4+-cell counts and increased serum IgG and IgA levels. In patients with both viruses, HCV and HIV RNA load correlated inversely with peripheral B-cell and CD4+-cell counts, respectively. HAART reduced levels of both viruses in the blood. Of the 25 patients with both viruses, HAART eliminated HCV in 2. In conclusion, immunologic dynamics differed between hemophiliac patients infected with HCV, HIV, or both. The relative dynamics of HCV viral load, peripheral B-cell count, and serum IgM level were similar to those of HIV viral load, CD4+-cell count, and serum IgA.
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Troisi, CL, FB Hollinger, WK Hoots, C. Contant, J. Gill, M. Ragni, R. Parmley, C. Sexauer, E. Gomperts, and G. Buchanan. "A multicenter study of viral hepatitis in a United States hemophilic population." Blood 81, no. 2 (January 15, 1993): 412–18. http://dx.doi.org/10.1182/blood.v81.2.412.412.

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Abstract Hemophilia A and B patients seen at nine US regional treatment centers were tested for serologic markers of hepatitis B virus (HBV), hepatitis C virus (HCV), and hepatitis delta virus (HDV) during 1987 and 1988. Because human immunodeficiency virus (HIV) infection, a potentially confounding variable, was present in 53% of the group, the population was divided by HIV status for analysis purposes. In the HIV-positive group (N = 382), less than 1% had not been infected with HBV, HCV, or HDV, whereas 75% had evidence of infection with HBV and 98% with HCV. HBsAg, a marker of active HBV infection, was present in 12% of subjects; 96% of these were HCV positive. Anti-HDV was detected in 35 subjects (9.1%); all were anti-HBc positive. Ten of the 35 (29%) also were positive for IgM anti-HDV, indicating current infection. All 10 were HBsAg positive and 7 of the 9 tested were HDV RNA positive. Severe/moderate hemophilia B patients were more likely to have experienced an HBV infection and to be anti-HDV positive than were similar hemophilia A patients (22% v 8%, P < .05). In the HIV-negative group (N = 345), the subjects were younger and had less severe hemophilia than the HIV-positive patients. No evidence of HBV, HCV, or HDV infection was found in 18%, whereas 33% had experienced HBV infection and 79% were anti-HCV positive. Within this group, 4% were HBsAg positive. All 13 subjects with anti-HDV (4% of the HIV-negative group) also possessed anti-HBc. One (7.7%) was IgM anti-HDV positive and the serum from another contained HDV RNA. Both of these individuals were HBsAg positive. As in the HIV-positive group, severe/moderate hemophilia B patients were more likely to be HBV and HDV positive than were hemophilia A patients (9% v 3%, P < .05). A prevalence study of viral hepatitis in a large US hemophilic population showed that active infection with HCV is common, occurring in 89% of all study patients regardless of HIV status. Evidence of active HBV infection was found in 8%; 19% of these were actively infected with HDV. HDV was more common in hemophilia B patients after controlling for disease severity.
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Troisi, CL, FB Hollinger, WK Hoots, C. Contant, J. Gill, M. Ragni, R. Parmley, C. Sexauer, E. Gomperts, and G. Buchanan. "A multicenter study of viral hepatitis in a United States hemophilic population." Blood 81, no. 2 (January 15, 1993): 412–18. http://dx.doi.org/10.1182/blood.v81.2.412.bloodjournal812412.

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Hemophilia A and B patients seen at nine US regional treatment centers were tested for serologic markers of hepatitis B virus (HBV), hepatitis C virus (HCV), and hepatitis delta virus (HDV) during 1987 and 1988. Because human immunodeficiency virus (HIV) infection, a potentially confounding variable, was present in 53% of the group, the population was divided by HIV status for analysis purposes. In the HIV-positive group (N = 382), less than 1% had not been infected with HBV, HCV, or HDV, whereas 75% had evidence of infection with HBV and 98% with HCV. HBsAg, a marker of active HBV infection, was present in 12% of subjects; 96% of these were HCV positive. Anti-HDV was detected in 35 subjects (9.1%); all were anti-HBc positive. Ten of the 35 (29%) also were positive for IgM anti-HDV, indicating current infection. All 10 were HBsAg positive and 7 of the 9 tested were HDV RNA positive. Severe/moderate hemophilia B patients were more likely to have experienced an HBV infection and to be anti-HDV positive than were similar hemophilia A patients (22% v 8%, P < .05). In the HIV-negative group (N = 345), the subjects were younger and had less severe hemophilia than the HIV-positive patients. No evidence of HBV, HCV, or HDV infection was found in 18%, whereas 33% had experienced HBV infection and 79% were anti-HCV positive. Within this group, 4% were HBsAg positive. All 13 subjects with anti-HDV (4% of the HIV-negative group) also possessed anti-HBc. One (7.7%) was IgM anti-HDV positive and the serum from another contained HDV RNA. Both of these individuals were HBsAg positive. As in the HIV-positive group, severe/moderate hemophilia B patients were more likely to be HBV and HDV positive than were hemophilia A patients (9% v 3%, P < .05). A prevalence study of viral hepatitis in a large US hemophilic population showed that active infection with HCV is common, occurring in 89% of all study patients regardless of HIV status. Evidence of active HBV infection was found in 8%; 19% of these were actively infected with HDV. HDV was more common in hemophilia B patients after controlling for disease severity.
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Goulder, Philip J. R., Marcus A. Altfeld, Eric S. Rosenberg, Thi Nguyen, Yanhua Tang, Robert L. Eldridge, Marylyn M. Addo, et al. "Substantial Differences in Specificity of HIV-Specific Cytotoxic T Cells in Acute and Chronic HIV Infection." Journal of Experimental Medicine 193, no. 2 (January 8, 2001): 181–94. http://dx.doi.org/10.1084/jem.193.2.181.

