Relevant bibliographies by topics / Antibody response to HIV

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

Academic literature on the topic 'Antibody response to HIV'

Author: Grafiati
Published: 4 June 2021
Last updated: 8 February 2022

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Journal articles on the topic "Antibody response to HIV"

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Kim, H. N., R. D. Harrington, H. M. Crane, S. Dhanireddy, T. H. Dellit, and D. H. Spach. "Hepatitis B vaccination in HIV-infected adults: current evidence, recommendations and practical considerations." International Journal of STD & AIDS 20, no. 9 (September 2009): 595–600. http://dx.doi.org/10.1258/ijsa.2009.009126.

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Immunization with hepatitis B (HBV) vaccine is recommended for all HIV-infected individuals without immunity to HBV. This patient population, however, has relatively poor HBV vaccine responses. Factors associated with this impaired HBV vaccine response in HIV-infected individuals may include older age, uncontrolled HIV replication, and low nadir CD4 cell count. Postvaccination testing for HBV surface antibody is recommended and vaccine non-responders should undergo repeat immunization with a full series. The benefit of double dosage, the appropriate strategy for HIV-infected patients with isolated HBV core antibody and the timing and number of vaccinations in persons with advanced immunosuppression on highly active antiretroviral therapy remain controversial areas.
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Overbaugh, J., and L. Morris. "The Antibody Response against HIV-1." Cold Spring Harbor Perspectives in Medicine 2, no. 1 (November 1, 2011): a007039. http://dx.doi.org/10.1101/cshperspect.a007039.

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BORMAN, STU. "HIV vaccine produces broad antibody response." Chemical & Engineering News 77, no. 3 (January 18, 1999): 15. http://dx.doi.org/10.1021/cen-v077n003.p015.

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Ye, Ling, Zhiyuan Wen, Ke Dong, Lei Pan, Zhigao Bu, Richard W. Compans, Huizhong Zhang, and Chinglai Yang. "Immunization with a Mixture of HIV Env DNA and VLP Vaccines Augments Induction of CD8 T Cell Responses." Journal of Biomedicine and Biotechnology 2010 (2010): 1–11. http://dx.doi.org/10.1155/2010/497219.

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The immune response induced by immunization with HIV Env DNA and virus-like particle (VLP) vaccines was investigated. Immunization with the HIV Env DNA vaccine induced a strong CD8 T cell response but relatively weak antibody response against the HIV Env whereas immunization with VLPs induced higher levels of antibody responses but little CD8 T cell response. Interestingly, immunization with a mixture the HIV Env DNA and VLP vaccines induced enhanced CD8 T cell and antibody responses. Further, it was observed that the mixing of DNA and VLP vaccines during immunization is necessary for augmenting induction of CD8 T cell responses and such augmentation of CD8 T cell responses was also observed by mixing the HIV Env DNA vaccine with control VLPs. These results show that immunization with a mixture of DNA and VLP vaccines combines advantages of both vaccine platforms for eliciting high levels of both antibody and CD8 T cell responses.
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Kadelka, Claus, Thomas Liechti, Hanna Ebner, Merle Schanz, Peter Rusert, Nikolas Friedrich, Emanuel Stiegeler, et al. "Distinct, IgG1-driven antibody response landscapes demarcate individuals with broadly HIV-1 neutralizing activity." Journal of Experimental Medicine 215, no. 6 (May 24, 2018): 1589–608. http://dx.doi.org/10.1084/jem.20180246.

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Understanding pathways that promote HIV-1 broadly neutralizing antibody (bnAb) induction is crucial to advance bnAb-based vaccines. We recently demarcated host, viral, and disease parameters associated with bnAb development in a large HIV-1 cohort screen. By establishing comprehensive antibody signatures based on IgG1, IgG2, and IgG3 activity to 13 HIV-1 antigens in 4,281 individuals in the same cohort, we now show that the same four parameters that are significantly linked with neutralization breadth, namely viral load, infection length, viral diversity, and ethnicity, also strongly influence HIV-1–binding antibody responses. However, the effects proved selective, shaping binding antibody responses in an antigen and IgG subclass–dependent manner. IgG response landscapes in bnAb inducers indicated a differentially regulated, IgG1-driven HIV-1 antigen response, and IgG1 binding of the BG505 SOSIP trimer proved the best predictor of HIV-1 neutralization breadth in plasma. Our findings emphasize the need to unravel immune modulators that underlie the differentially regulated IgG response in bnAb inducers to guide vaccine development.
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Stratov, Ivan, Amy Chung, and Stephen J. Kent. "Robust NK Cell-Mediated Human Immunodeficiency Virus (HIV)-Specific Antibody-Dependent Responses in HIV-Infected Subjects." Journal of Virology 82, no. 11 (March 19, 2008): 5450–59. http://dx.doi.org/10.1128/jvi.01952-07.

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ABSTRACT Antibody-dependent cellular cytotoxicity (ADCC) is a potentially effective adaptive immune response to human immunodeficiency virus (HIV) infection. The study of ADCC responses has been hampered by the lack of simple methods to quantify these responses and map effective epitopes. We serendipitously observed that standard intracellular cytokine assays on fresh whole blood from a cohort of 26 HIV-infected subjects identified non-T lymphocytes expressing gamma interferon (IFN-γ) in response to overlapping linear peptides spanning HIV-1 proteins. The effector cells were CD3− CD4− CD8− CD14− CD2+ CD56+/− NK lymphocytes and degranulated granzyme B and perforin in response to antigen stimulation. Serum transfer assays demonstrated that the specific response was mediated by immunoglobulin G. Fresh blood samples from half of the HIV-infected cohort demonstrated robust HIV peptide-specific IFN-γ expression by NK cells, predominately to Env, Pol, and Vpu HIV-1 proteins. Responses were readily mapped to define minimal epitopes utilizing this assay. Antibody-dependent, HIV-specific NK cell recognition, involving components of both innate and adaptive immune systems, represents a potentially effective immune response to induce by vaccination.
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Zhou, Yinggao, Kuan Yang, Kai Zhou, and Chunling Wang. "Optimal Treatment Strategies for HIV with Antibody Response." Journal of Applied Mathematics 2014 (2014): 1–13. http://dx.doi.org/10.1155/2014/685289.