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Cytotoxic T lymphocytes (CTLs) play a vital part in controlling viral replication during human viral infections. Most studies in human infections have focused on CTL specificities in chronic infection and few data exist regarding the specificity of the initial CTL response induced in acute infection. In this study, HIV-1 infection in persons expressing human histocompatibility leukocyte antigen (HLA)-A*0201 was used as a means of addressing this issue. In chronic infection, the dominant HLA-A*0201–restricted CTL response is directed towards the epitope SLYNTVATL (“SL9”) in p17 Gag (residues 77–85). This epitope is targeted by 75% of HLA-A*0201–positive adults, and the magnitude of this A*0201-SL9 response shows a strong negative association with viral load in progressive infection. Despite using the highly sensitive peptide–major histocompatibility complex tetramer and intracellular cytokine assays, responses to the SL9 epitope were not detectable in any of 11 HLA-A*0201–positive subjects with acute HIV-1 infection (P = 2 × 10−6), even when assays were repeated using the SL9 peptide variant that was encoded by their autologous virus. In contrast, multiple responses (median 3) to other epitopes were evident in 7 of the 11 A*0201–positive subjects. Longitudinal study of two subjects confirmed that the A*0201-SL9 response emerged later than other CTL responses, and after viral set point had been reached. Together, these data show that the CTL responses that are present and that even may dominate in chronic infection may differ substantially from those that constitute the initial antiviral CTL response. This finding is an important consideration in vaccine design and in the evaluation of vaccine candidates.
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Ong, Catherine Wei Min, Giovanni Battista Migliori, Mario Raviglione, Gavin MacGregor-Skinner, Giovanni Sotgiu, Jan-Willem Alffenaar, Simon Tiberi, et al. "Epidemic and pandemic viral infections: impact on tuberculosis and the lung." European Respiratory Journal 56, no. 4 (June 25, 2020): 2001727. http://dx.doi.org/10.1183/13993003.01727-2020.

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Major epidemics, including some that qualify as pandemics, such as severe acute respiratory syndrome (SARS), Middle East respiratory syndrome (MERS), HIV, influenza A (H1N1)pdm/09 and most recently COVID-19, affect the lung. Tuberculosis (TB) remains the top infectious disease killer, but apart from syndemic TB/HIV little is known regarding the interaction of viral epidemics and pandemics with TB. The aim of this consensus-based document is to describe the effects of viral infections resulting in epidemics and pandemics that affect the lung (MERS, SARS, HIV, influenza A (H1N1)pdm/09 and COVID-19) and their interactions with TB. A search of the scientific literature was performed. A writing committee of international experts including the European Centre for Disease Prevention and Control Public Health Emergency (ECDC PHE) team, the World Association for Infectious Diseases and Immunological Disorders (WAidid), the Global Tuberculosis Network (GTN), and members of the European Society of Clinical Microbiology and Infectious Diseases (ESCMID) Study Group for Mycobacterial Infections (ESGMYC) was established. Consensus was achieved after multiple rounds of revisions between the writing committee and a larger expert group. A Delphi process involving the core group of authors (excluding the ECDC PHE team) identified the areas requiring review/consensus, followed by a second round to refine the definitive consensus elements. The epidemiology and immunology of these viral infections and their interactions with TB are discussed with implications for diagnosis, treatment and prevention of airborne infections (infection control, viral containment and workplace safety). This consensus document represents a rapid and comprehensive summary on what is known on the topic.
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Manapova, E. R., V. Kh Fazylov, and A. T. Beshimov. "Clinical and immunological characteristic of natural course at the early stages of HIV infection." Medical Immunology (Russia) 22, no. 3 (May 21, 2020): 519–26. http://dx.doi.org/10.15789/1563-0625-cai-1866.

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An early-stage infection induces the most powerful reactions of immune system. 137 clinical histories of patients with HIV infection, and HCV/HIV-infected at the early stages of HIV infection were subjected to analysis. Patients and methods: a group of 45 patients at early terms of HIV infection included 25 cases of HCV/HIV-infected patients (first group), and 20 cases with HIV mono-infection (second group). Duration of infection was less than 1 year (with positive ELISA test), with mean terms of HIV immunoblot positivity of 5.5±0.6 months. For comparative analysis, the natural course group was examined, i.e., 43 patients with combined HCV/HIV infection (third group), and 49, with HIV monoinfection (fourth group) with a duration of HIV infection for 4.4±0.21 years. The group of healthy controls included 52 persons. We aimed to perform a comparative evaluation of clinical course and immunological features from the early stages of infection in the patients with combined HCV/HIV and HIV infection. Results: at early stages of infection, clinical pattern in HCV/HIV-infected patients was dominated by purulent-inflammatory, fungal infections and secondary diseases, along with more pronounced inhibition of cellular immunity and increased viral load of RNA HIV, as compared to data on HIV-infected patients.
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More sources

Dissertations / Theses on the topic "HIV; Immunology; Viral infections"

1

Huang, Kenneth Hsing-Chung. "Immune correlates of viral control in chronic HIV infection." Thesis, McGill University, 2008. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=111908.

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There are currently an estimated 33.2 million people living with human immunodeficiency virus (HIV) worldwide. For these individuals, long-term use of combination antiretroviral therapy (cART) is not feasible for a variety of reasons including major adverse complications, multi-drug resistance, poor adherence, and high cost. Hence, development of novel therapeutic strategies that can reduce the life-long dependency on cART is highly desired. In order to develop effective therapeutic strategies such as a therapeutic vaccine, we need to have a greater understanding of the immune correlates of viral control in chronic HIV infection. In this thesis, we used treatment interruption (TI) as a tool to test the efficacy of several therapeutic approaches and immune parameters for their association with effective control of viral replication.
In Chapter 2 we showed that cART intensification and Remune vaccination resulted in reduced viral load (VL) plateau during sequential TIs. Although HIV-specific immune responses measured by interferon-gamma (IFN-gamma) enzyme-linked immunospot assay (ELISPOT) increased in the same time frame, neither their breadth nor magnitude correlated with the decrease in VL plateau. In Chapter 3 the effect of ALVAC-vCP1425 plus Remune vaccination on HIV proteome-wide HIV-specific responses was monitored using a dual color IFN-gamma/interleukin-2 (IL-2) ELISPOT assay. We observed an increase in the magnitude of HIV-specific IFN-gamma/IL-2 responses, as well as in the breadth of Gag-specific IFN-gamma responses in the vaccinated groups compared to placebo groups. A shift towards an increased contribution of Gag-specific responses to total HIV-specific vaccine induced immune response was associated with longer delay to viral rebound during TI. In Chapters 4 and 5, we examined baseline pre-TI immune parameters and their association with viral rebound and CD4 count change during TI in HIV-infected individuals in the chronic phase of infection experiencing virologic failure before TI (Chapter 4) or with different levels of VL control while on therapy prior to TI (Chapter 5). We saw that chronic antigen stimulation from persistent viremia as well as co-infections such as with cytomegalovirus are associated with T-cell senescence, which may result in less favourable clinical outcomes during TI.
Consequently, results from this thesis contribute to further understanding of immune correlates of viral control in chronic HIV infection. New therapeutic vaccines and interventions should induce polyfunctional HIV-specific immune responses, broad Gag-specific immune responses, as well as reducing chronic antigen stimulation to prevent irreversible T-cell exhaustion. Taken together, these insights could potentially lead to the development of novel treatment interventions that could effectively control viral replication off cART.
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Rowland-Jones, Sarah Louise. "The role of class I MHC molecules in the presentation of viral antigens to cytotoxic T lymphocytes." Thesis, University of Oxford, 1994. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.296832.

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Azizi, Ali. "Humoral and cellular immune responses in RNA viral infections: Immunogenicity of HIV-1, HCV and SARS-CoV candidate vaccines in animal models." Thesis, University of Ottawa (Canada), 2006. http://hdl.handle.net/10393/29278.

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It is difficult to induce protective immunity against most RNA viruses. However, there is strong evidence that humoral and especially cellular immune responses play crucial roles in the control of established RNA viral infections. Thus, an ideal vaccine should be able to induce strong specific antibody titer as well as a robust T-helper and T-cell cytotoxic response. Here, correlates of protective immunity against HIV-1, HCV and SARS-CoV were assessed. Monocistronic and polycistronic DNA constructs containing structural HIV-l, and SARS genes were designed. The structural proteins (HIV- gpl20, gag, pol, HCV-core, E1/E2 and SARS-NC) were also expressed, purified and characterized in mammalian and bacterial cell lines. HLA-A2.1 and B6 mice were immunized with different combinations of DNA constructs, recombinant proteins and novel adjuvants. Humoral responses were measured by titrating of specific antibodies and cell-mediated immune responses were identified by Th1/Th2 cytokine expression, lymphocyte proliferation, intracellular cytokine staining, HLA-peptide dimer assay, and ELISPOT. The first study in HIV-1 showed that a combination of DNA single constructs, protein and adjuvant induce a higher immune response compared to the DNA or/and protein alone. In the second HIV-1 approach, a synergistic effect between HIV/HCV antigens was detected that may lead to induction of multi-specific immune responses against both HIV and HCV. In the third study (SARS project), a high level of specific SARS-CD8+ T-cell response was demonstrated in mice that received DNA encoding the SARS-nucleocapsid, protein and XIAP (X-link inhibitor of apoptosis) as an adjuvant.
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Ogbu, Stella Chinyere. "Role of Topoisomerase II alpha in DNA Topology and T cell responses during Chronic Viral Infections." Digital Commons @ East Tennessee State University, 2019. https://dc.etsu.edu/etd/3661.