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Numerical analysis and optimization tools are used to suggest improved therapies to try and cure HIV infection. An HIV model of ordinary differential equation, which includes immune response, neutralizing antibodies, and multidrug effects, is improved. For a fixed time, single-drug and two-drug treatment strategies are explored based on Pontryagin’s maximum principle. Using different combinations of weight factor pairs combining with special upper-bound pairs for controls, nine types of treatment policies are determined and different therapy effects are numerically simulated with a gradient projection method. Some strategies are effective, but some strategies are not particularly helpful for the therapy of HIV/AIDS. Comparing the effective treatment strategies, we find a more appropriate strategy with maximizing the number of uninfected CD4+T-cells and minimizing the number of active virus.
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Crothers, Kristina, Kieran R. Daly, David Rimland, Matthew Bidwell Goetz, Cynthia L. Gibert, Adeel A. Butt, Amy C. Justice, Kpandja Djawe, Linda Levin, and Peter D. Walzer. "Decreased Serum Antibody Responses to RecombinantPneumocystisAntigens in HIV-Infected and Uninfected Current Smokers." Clinical and Vaccine Immunology 18, no. 3 (December 29, 2010): 380–86. http://dx.doi.org/10.1128/cvi.00421-10.

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ABSTRACTSerologic studies can provide important insights into the epidemiology and transmission ofPneumocystis jirovecii. Exposure toP. jiroveciican be assessed by serum antibody responses to recombinant antigens from the major surface glycoprotein (MsgC), although factors that influence the magnitude of the antibody response are incompletely understood. We determined the magnitudes of antibody responses toP. jiroveciiin comparison to adenovirus and respiratory syncytial virus (RSV) in HIV-infected and uninfected patients and identified predictors associated with the magnitude of the response. We performed a cross-sectional analysis using serum samples and data from 153 HIV-positive and 92 HIV-negative subjects enrolled in a feasibility study of the Veterans Aging Cohort 5 Site Study (VACS 5). Antibodies were measured using an enzyme-linked immunosorbent assay (ELISA). Independent predictors of antibody responses were determined using multivariate Tobit regression models. The results showed that serum antibody responses toP. jiroveciiMsgC fragments were significantly and independently decreased in current smokers. Antibodies toP. jiroveciialso tended to be lower with chronic obstructive pulmonary disease (COPD), hazardous alcohol use, injection drug use, and HIV infection, although these results were not statistically significant. These results were specific toP. jiroveciiand did not correlate with adenovirus. Antibody responses to RSV were in the inverse direction. Thus, current smoking was independently associated with decreasedP. jiroveciiantibody responses. Whether smoking exerts an immunosuppressive effect that affects theP. jiroveciiantibody response, colonization, or subsequent risk for disease is unclear; prospective, longitudinal studies are needed to evaluate these findings further.
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Tannig, Pierre, Antonia Sophia Peter, Dennis Lapuente, Stephan Klessing, Dominik Damm, Matthias Tenbusch, Klaus Überla, and Vladimir Temchura. "Modulation of Vaccine-Induced HIV-1-Specific Immune Responses by Co-Electroporation of PD-L1 Encoding DNA." Vaccines 8, no. 1 (January 14, 2020): 27. http://dx.doi.org/10.3390/vaccines8010027.

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The importance of a balanced TH1/TH2 humoral immune response against the HIV-1 envelope protein (Env) for antibody-mediated HIV-1 control is increasingly recognized. However, there is no defined vaccination strategy to raise it. Since immune checkpoints are involved in the induction of adoptive immunity and their inhibitors (monoclonal antibodies) are licensed for cancer therapy, we investigated the effect of checkpoint blockade after HIV-1 genetic vaccination on enhancement and modulation of antiviral antibody responses. By intraperitoneal administration of checkpoint antibodies in mice we observed an induction of anti-drug antibodies which may interfere with immunomodulation by checkpoint inhibitors. Therefore, we blocked immune checkpoints locally by co-electroporation of DNA vaccines encoding the active soluble ectodomains of programmed cell death protein-1 (PD-1) or its ligand (PD-L1), respectively. Plasmid-encoded immune checkpoints did not elicit a detectable antibody response, suggesting no interference with their immunomodulatory effects. Co-electroporation of a HIV-1 DNA vaccine formulation with soluble PD-L1 ectodomain increased HIV-1 Env-specific TH1 CD4 T cell and IgG2a antibody responses. The overall antibody response was hereby shifted towards a more TH1/TH2 balanced subtype pattern. These findings indicate that co-electroporation of soluble checkpoint ectodomains together with DNA-based vaccines has modulatory effects on vaccine-induced immune responses that could improve vaccine efficacies.
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Mascola, John. "Defining the Protective Antibody Response for HIV-1." Current Molecular Medicine 3, no. 3 (May 1, 2003): 209–16. http://dx.doi.org/10.2174/1566524033479799.

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Dissertations / Theses on the topic "Antibody response to HIV"

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Smalls-Mantey, Adjoa. "The innate immune effector cell response against HIV-1." Thesis, University of Oxford, 2013. http://ora.ox.ac.uk/objects/uuid:d97fadc3-bb4a-43dd-9138-6ab023aef60d.