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The clearance of viruses is largely dependent upon the activation of T cells to generate a robust immune response. However, host responses are suppressed during chronic viral infections. In this thesis, we explored the role of Top2α in DNA topology in individuals with chronic HBV, HCV, and HIV infections. We found that Top2α protein expression and activity were low in T cells derived from chronically virus-infected individuals compared to healthy subjects. Using CD4+ T cells treated with Top2α inhibitor or poisoner as a model, we demonstrated that Top2α inhibition disrupts the DNA topology, suppresses DNA repair kinase (ATM), and telomere protein (TRF2) expression, and induces T cell dysfunction. These findings reveal that Top2α inhibition is a mechanism by which viruses evade the host responses and establish persistent infection, and thus, restoring Top2α levels could be a way of boosting immune responses during chronic viral infections.
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Peng, Yanchun. "HLA-B51 associated HIV-1 viral control." Thesis, University of Oxford, 2013. http://ora.ox.ac.uk/objects/uuid:8e06bed0-bd8d-4774-b137-c12f5e3547fc.

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Polymorphism in the Human Leucocyte Antigen (HLA) region of chromosome is the major source of host genetic variability in outcome of HIV-1 infection. However, there is limited understanding of the mechanisms underlying the beneficial effect of protective class I alleles such as HLA-B57, B27 and B51. Taking advantage of a unique cohort (SM cohort) infected with clade B’ HIV-1 through contaminated blood, in which many variables, such as the length of infection, the infecting viral strain and host genetic background are controlled, we performed a comprehensive study in order to understand HLA-B51 associated HIV-1 control. We first focused on the T cell responses against three dominant HLA-B51 restricted epitopes: GagNI9 (NANPDCKTI), Pol TV8 (TAFTIPSV) and Pol LI9 (LPPVVAKEI), and HLA-B51 associated escape mutations in these three epitopes. A sequential selection of epitope mutations (i.e., epitope Pol LI9, Pol TV8 and Gag NI9) was observed. Good control of viral load and higher CD4+ counts were significantly associated with at least one detectable T cell response to un-mutated epitopes. HLA-B51 restricted CD8+ T-cell clones, generated from the patients, could effectively inhibit HIV-1 replication when wild type epitopes are properly processed and presented. We then assessed the evolution of escape mutations under the selecting pressure of HLA-B51 CTLs in vitro by co-culturing HLA-B51 CTL clones with HIV-1 infected target cells (Virus Evolution Assay). Our data showed that three dominant HLA-B51 restricted CTL responses have driven the sequential escape mutations within the epitopes, leading to the loss of viral control, which confirmed our in vivo findings. Furthermore, applying Virus Evolution Assay, we assessed the impact of antigen sensitivity and TCR usage as well as founder virus effect on HIV-1 evolution and control. Our data suggested that antigen sensitivity plays an important role in anti-viral efficacy of CTLs; the TCR usage of CTLs has stronger effect on virus evolution. More importantly, our study highlighted the major impact of the founder virus sequence on viral control. It has been shown that HIV-1 has adapted to the T-cell responses to epitope Pol TI8 in other HLA-B51+ patient cohorts. However, in our cohort, T-cell responses targeting this epitope, with Valine at position 8 (Pol TV8), provide the hosts with a long-term protection against HIV-1 infection, because of a fine balance of efficient viral control, lower level of immune pressure and the slower rate of development of escape mutations. In addition, we assessed the ex vivo phenotypic characteristics of HLA-B51 restricted dominant T cell responses and our preliminary data indicated that the early differentiated and less senescence phenotype of CD8+ T cell responses in HIV-1 chronic infection is likely to be a result of low viral antigen exposure due to T cell driven escape. In conclusion, immune-dominant T-cell responses targeting three HLA-B51 restricted epitopes (Pol LI9, Pol TV8 and Gag NI9) could be advantageous for the host. In particular, the responses against epitope Gag NI9 with slow development of escape mutations or epitope Pol TV8 with a fine balance of moderate immune pressure and delayed escape mutations, are beneficial for long-term control of HIV-1 infection.
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Fernandez, Maria Helen. "The role of viral variation on CD4⁺ T cell recognition in HIV-1." Thesis, University of London, 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.325677.

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Williams, James Philip. "Characterisation of the HIV-1 reservoir and the potential for viral eradication." Thesis, University of Oxford, 2014. http://ora.ox.ac.uk/objects/uuid:5ca5dd43-8045-47d9-a2b7-58713554e359.