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Since being identified as the cause of AIDS in 1983, HIV-1 infection has reached pandemic proportions. Despite public awareness about prevention, the growing incidence of HIV-1 infection and the limitations of current antiretroviral therapy underscore the imperative need for a vaccine. Understanding the basis of an immune response that controls infection or provides sterilizing immunity remains a major goal in the search for effective vaccines or immunotherapies. Research into correlates of immunity to HIV-1 have largely focused on CD8+ T cells or neutralising antibodies (NAbs) but to date these responses have not proved effective in containing viral replication in vaccinees who become infected. Natural killer cells (NKs), monocytes (MCs), and neutrophils (PMNs) are cells of the innate immune system with intrinsic cytotoxic function that can be enhanced by antibodies (Abs) in what is termed antibody-dependent cellular cytotoxicity (ADCC). In my studies I investigated the production of PMNs from human stem cells, the elimination of HIV-1 infected cells by these effector cells, the modulation of cellular cytotoxicity by Ab, and characterized how Abs facilitate a potent ADCC response. I developed a novel flow cytometry assay to measure cytotoxic activity against HIV-1 infected CD4+ T cells. Using this, effector cells were shown to have different cytotoxic capacities which were enhanced by Ab. Comparing ADCC mediated by patient serum revealed that higher levels correlated with IgG binding to infected cells. I observed no correlation between serum-mediated ADCC and markers of disease progression including patient status, viral RNA load, CD4+ T cell count, or NAb titers. The data presented here have implications for acquisition and control of early HIV-1 infection by NKs, MCs, and PMNs prior to activation of an adaptive immune response, at later stages in the presence of HIV-1-specific Abs, and are relevant to vaccine-induced anti- HIV-1 Ab-based effector mechanisms.
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Simmonds, Peter. "Detection of antibody responses to infection with herpes simplex virus and human immunodeficiency virus." Thesis, University of Edinburgh, 1988. http://hdl.handle.net/1842/26933.

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Chen, Yuxin. "Characterization of Envelope-Specific Antibody Response Elicited by HIV-1 Vaccines: A Dissertation." eScholarship@UMMS, 2001. http://escholarship.umassmed.edu/gsbs_diss/760.

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Despite 30 years of intensive research，an effective human immunodeficiency virus (HIV) vaccine still remains elusive. The desirable immune response capable of providing protection against HIV acquisition is still not clear. The accumulating evidence learned from a recent vaccine efficacy correlate study not only confirmed the importance of antibody responses, but also highlighted potential protective functions of antibodies with a broad repertoire of HIV-1 epitope specificities and a wide range of different antiviral mechanisms. This necessitates a deep understanding of the complexity and diversity of antibody responses elicited by HIV-1 vaccines. My dissertation characterizes antibody response profiles of HIV-1 Env antibodies elicited by several novel immunogens or different immunization regimens, in terms of magnitude, persistence, epitope specificity, binding affinity, and biological function. First, to overcome the challenge of studying polyclonal sera without established assays, we expanded a novel platform to isolate Env-specific Rabbit mAbs (RmAb) elicited by DNA prime-protein boost immunization. These RmAbs revealed diverse epitope specificity and cross-reactivity against multiple gp120 antigens from more than one subtype, and several had potent and broad neutralizing activities against sensitive Tier 1 viruses. Further, structural analysis of two V3 mAbs demonstrated that a slight shift of the V3 epitope might have a dramatic impact on their neutralization activity. All of these observations provide a useful tool to study the induction of a desired type of antibody by different immunogens or different immunization regimens. Since heavily glycosylated HIV Env protein is a critical component of an HIV vaccine, we wanted to determine the impact of the HIV Env-associated glycan shield on antibody responses. We were able to produce Env proteins with a selective and homogeneous pattern of N-glycosylation using a glycoengineered yeast cell line. Antigenicity of these novel Env proteins was examined by well-characterized human mAbs. Immunogenicity studies showed that they were immunogenic and elicited gp120- specific antibody responses. More significantly, sera elicited by glycan-modified gp120 protein immunogens revealed better neutralizing activities and increased diversity of epitopes compared to sera elicited by traditional gp120 produced in Chinese Hamster Ovary (CHO) cells. Further, we examined the impact of the delivery order of DNA and protein immunization on antibody responses. We found that DNA prime-protein boost induced a comparable level of Env-specific binding Abs at the peak immunogenicity point to codelivery of DNA. However, antibody responses from DNA prime-protein boost had high avidity and diverse specificities, which improved potency and breadth of neutralizing Abs against Tier 1 viruses. Our data indicate that DNA vaccine priming of the immune system is essential for generation of high-quality antibodies. Additionally, we determined the relative immunogenicity of gp120 and gp160 Env in the context of DNA prime-protein boost vaccination to induce high-quality antibody responses. Immunized sera from gp120 DNA primed animals, but not those primed with gp160 DNA, presented with distinct antibody repertoire specificities, a high magnitude of CD4 binding site-directed binding capabilities as well as neutralizing activities. We confirmed the importance of using the gp120 Env form at the DNA priming phase, which directly determined the quality of antibody response.
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Chen, Yuxin. "Characterization of Envelope-Specific Antibody Response Elicited by HIV-1 Vaccines: A Dissertation." eScholarship@UMMS, 2015. https://escholarship.umassmed.edu/gsbs_diss/760.

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Despite 30 years of intensive research，an effective human immunodeficiency virus (HIV) vaccine still remains elusive. The desirable immune response capable of providing protection against HIV acquisition is still not clear. The accumulating evidence learned from a recent vaccine efficacy correlate study not only confirmed the importance of antibody responses, but also highlighted potential protective functions of antibodies with a broad repertoire of HIV-1 epitope specificities and a wide range of different antiviral mechanisms. This necessitates a deep understanding of the complexity and diversity of antibody responses elicited by HIV-1 vaccines. My dissertation characterizes antibody response profiles of HIV-1 Env antibodies elicited by several novel immunogens or different immunization regimens, in terms of magnitude, persistence, epitope specificity, binding affinity, and biological function. First, to overcome the challenge of studying polyclonal sera without established assays, we expanded a novel platform to isolate Env-specific Rabbit mAbs (RmAb) elicited by DNA prime-protein boost immunization. These RmAbs revealed diverse epitope specificity and cross-reactivity against multiple gp120 antigens from more than one subtype, and several had potent and broad neutralizing activities against sensitive Tier 1 viruses. Further, structural analysis of two V3 mAbs demonstrated that a slight shift of the V3 epitope might have a dramatic impact on their neutralization activity. All of these observations provide a useful tool to study the induction of a desired type of antibody by different immunogens or different immunization regimens. Since heavily glycosylated HIV Env protein is a critical component of an HIV vaccine, we wanted to determine the impact of the HIV Env-associated glycan shield on antibody responses. We were able to produce Env proteins with a selective and homogeneous pattern of N-glycosylation using a glycoengineered yeast cell line. Antigenicity of these novel Env proteins was examined by well-characterized human mAbs. Immunogenicity studies showed that they were immunogenic and elicited gp120- specific antibody responses. More significantly, sera elicited by glycan-modified gp120 protein immunogens revealed better neutralizing activities and increased diversity of epitopes compared to sera elicited by traditional gp120 produced in Chinese Hamster Ovary (CHO) cells. Further, we examined the impact of the delivery order of DNA and protein immunization on antibody responses. We found that DNA prime-protein boost induced a comparable level of Env-specific binding Abs at the peak immunogenicity point to codelivery of DNA. However, antibody responses from DNA prime-protein boost had high avidity and diverse specificities, which improved potency and breadth of neutralizing Abs against Tier 1 viruses. Our data indicate that DNA vaccine priming of the immune system is essential for generation of high-quality antibodies. Additionally, we determined the relative immunogenicity of gp120 and gp160 Env in the context of DNA prime-protein boost vaccination to induce high-quality antibody responses. Immunized sera from gp120 DNA primed animals, but not those primed with gp160 DNA, presented with distinct antibody repertoire specificities, a high magnitude of CD4 binding site-directed binding capabilities as well as neutralizing activities. We confirmed the importance of using the gp120 Env form at the DNA priming phase, which directly determined the quality of antibody response.
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Cleveland, S. Matthew. "HIV-1-specific antibody responses to a plant virus-HIV chimera." Thesis, University of Warwick, 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.340090.

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Moyo, Thandeka. "Role of envelope compactness and glycosylation in HIV-1 resistance to neutralising antibody responses." Doctoral thesis, University of Cape Town, 2017. http://hdl.handle.net/11427/26866.

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Understanding the mechanisms used by HIV-1 to evade antibody neutralisation may contribute to the design of a high-coverage vaccine. This thesis explores the mechanism used by a Tier 3 virus leading to its high antibody neutralisation resistance phenotype. This thesis also describes how the glycans at the base of the V3 loop contribute to (i) breadth and potency in a cohort of unselected HIV-1-infected individuals and (ii) the selective pressures resulting from the V3/glycans shielding the virus from neutralisation and the glycans themselves being targets of broad antibody responses. HIV-1 isolates that are highly resistant to broadly neutralising antibodies could limit the efficacy of an antibody-based vaccine. For this reason, it is important to understand the mechanisms behind high HIV-1 resistance to neutralising antibodies. Chapter 2 and Chapter 3 of this thesis describe virus 253-11, a highly neutralisation resistant virus, which is particularly resistant to commonly-elicited, anti-membrane proximal external region (MPER) antibodies in sera. To further understand its resistance, mutations in the MPER were introduced that are known to delay fusion following CD4-binding and thus increase the time the virus spends in the open conformation. Interestingly, we found that these mutations affect the 253-11 Envelope (Env) spike before CD4-binding by destabilising the closed trimer structure. From these data, we hypothesized that the neutralisation resistance of 253-11 was due to an unusually tight, compact pre-fusion Env trimer that resists transient changes to the open conformation. The open conformation frequently exposes narrowly-neutralising antibody epitopes. Because the unliganded 253-11 Env presumably transitions infrequently into the open conformation, it would be able to evade these responses. 253-11 was sensitive to most but not all of the most potent broadly neutralising antibodies (bnAbs) tested, most likely because those broadly neutralising antibodies can access their epitopes in the pre-fusion Env conformation. To gain further information about the structure of the 253-11 Env, we designed a recombinant 253-11 SOSIP trimer and found it to be stable and predominantly adopt a closed conformation. The crystal structure of the SOSIP trimer revealed structural elements likely responsible for 253-11 Env compactness including the inward disposition of the heptad repeat helices and gp120 protomers towards the trimer axis. Taken together, the data from Chapter 2 and Chapter 3 highlight an underappreciated Env compactness mechanism of HIV-1 resistance to neutralising antibodies and these data may be useful in HIV-1 immunogen design research. Previous candidate HIV vaccines have failed to induce wide-coverage neutralising antibodies capable of substantially protecting vaccinees. A key approach in HIV immunogen development has been to define and model epitopes recognised by anti-HIV bnAbs. Candidate immunogen models identified by bnAbs include the V3/glycans, the V2/apex and the MPER epitopes. Autoreactivity and polyreactivity of anti-V3/glycan and anti-MPER antibodies are thought to pose both direct and indirect barriers to achieving neutralisation breadth. Chapter 4 of this thesis explored which of these bnAb epitopes were associated with breadth and potency in a South African cohort of chronically HIV-infected individuals. The study found that antibodies targeting the V3/glycans were associated with breadth and potency. In contrast, antibodies to the V2/apex were not associated with neutralisation breadth/potency. This suggests that auto/polyreactivity are not critical factors in the development of breadth and potency and that the V3/glycans should remain a high-priority vaccine candidate. Since targeting the V3/glycans was associated with breadth and potency in this cohort, the study continued to look at this epitope to investigate the role of these glycans in neutralisation resistance of Tier 2 viruses. The HIV-1 Env is surrounded by glycans that often prevent antibody neutralisation, leading to the term the "glycan shield", however some bnAbs have evolved to recognise these carbohydrates. Chapter 4 of this thesis describes how the N-linked glycan at position N301 is critical for maintaining neutralisation resistance of one subtype C virus (Du156.12), but not for another subtype-matched virus (CAP45.2.00.G3). Thus, the loss of the N301 glycan may have a substantial antibody-related fitness cost for some viruses but not others. The N301 glycan, as well as glycans at positions 332 and 334, are the primary targets of the anti-V3/glycan class of neutralising antibodies, which may select for loss of the targeted glycan. The evidence presented in Chapter 4 suggests that in some viruses, loss of the N301 glycan may result in evasion of anti-V3/glycan antibody responses while maintaining overall neutralisation resistance. This phenomenon may impair efficacy of passively-infused anti-V3/glycan bnAbs or a therapeutic vaccine.
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Long, Joanna Elizabeth. "Psychosocial factors, physical activity status and antibody response to vaccination in healthy and HIV positive populations." Thesis, University of Birmingham, 2012. http://etheses.bham.ac.uk//id/eprint/3246/.