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The HIV-1 reservoir is the major barrier to eradication and cure of HIV-1 infection. The aim of this thesis was to characterise the HIV-1 reservoir in PHI and to investigate two potential reservoir clearance strategies. Sensitive Q-PCR assays that quantify HIV-1 DNA reservoir level were developed and applied to characterise the HIV-1 reservoir in acutely infected patients enrolled in the SPARTAC trial. HIV-1 DNA levels were found to be a useful biomarker for predicting clinical progression and the time of viral remission in patients, after HAART interruption. Since low HIV-1 DNA reservoir levels were clinically beneficial, potential therapies aimed at decreasing the reservoir burden were investigated. Thermotherapy was employed as a possible method for increasing CTL killing ability of HIV-1-infected cells. This may increase the likelihood of virological control and functional cure. SPION uptake impacted negatively on the natural killing ability of CTL that expressed the high affinity 868-TCR. However, localised thermotherapeutic heat generation was insufficient to cause direct thermal ablation of bound target cells or to enhance the natural killing ability of CTL. 868-TCR transduced CTL were employed directly as a means to target the latent viral reservoir by the ‘kick and kill’ hypothesis. Latent HIV-1 was reactivated in a variety of latent cell line models, but inconclusively in a primary model. 868-TCR transduced CTL killing of latently infected cells was observed. However, reactivation of latent virus did not necessarily relate to increased antigenicity of latent cells, perhaps in part due to anti-latency drug-induced alterations in MHC class I expression. Despite recent and sustained interest in HIV-1 cure strategies, the prospect still remains elusive. Only through the development of sensitive assays that measure the HIV-1 reservoir and their application to novel and innovative cure strategies will HIV-1 ever be functionally cured or eradicated in patients on a large scale.
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Kishko, Michael G. "Molecular and Functional Properties of Transmitted HIV-1 Envelope Variants: A Dissertation." eScholarship@UMMS, 2011. https://escholarship.umassmed.edu/gsbs_diss/519.

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In 2008 the Nobel Prize in Physiology or Medicine was awarded to the co-discoverers of the Human Immunodeficiency Virus Type 1 (HIV-1), the causative agent of Acquired Immunodeficiency Syndrome (AIDS). This award acknowledged the enormous worldwide impact of the HIV-1/AIDS pandemic and the importance of research aimed at halting its spread. Since the syndrome was first recognized, 25 million people have succumbed to AIDS and over 33 million are currently infected with HIV-1 (www.unaids.org). The most effective strategy for ending the pandemic is the creation of a prophylactic vaccine. Yet, to date, all efforts at HIV-1 vaccine design have met with very limited success. The consistent failures of vaccine candidates stem in large part from the unprecedented diversity of HIV-1. Among the novel theories of vaccine design put forward to address this diversity is the targeted vaccine approach. This proposal is based on the finding that mucosal transmission of HIV-1, the most prevalent form, occurs across a selective bottleneck such that typically only a single (or a few) variants of the viral swarm present in a donor are passed to the recipient. While the mechanisms controlling the selection are largely unknown, the targeted vaccine approach postulates that once they are identified, we can utilize this understanding to design vaccines specifically targeted to the characteristics shared by the rare, mucosally transmissible HIV-1 variants. The studies described in this work were conducted to improve our understanding of the factors influencing viral variant selection during mother-to-child-transmission of HIV-1, a route of mucosal transmission which has globally become the leading cause of child infection. A unique panel was generated, consisting of nearly 300 HIV-1 envelope genes cloned from infected mother-infant pairs. Extensive characterization of the genotypes, phenotypes and phylogeny of these clones was then done to identify attributes differentiating early infant from maternal variants. Low genetic diversity of HIV-1 envelope variants was detected in early infant samples, suggesting a bottleneck and active selection of variants for transmission. Transmitted variants did not differ from non-transmitted variants in CD4 and CCR5 use. Infant isolates replicated poorly in macrophages; a cell subtype hypothesized to be important in the establishment of infection. The sensitivity of infant envelope variants to neutralization by a panel of monoclonal antibodies, heterologous and autologous plasmas and HIV-1 entry inhibitors varied. Most intriguingly, envelopes cloned from infants infected during delivery exhibited a faster entry phenotype than maternal isolates. Together, these findings provide further insight into viral variant selection during mother-to-child transmission. Identification of properties shared by mucosally transmitted viral variants may allow them to be selectively targeted, resulting in improved methods for preventing HIV-1 transmission.
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Auma, Ann Winniefred Nangobi. "THE IMPACT OF DIRECT-ACTING ANTI-VIRAL THERAPY ON NAIVE CD4+ T CELL LYMPHOPENIA AND CELLULAR IMMUNE ACTIVATION IN HCV INFECTION AND HCV/HIV CO-INFECTION." Case Western Reserve University School of Graduate Studies / OhioLINK, 2021. http://rave.ohiolink.edu/etdc/view?acc_num=case1625764728651756.

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Ozen, Aysegul. "Structure and Dynamics of Viral Substrate Recognition and Drug Resistance: A Dissertation." eScholarship@UMMS, 2005. http://escholarship.umassmed.edu/gsbs_diss/677.

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Drug resistance is a major problem in quickly evolving diseases, including the human immunodeficiency (HIV) and hepatitis C viral (HCV) infections. The viral proteases (HIV protease and HCV NS3/4A protease) are primary drug targets. At the molecular level, drug resistance reflects a subtle change in the balance of molecular recognition; the drug resistant protease variants are no longer effectively inhibited by the competitive drug molecules but can process the natural substrates with enough efficiency for viral survival. Therefore, the inhibitors that better mimic the natural substrate binding features should result in more robust inhibitors with flat drug resistance profiles. The native substrates adopt a consensus volume when bound to the enzyme, the substrate envelope. The most severe resistance mutations occur at protease residues that are contacted by the inhibitors outside the substrate envelope. To guide the design of robust inhibitors, we investigate the shared and varied properties of substrates with the protein dynamics taken into account to define the dynamic substrate envelope of both viral proteases. The NS3/4A dynamic substrate envelope is compared with inhibitors to detect the structural and dynamic basis of resistance mutation patterns. Comparative analyses of substrates and inhibitors result in a solid list of structural and dynamic features of substrates that are not shared by inhibitors. This study can help guiding the development of novel inhibitors by paying attention to the subtle differences between the binding properties of substrates versus inhibitors.
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Books on the topic "HIV; Immunology; Viral infections"

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Nair, Madhavan P. N., and Stanley Schwartz. Immunology of HIV infection. Edited by Research Signpost (Trivandrum India). Trivandrum, India: Research Signpost, 2003.

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International Workshop on Viral Quantitation in HIV Infection (1991 Paris, France). Viral quantitation in HIV infection: Proceedings of the International Workshop on Viral Quantitation in HIV Infection, June 13-14, 1991, Paris, France. Edited by Andrieu Jean-Marie. Montrouge, France: John Libbey Eurotext, 1991.

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Viral sex: The nature of AIDS. New York: Oxford University Press, 1997.

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M, Parkin J., ed. HIV and AIDS. Oxford, UK: Bios Scientific Publishers, 1994.

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International Symposium of the Immune Response to Viral Infections (1988 Florence, Italy). The immune response to viral infections. New York: Plenum Press, 1989.

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Trinity, College (Dublin Ireland) Dept of Community Health and General Practice. Hepatitis B, hepatitis C, and HIV in Irish prisoners, part II: Prevalence and risk in committal prisoners 1999 : report prepared for the Minister for Justice, Equality, and Law Reform. [Dublin?: Stationary Office?, 2000.

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Wick, W. David. War in the body: The evolutionary arms race between HIV and the human immune system and the implications for vaccines. New York: Springer, 2013.

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O, Freed Eric, and SpringerLink (Online service), eds. HIV Interactions with Host Cell Proteins. Berlin, Heidelberg: Springer-Verlag Berlin Heidelberg, 2010.

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Models of protection against HIV/SIV: Avoiding AIDS in humans and monkeys. Amsterdam: Academic Press, 2012.

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Mulder, C. L. Psycho-immunology and HIV infection: Biopsychosocial determinants of distress, immunological parameters, and disease progression in homosexual men infected with human immunodeficiency virus-1. Amsterdam: Thesis, 1994.

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Book chapters on the topic "HIV; Immunology; Viral infections"

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Astrin, S. M., E. Schattner, J. Laurence, R. I. Lebman, and C. Rodriguez-Alfageme. "Does HIV Infection of B Lymphocytes Initiate AIDS Lymphoma? Detection by PCR of Viral Sequences in Lymphoma Tissue." In Current Topics in Microbiology and Immunology, 399–407. Berlin, Heidelberg: Springer Berlin Heidelberg, 1992. http://dx.doi.org/10.1007/978-3-642-77633-5_51.

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Morgello, Susan. "HIV." In Neurotropic Viral Infections, 21–74. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-33189-8_2.

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Bobat, Raziya, and Moherndran Archary. "HIV Infection." In Viral Infections in Children, Volume I, 69–100. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-54033-7_3.

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Ishay, Yuval, and Yaron Ilan. "Hepatitis A and Other Viral Infections." In Liver Immunology, 227–53. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-51709-0_15.

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Stoiber, Heribert, and Doris Wilflingseder. "Immunology of HIV." In Sexually Transmitted Infections and Sexually Transmitted Diseases, 271–85. Berlin, Heidelberg: Springer Berlin Heidelberg, 2011. http://dx.doi.org/10.1007/978-3-642-14663-3_24.

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Biron, Christine A., Marc Dalod, and Thais P. Salazar-Mather. "Innate Immunity and Viral Infections." In Immunology of Infectious Diseases, 139–60. Washington, DC, USA: ASM Press, 2014. http://dx.doi.org/10.1128/9781555817978.ch11.

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Szomolanyi-Tsuda, Eva, Micheal A. Brehm, and Raymond M. Welsh. "Acquired Immunity against Viral Infections." In Immunology of Infectious Diseases, 247–65. Washington, DC, USA: ASM Press, 2014. http://dx.doi.org/10.1128/9781555817978.ch18.

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Onakewhor, Joseph, Toby Kenneth Maduako, and Friday Okonofua. "Non-HIV Viral Infections in Pregnancy." In Contemporary Obstetrics and Gynecology for Developing Countries, 397–408. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-75385-6_36.

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Sissons, J. G. P. "The Immunopathology of Viral and Bacterial Infections." In Immunology of Infection, 133–57. Dordrecht: Springer Netherlands, 1994. http://dx.doi.org/10.1007/978-94-011-1430-1_7.

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Zarnitsyna, Veronika I., Philip L. F. Johnson, Joseph N. Blattman, and Rustom Antia. "Modeling Immunopathology During Persistent Viral Infections." In Mathematical, Computational and Experimental T Cell Immunology, 109–20. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-57204-4_7.

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Conference papers on the topic "HIV; Immunology; Viral infections"

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Celis, Esteban. "Abstract IA16: Designing cancer vaccines that mimic viral infections." In Abstracts: AACR Special Conference: Tumor Immunology and Immunotherapy: A New Chapter; December 1-4, 2014; Orlando, FL. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/2326-6074.tumimm14-ia16.