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This thesis examines the effects of psychosocial factors and physical activity on antibody response to vaccination in healthy young, older, and HIV+ populations. Chapter Two found that a brisk walk prior to vaccination did not improve antibody response to pneumococcal or influenza vaccinations in young (18-30yrs) or older (50-64yrs) adults. Chapter Three examined whether a lifestyle physical activity intervention affected antibody response to pneumococcal vaccination in sedentary middle-aged women. There was no effect on antibody response, body composition or fitness measures, although there was an improvement in quality of life for the intervention group. Finally, Chapter Four investigated the relationship between psychosocial and physical activity status and antibody response to vaccination in HIV+ patients. Antibody response to some strains of the pneumococcal vaccine were predicted by higher physical activity levels (pn1, pn6b, pn18c), greater social support (pn3) and lower life events stress (pn1). However, the majority of analyses found that antibody response to vaccination was not affected by these measures. In conclusion, neither acute nor chronic walking interventions improve antibody response to vaccination, and only limited relationships are seen between psychosocial factors, physical activity status and antibody response to a variety of vaccinations.
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Wan, Lai Kin Derek. "The design and development of an HIV-1 vaccine to elicit a broadly neutralising antibody response." Thesis, University of Oxford, 2012. http://ora.ox.ac.uk/objects/uuid:5de89b0d-a0bd-47e4-b577-87adf68bfb69.

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Despite 30 years of research, a prophylactic vaccine against HIV-1 is still lacking and is urgently needed in order to control the global AIDS pandemic. The discovery of broadly neutralising antibodies (BNAbs) was an important step for HIV-1 research but no vaccine candidate tested so far has been able to reproduce responses containing such antibodies, and it remains unclear how this could be achieved via immunisation. In this thesis, I attempted to explore this gap of knowledge in two ways. First, certain features (‘signatures’) of the Env protein that were associated with a broadly neutralising response were identified through machine learning. Further characterisation of these signatures revealed several ways by which these naturally-occurring mutations might alter the immunogenicity of the Env protein that could result in the elicitation of a broadly neutralising response. The incorporation of such signatures in future vaccine design could be useful as the Env protein might adopt a conformation that encourages the elicitation of a broadly neutralising response. Second, 3 novel vaccination approaches were proposed aiming to induce a BNAb antibody response. The development of 2 approaches proved to be difficult and was not continued. For the third approach, non-neutralising immunogen-derived antibodies were used to mask immunodominant epitopes on the Env protein (i.e. ‘antibody-shielding’), thus allowing the antibody response to be focused to the highly conserved CD4 binding site (CD4bs). Subsequent immunisation of the antibody-shielded gp120 proteins in mice and rabbits demonstrated that antibody-shielding was able to significantly dampen the V3-specific antibody response while retaining the CD4bs-specific response. However, the antibody response to the V1/V2 loop was enhanced upon V3-dampening which indicates that further optimisation of the antibody-shield is needed in order to eliminate any antibody response towards the immunodominant regions. In conclusion, these results are the first description of a number of novel vaccination ideas and provide valuable insights into how these approaches could be optimised to become effective HIV-1 vaccines that can lead to the elicitation of a broadly neutralising antibody response.
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Jacob, Rajesh Abraham. "Evaluating the neutralizing antibody response to HIV-1 membrane proximal external regional; Implications for vaccine design." Doctoral thesis, University of Cape Town, 2014. http://hdl.handle.net/11427/8707.

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Inducing broadly neutralizing antibodies targeting the HIV-1 envelope is thought to be crucial for developing an effective vaccine. The Membrane Proximal External Region (MPER) within the HIV- 1 gp41 envelope is a promising vaccine target. The MPER is highly conserved, functionally constrained, facilitates virus fusion and is targeted by broadly neutralizing monoclonal antibodies. The objectives of this research were 1) To evaluate the neutralization breadth of antibodies induced by epitopes within the MPER compared to the PG9/16-site in chronically HIV-1-infected individuals, 2) to identify neutralization resistant HIV-1 isolates (using plasma samples infected with the same subtype) and to characterize their sensitivity to anti-MPER antibodies and 3) to determine the accessibility of the MPER to HIV-1 induced polyclonal anti-MPER antibodies in a highly neutralization resistant virus (253-11; CRF02_AG subtype).
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Davis, Katie L. "Analysis of HIV-1 variable loop 3-specific neutralizing antibody responses by HIV-2/HIV-1 envelope chimeras." Thesis, Birmingham, Ala. : University of Alabama at Birmingham, 2008. https://www.mhsl.uab.edu/dt/2009r/davis.pdf.

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Books on the topic "Antibody response to HIV"

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Cleveland, S. Matthew. HIV-1-specific antibody responses to a plant virus-HIV chimera. [s.l.]: typescript, 1999.

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Federal Centre for AIDS (Canada). AIDS and the HIV antibody test. Ottawa, Ont: Minister of Supply and Services Canada = Ministre des approvisionnements et services Canada, 1989.

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Illinois. Dept. of Public Health. AIDS antibody testing. Springfield, IL]: Illinois Dept. of Public Health, 1999.

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Burns, Debra L. HIV antibody test-linked counseling in Minnesota. [Minneapolis, Minn.]: Minnesota Dept. of Health, 1989.