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Roubinian, Nareg, Laurence Huang, Eunice Chen, William Worodria, Samuel Yoo, Delphine Huang, Serena Fong, et al. "Prevalence Of Viral Infections In HIV-Infected Individuals With Opportunistic Pneumonia In Kampala, Uganda." In American Thoracic Society 2011 International Conference, May 13-18, 2011 • Denver Colorado. American Thoracic Society, 2011. http://dx.doi.org/10.1164/ajrccm-conference.2011.183.1_meetingabstracts.a6255.

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Hu, Bin, and Sarah L. Kieweg. "Numerical Study of Epithelial Deformation During Vaginal Application of a Viscoelastic Gel Using a Fluid-Structure Interaction Model." In ASME 2012 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2012. http://dx.doi.org/10.1115/sbc2012-80783.

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This paper is one of the components of our research on how to optimize polymeric anti-HIV gels, microbicides [1]. Microbicides are delivered to the vaginal epithelium to protect it from HIV and other sexually transmitted infections. Microbicides may provide a physical barrier amplifying the normal vaginal defenses, as well as destroy the pathogens chemically or inhibit viral infection. Microbicides are a promising solution to provide a low-cost, female-controlled method for protection against HIV and other sexually transmitted pathogens.
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Hu, Bin, and Sarah L. Kieweg. "The Effect of Surface Tension on the Epithelial Spreading of Non-Newtonian Drug Delivery Vehicles: Numerical Simulations." In ASME 2009 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2009. http://dx.doi.org/10.1115/sbc2009-206565.

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This paper is one of the components of our research on how to optimize polymeric drug delivery vehicles. One of the applications is in the topical delivery of anti-human immunodeficiency virus (HIV) gels called microbicides [1]. Microbicides are delivered to vaginal or rectal epithelium to protect it from HIV and other sexually transmitted infections. Microbicides may provide a physical barrier amplifying the normal vaginal defense, as well as destroy the pathogens chemically or inhibit viral infection. The microbicide may consist of an anti-HIV active agent in some delivery vehicle, such as a gel, cream or foam. Microbicides are a promising solution to provide a low-cost, female-controlled method for protection against HIV and other sexually transmitted pathogens.
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Shah, Neil J., Ghassan AL-Shbool, Matthew Blackburn, Michael Cook, William J. Kelly, Anas Belouali, Sebastian Ochoa, et al. "Abstract 3230: Safety and efficacy of immune checkpoint inhibitors (ICIs) in patients with HIV, hepatitis B, or hepatitis C viral infections." In Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.am2019-3230.

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Shah, Neil J., Ghassan AL-Shbool, Matthew Blackburn, Michael Cook, William J. Kelly, Anas Belouali, Sebastian Ochoa, et al. "Abstract 3230: Safety and efficacy of immune checkpoint inhibitors (ICIs) in patients with HIV, hepatitis B, or hepatitis C viral infections." In Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.sabcs18-3230.

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Evatt, B. L. "VIRUS INACTIVATION AND COAGULATION FACTOR PREPARATIONS." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644754.

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Nonheat-treated factor concentrates were used for the therapy of congenital and acquired coagulation deficiencies until 1984. These unheated factor crticentrates, which are manufactured from pooled plasma obtained from between 2500 and 25,000 blood or plasma donors, have been epidemiologically implicated in exposure of large numbers of hemophilia patients to several viral infections Including human immunodeficiency virus (HIV), hepatitis B, and non-A non-B hepatitis. Of these, HIV has been fdund to be very heat labile. After the introduction in 1984-85 of heat treatment of concentrates to reduce the risk of! hepatitis to recipients, several studies documented a lack of HIV serconversion in patients treated with clotting-fadtor concentrates. However, subsequent reports described a few hemophilia patients who had seroconverted to HIV! after receiving heat-treated concentrate from unscreened donors. To determine the significance of these seroconvers(ions, an international survey was conducted on 11 hemophilia treatment centers in Europe, Canada, and the United Kingdcpn whose total patient population comprised more than 2300 hemophilia A patients and 400 hemophilia B patients. Only three patients were found who seroconverted beyond a 6-month period after switching to heat-treated material, a(nd no seroconversions have occurred in these centers between November 1985 and February 1987. In addition no cases of seroconversion on donor screened heat-treated concentrate have been reported since its widespread introduction to the hemophilia patients during 1985-1986. Other modes of viral inactivation are currently being tested, and they appeiar to be effective in inactivating HIV and hepatitis B virus. Some of these methods have shown some promise for the inactivation of non-A and non-B hepatitis, but more data are needed for final assessment of these methods.
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Pigul, Evgeniia Yu, Galina F. Filimonova, Ivan B. Tokin, and Ivan I. Tokin. "Cluster analysis in assessing the interdependencies of clinical and morphological parameters of patients with mixed infections (pulmonary tuberculosis, chronic viral hepatitis, HIV infection) and heroin addiction." In 2015 International Conference "Stability and Control Processes" in Memory of V.I. Zubov (SCP). IEEE, 2015. http://dx.doi.org/10.1109/scp.2015.7342204.

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Levine, P. H. "ACQUIRED IMMUNODEFICIENCY SYNDROME, HUMAN IMMUNODEFICIENCY VIRUS AND HEMOPHILIA." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644752.