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Burns, Debra L. Laboratory quality related to HIV antibody testing in Minnesota. [St. Paul, Minn.]: Minnesota Dept. of Health, 1989.

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Hammett, Theodore M. HIV antibody testing: Procedures, interpretation, and reliability of results. [Washington, D.C.]: U.S. Dept. of Justice, National Institute of Justice, 1988.

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Great Britain. Department of Health. Department of Health guidance: Additional sites for HIV antibody testing ; Offering voluntary named HIV antibody testing to women receiving antenatal care ; Partner notification for HIV infection. London: Department of Health, 1992.

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Sandfort, Theo. The Dutch Response To HIV. London: Taylor & Francis Inc, 2002.

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United States. Agency for International Development. USAID's expanded response to HIV/AIDS. Washington, D.C.]: U.S. Agency for International Development, 2002.

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Chateauvert, Michel. Human immunodeficiency virus antibody testing: Counselling guidelines from the Canadian Medical Association. Ottawa: Canadian Medical Association, 1990.

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Book chapters on the topic "Antibody response to HIV"

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Makvandi-Nejad, Shokouh. "Antibody Response to HIV-2." In Encyclopedia of AIDS, 55–58. New York, NY: Springer New York, 2018. http://dx.doi.org/10.1007/978-1-4939-7101-5_50.

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Makvandi-Nejad, Shokouh. "The Antibody Response to HIV-2." In Encyclopedia of AIDS, 1–5. New York, NY: Springer New York, 2015. http://dx.doi.org/10.1007/978-1-4614-9610-6_50-1.

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Moldoveanu, Zina, and Jiri Mestecky. "Mucosal Antibody Responses to HIV." In Methods in Molecular Biology, 333–45. Totowa, NJ: Humana Press, 2009. http://dx.doi.org/10.1007/978-1-59745-170-3_22.

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Parren, Paul W. H. I., and Dennis R. Burton. "Antibodies against HIV-1 from Phage Display Libraries: Mapping of an Immune Response and Progress towards Antiviral Immunotherapy (Part 1 of 2)." In Antibody Engineering, 18–37. Basel: KARGER, 1996. http://dx.doi.org/10.1159/000319346.

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Parren, Paul W. H. I., and Dennis R. Burton. "Antibodies against HIV-1 from Phage Display Libraries: Mapping of an Immune Response and Progress towards Antiviral Immunotherapy (Part 2 of 2)." In Antibody Engineering, 38–56. Basel: KARGER, 1996. http://dx.doi.org/10.1159/000319347.

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Lewis, George K. "Non-neutralizing Antibody Responses and Protection Against HIV-1." In Encyclopedia of AIDS, 1–6. New York, NY: Springer New York, 2014. http://dx.doi.org/10.1007/978-1-4614-9610-6_140-1.

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Lewis, George K. "Non-neutralizing Antibody Responses and Protection Against HIV-1." In Encyclopedia of AIDS, 1539–44. New York, NY: Springer New York, 2018. http://dx.doi.org/10.1007/978-1-4939-7101-5_140.

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Lenzi, M., M. Fusconi, L. Selleri, A. Caselli, F. Cassani, A. Craxi, and F. B. Bianchi. "Characterization of Anti Liver Kidney Microsomal Antibody Associated with Chronic HDV Infection by Immunoblotting." In The Immune Response to Viral Infections, 255–56. Boston, MA: Springer US, 1989. http://dx.doi.org/10.1007/978-1-4684-5712-4_25.

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Silfverdal, Sven Arne, Lennart Bodin, Marina Ulanova, Mirjana Hahn-Zoric, Lars Å. Hanson, and Per Olcén. "Antibody Response to Haemophilus Influenzae Type B (HIB) in Children with Invasive HIB Infection in Relation to Duration of Exclusive Breastfeeding." In Advances in Experimental Medicine and Biology, 311–13. Boston, MA: Springer US, 2002. http://dx.doi.org/10.1007/978-1-4615-0559-4_60.

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de St. Grothan, S. Fazekas, and R. G. Webster. "The Antibody Response." In Ciba Foundation Symposium - Cellular Biology of Myxovirus Infections, 246–71. Chichester, UK: John Wiley & Sons, Ltd., 2008. http://dx.doi.org/10.1002/9780470719367.ch11.

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Conference papers on the topic "Antibody response to HIV"

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GOMPERTS, E. D., and K. WEINBERG. "LOSS OF IMMUNE TO RECALL ANTIGENS IN THERE HIV+ HEMOPHILIC CHILDREN." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644140.

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Three children with severe inherited bleeding disorders have been followed for a number of years at this center. One child (DOB 3/71) initially presented with mild hemophilia A, (Factor VIII 6%). He subsequently developed an inhibitor to Factor VIII (maximum 45 B. U.) and seroconverted to HIV+ Status 12/83. In 12/86 he had virtually lost his antibody response to infused Factor VIII (previously withheld), with a maximum increase in inhibitor titre to1 B. U. on challenge. In addition, his antitetanus antibody titre was very low at 0.01 u/ml earlier in theyear. His absolute T4 cell number at this time was very low at 64 and did not respond to skin antigen testing to PPD, tetanus and Candida.The second patient (severe hemophilia A DOB 7/76) had seroconvertedto HIV+ Status in 9/78. This child has lost his a-HBs seropositive status with an absolute T4 count of 239. His current anti-tetanus titre is 0.01 u/ml.The third patient (von Willebrand disease, Type III, DOB 7/74) seroconverted to HIV+E status by 5/83. His T4 absolute numbers have fallen to 53. His anti-tetanus antibody titre has fallen to extremely low levels (0.01 u/ml), and this failed to respond to re-immunization with tetanus toxoid. These three patients indicate that previously immunized children may lose their immune status and their ability to respond to recall antigens. It is pertinent to note that lymphocytes from all 3 patients failed to respond mitogenically in vitro to tetanus antigen pari passu with the observed very low anti-tetanus antibody titres. These phenomena would indicate that these patients are probably susceptible to previously preventable infectious agents including poliovirus, measles, mumps, rubella, diphtheria, tetanus and hepatitis B virus.
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Wood, Gwendolyn, Stefanie Iverson Cabral, Lisa Manhart, Sylvan Lowens, Catherine Gillespie, and Patricia Totten. "P797 Antibody response tomycoplasma genitaliumin longitudinally infected men with non-gonococcal urethritis." In Abstracts for the STI & HIV World Congress (Joint Meeting of the 23rd ISSTDR and 20th IUSTI), July 14–17, 2019, Vancouver, Canada. BMJ Publishing Group Ltd, 2019. http://dx.doi.org/10.1136/sextrans-2019-sti.851.

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Karpatkin, S. "MECHANISMS OF IMMUNOLOGIC THROMBOCYTOPENIA IN INDIVIDUALS AT RISK FOR AIDS." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644759.

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HIV-seropositive homosexuals, narcotic addicts and hemophiliacs develop a new syndrome of immunologic thrombocytopenic purpura (ITP) which is clinically indistinguishable from classic autoimmune thrombocytopenic purpura (ATP) with respect to increased megakaryocytes in the bone marrow, peripheral destruction of antibody-coated platelets, negative serology for SLE, response to treatment with prednisone and/or splenectomy. However, their platelet immunologic profiles are different.Homosexuals appear to have an immune complex-mediated mechanism: markedly elevated platelet-bound IgG and C3C4 (3.8 and 4.2-fold greater than classic ATP, respectively), elevated circulating immune complexes (3-fold greater than classic ATP), anti-F(ab')2 antibodies and absence of 7S anti-platelet IgG. There is no inverse correlation between platelet count and platelet-bound IgG or platelet-elutable anti-platelet antibody as in classic ATP.Hemophiliacs appear to have an autoimmune 7S IgG-mediated mechanism similar to classic ATP: inverse relationship betweem platelet count and platelet-bound IgG, r = 0.84, p less than 0.001, 26 df, anti-platelet reactive 7S IgG which reacts by its F(ab')2 domain, (reactive at 60-130 ug/ml compared to control IgG), platelet-elutable anti-platelet antibody. However, these patients also have elevated circulating immune complexes (2.4-fold classic ATP level) and markedly elevated platelet-bound IgG and C3C4 (3.4 and 1.2-fold classic ATP level, respectively). Anti-HIV antibody correlated with circulating immune complexes, r = 0.833, p less than 0.001.Narcotic addicts appear to have a mixture of both mechanisms (immune complex as well as autoimmune 7S IgG): markedly elevated platelet-bound IgG and C3C4 (2.6 and 2.4-fold classic ATP level, respectively), elevated circulating immune complexes (7.3-fold classic ATP level), anti-F(ab')2 antibodies, absence of an inverse correlation between platelet count and platelet-bound IgG. However, these patients do have specific 7S IgG anti-platelet antibody, which reacts by its F(ab')2 domain.F(ab')2antibodies were of the IgG class and correlated with circulating immune complex level. They react with autologous, homologous patient and healthy control F(ab')2 fragments. Some anti-F(ab')2 antibodies have broad reactivity, others are more limited. Some immune complexes were shown to contain HIV antibody. It is postulated that the immune complex platelet deposition noted with homosexual and narcotic addict thrombocytopenia may in part be due to HIV antibody complexes, some of which may exist as anti-antibody complexes.
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Djawe, Kpandja, Laurence Huang, Kieran Daly, Linda Levin, Serena Fong, Anuradha Subramanian, Katherine Grieco, Leah Jarlsberg, July Koch, and Peter Walzer. "Independent Predictors Of High Antibody Responses To MsgC In HIV-infected Patients With Pneumocystis Pneumonia (PcP)." In American Thoracic Society 2010 International Conference, May 14-19, 2010 • New Orleans. American Thoracic Society, 2010. http://dx.doi.org/10.1164/ajrccm-conference.2010.181.1_meetingabstracts.a5218.

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Kasper, C. K., N. L. Sanders, and N. P. Ewing. "IMMUNE TOLERANCE INDUCTION IN HEMOPHILIA A WITH INHIBITOR." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644715.

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Factor VIII (FVIII), 50 U/Kg/day, was given without immunosuppressive drugs to 11 patients with hemophilia A and inhibitor. Interval since inhibitor diagnosis was 4-6 years (yr) in 3 cases and 12-27 yr in others. Six had received no FVIII since inhibitor diagnosis. Intervals since last FVIII use were 2 months (mo) in 3 cases and 3-15 yr in others. Historic peak inhibitor levels were 3,8,9,10,25,27,64,375,809,1100 and 2780 Bethesda units (BU). Levels at start of protocol (baseline) were under one BU in 7 cases and 2,42,265 and 398 in others. Evidence of HIV. infection exists in 10 patients: 8 of 9 tested have HIV antibody, 7 of 11 tested have low T4 cell counts and 4 currently have AIDS-related complex. Results after 4-31 mo (median 10) are as follows. Peak inhibitor levels on protocol exceeded baseline in only 6 cases and exceeded historic peaks in only 2 cases. All peaks occurred during the first mo and levels fell markedly by the second. All patients but one had levels below baseline by the third mo. Among 7 patients with one BU or less baseline, no inhibitor was detected after one mo in 4 cases and after 3 mo in 2 cases; another child still has trace inhibitor after 8 mo. A child with baseline 2 BU had no inhibitor after 4 mo. Three older patients have not responded completely. In 2 adults who began the protocol 2 mo after intense FVIII use for hemorrhages, baselines of 275 and 398 BU fell rapidly in the first 4 mo but then plateaued around 20-30 BU despite 9 and 26 mo further therapy. In a teenager who began the protocol 4 yr after intense FVIII use, the baseline of 42 BU has not fallen in 4 mo of therapy. Thus, rapid induction of immune tolerance was achieved in 7 of 8 patients with low baselines; the program was less useful in patients with high baselines. Of 4 patients resistant to full induction of immune tolerance, all have evidence of HIV infection; 3 were tested and have HIV antibody, 2 have low T4 counts and 2 have ARC. Thus, the immune suppression of HIV infection may not potentiate induction of FVIII tolerance. All patients achieving FVIII tolerance remain of FVIII prophylaxis. In some, low-level inhibitors emerged on attempts at withdrawal. Induction of immune tolerance with FVIII is advised for patients with currently-low inhibitor levels because of the high success rate.
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Brace, L. D., J. Fareed, and D. Hoppensteadt. "EFFECTS OF THROMBOXANE PATHWAY ANTAGONISTS ON HEPARIN-INDUCED PLATELET AGGREGATION (H-IPA) AND TESTING FOR HEPARIN-INDUCED THROMBOCYTOPENIA (HIT)." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643383.