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Less than 15 years ago the National Heart, Lung and Blood Institute surveyed physicians in the United States in order to characterize the demographics of hemophilia. The average age of persons with hemophilia in the United States was found to be 11.5 years old. By 10 years later, the life expectancy was predicted to be normal, and indeed the average age of persons with hemophilia in the U.S. is now in the early twenties. Early, intensive and predictably efficacious control of hemorrhage has made this result possible, and the therapeutic product which has allowed such control is commercial clotting factor concentrate.We now know that starting in 1978, and with great frquency during 1982 and 1983, the majority of U.S. hemophiliacs were infected with human immunodeficiency virus (HIV). It is estimated that as of January, 1987, approximately two thirds of the 20,000' persons with hemophilia in the United States have been infected with HIV. Among those with severe factor VIII deficiency, more than 9056 are seropositive. As of 1/5/87, there were 288 cases of AIDS among U.S. hemophiliacs, for an AIDS rate of approximately 2.256 of those with HIV infection. This number included 185 with severe, 32 with moderate and 28 with mild hemophilia A; 12 with severe, 6 with moderate and 1 with mild hemophilia B; 9 with vWD, and 4 others. A disproportionate number were older patients: 55 were ages 1-19; 62 ages 20-29; 85 ages 30-39, and 86 age 40 or older. Although the AIDS attack rate is no longer climbing logarhythmically, new cases are certainly still occurring.A variety of other HIV-related syndromes have emerged. Of great concern is immune thrombocytopenia, which is now relatively common; among a group of 209 carefully followed HIV-positive patients at our center, 31 (1556) are or have been thrombocytopenic. Progressive failure to normally gain height and weight in children with hemophilia has recently been shown by our group to correlate with HIV antibody positivity, and also with decreased T4/T8 ratio, decreased T4 cell count, decreased skin test reactivity, and subsequent development of ARC or AIDS in some such children. Finally, a picture of progressive fall in T4 count associated with recurrent non-specific infections and increased likelihood of positive viral culture, may predict an increased risk of developing AIDS.We know that the immune dysfunction in hemophilia is complex, and not wholly explained by HIV infection. One important factor may be the many foreign proteins contained in commercial clotting factor concentrates, and their ability to stimulate T cells. It is known that latent HIV infection in cultured T4 lymphocytes can be induced to enter the proliferative, viral secretory phase by the addition of soluble foreign antigens to the cell culture. Recent data of Brettler and colleagues, to be presented at this meeting, suggest that the use of highly purified VI!I:C (specific activity >3000 u/mg) in place of the present extremely impure products, may improve the immune dysfunction in hemophilia. This observation offers a new hypothetical approach to the prevention of progressive T4 cell depletion in HIV infected hemophiliacs, and requires immediate and extensive further study.The psychosocial burden of HIV infection is immense. The need for extensive, formal education and support programs is largely unmet in most parts of the world. Such programs are best run out of hemophilia treatment centers in most cases, and must include an active program on prevention of sexual transmission, provision of HIV testing before and during pregnancies, provision for maintenance of confidentiality, etc. Education concerning HIV is like all other forms of education. It requires formal organization, a curriculum, active rather than passive learning in which there is interaction between the teacher and the pupil, time for planned repetition, reinforcement with written materials, and assessment of goals achieved. For all of these reasons it is inappropriate to assume that the physician at the hemophilia center will be able to provide an adequate education program. Adquate paramedical personnel will need to undertake this effort, under the directjon of the physician.
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Addiego, J. E., P. Bailey, M. Bradley, S. Courter, and M. Lee. "RECOVERY AND SURVIVAL STUDIES OF A NEW FACTOR VIII PRODUCT." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644052.

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Lyophilized protein concentrates are the international treatment of choice to manage bleeding in hemophiliacs. These pooled plasma products, however, expose the recipient of treatment to an increased risk of viral infections. While current manufacturing techniques of these products appear to be effective in eradicating the human immunodeficiency virus (HIV), transmission of other viruses, especially non-A/non-B (NANB) hepatitis, is still a majoor complication of concentrate therapy. Hyland Therapeutics Division Travenol Laboratories, Inc., has developed a new process using the techniques of immunoaffinity chromatography and organic solvent/detergent treatment to prepare a high specific activity product; Antihemophilic Factor (Human), Method M (AHF-M); that may render it free of pathogenic viruses. To determine the recovery and half-life of factor VIII in this product five severe hemophiliacs in a nonbleeding state were given! 50 U/kg of M-AHF and 50 U/kg of a currently licensed factor concentrate (HEMOFILe CT) in a crossover blinded study with a seven day interval between the respective infusions. The table below shows the recovery and half-life results for the five patients studiedThe factor VIII recoveries and half-lifes were similar for both products. No significant adverse clinical reactions were detected in any patient either during or after their infusions. This product appears to produce adequate circulating levels of factor VIII. It also appears to be safe for administration in humans. Further studies are on-going to test the overall efficacy of this product and to confirm that the manufacturing process is effective in eliminating pathogenic viruses
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Reports on the topic "HIV; Immunology; Viral infections"

1

Roderick Slavcev, Roderick Slavcev. Can bacterial viruses be engineered to protect against human viral infections like HIV? Experiment, May 2014. http://dx.doi.org/10.18258/2564.

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