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We have reported that heparin and heparin fractions can induce platelet aggregation (PA) in a substantial number of normal healthy drug-free donors. H-IPA was shown to depend upon the molecular weight and concentration of the heparin preparation used, but its mechanism remains unknown. Therefore, we performed experiments with antagonists of the thromboxane pathway to determine whether arachidonic acid metabolites contribute to H-IPA. When indomethacin or 13-azaprostanoic (a thromboxane receptor anatagonist) was added to the PRP of donors whose platelets had been shown to aggregate in response to heparin, H-IPA was completely inhibited: heparin (bovine or porcine) caused 75% PA, while pretreatment with indomethacin or 13-APA reduced the response to 6%. Similarly, if the same donors ingested 650 mg aspirin 3 hours prior to phlebotomy, the PA response to heparin was reduced to approx. 10%. These results demonstrate that at least part of the mechanism of H-IPA is mediated through thromboxane generation. However, the mechanism by which'heparin stimulates thromboxane production in platelets remains unknown.In some patients, heparin is known to induce an immune response that causes severe thrombocytopenia (HIT) and is associated with arterial and venous thrombosis. Fratantoni, et al. (Blood 45:395-401, 1975) have introduced a PA method for the diagnosis of HIT. We have used a modification of this method to show that the PA observed when heparin is added to a mixture of normal donor PRP and HIT patient’s serum or plasma can be inhibited by antagonists of the thromboxane pathway. When normal donor PRP was pretreated with indomethacin or 13-APA and then mixed with serum from a HIT patient (290 uL PRP:160 uL serum), the PA response to heparin was reduced from 75% to 10% or less. Similarly, if the PRP donors ingested 650 mg aspirin prior to phlebotomy, PA in the HIT test was reduced from 75% to 10% or less. Thus, the interaction of heparin with the antibody and platelets causes thromboxane generation and leads to PA. Cyclo-oxygenase specific antiplatelet drugs and inhibitors of thromboxane generation may be useful in the clinical management of HIT and H-IPA.
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Zinin, Pavel V., Ningjie Hu, Lori E. Kamemoto, Qigui Yu, Anupam K. Misra, and Shiv K. Sharma. "Raman spectroscopy of HIV-1 antigen and antibody." In SPIE Defense, Security, and Sensing, edited by Brian M. Cullum and Eric S. McLamore. SPIE, 2011. http://dx.doi.org/10.1117/12.887169.

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Moroi, M., S. M. Jung, N. Yoshida, N. Aoki, and K. Tanoue. "THROMBASTHENIA WITH AN ABNORMAL PLATELET MEMBRANE GPIIb OF DIFFERENT MOLECULAR WEIGHT." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644741.

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We describe several individuals with abnormal platelet glycoprotein lib (GPIIb) of different molecular weight (MW), a novel defect in that previously reported thrombasthenics have not shown GPIIb molecules of abnormal MW. Patient 1 shows 2 bands of GPIIb (one with normal MW and one with abnormal MW) in SDS-PAGE (lectin and antibody staining). This patient has a mild bleeding tendency, and her platelets did not aggregate in response to ADP (2-10 μM) and had severely depressed collagen induced aggregation ,but responded normally to ristocetin. The MW of the abnormal GPIIb band was calculated to be 122 KDa (compared to the 129 kDa of normal GPIIb) in non-reduced SDS-PAGE; the MW was 128 kDa (compared to the normal 118 kDa) in reduced SDS-PAGE. The amount of each GPIIb band, calculated from densitometry, was approximately 35% for the GPIIb of abnormal MW and 20% for the normal MW GPIIb, relative to the amounts of GPIIb found in normal individuals. Assays of fibrinogen binding to the patient`s platelets indicate that they contain 25% of the fibrinogen receptor as compared to normal platelets. Crossed immunoelectrophoresis showed the formation of the GPIIb/IIIa complex, which was found to consist mostly of normal MW GPIIb and GPIIIa. The patient's father showed decreased aggregability in response to ADP, and his platelets also contained abnormal and normal GPIIb. The father's platelets, however, contained about 50% normal GPIIb as compared to normal platelets, and his platelets have about 50% the number of fibrinogen receptors compared to normal platelets. From these results, the patient was suggested to have heterozygous GPIIb molecules, and the observed defects in aggregability would be attributable to the decrease of normal GPIIb to 20-30% of the normal level. Quite recently, we found another thrombasthenic individual who has homozygous abnormal GPIIb molecules. Electrophoretic mobilities of his abnormal GPIIb on SDS-PAGE indicated that the abnormal GPIIb's were very similar between the 2 cases, and two-dimensional, unreduced-reduced SDS-PAGE suggested that the abnormal GPIIb consists of a single chain.
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Olorunsola, BO, OT Adedoyin, and SK Ernest. "G587(P) Measles antibody levels among vaccinated HIV-infected and HIV uninfected children in nigeria." In Royal College of Paediatrics and Child Health, Abstracts of the RCPCH Conference–Online, 25 September 2020–13 November 2020. BMJ Publishing Group Ltd and Royal College of Paediatrics and Child Health, 2020. http://dx.doi.org/10.1136/archdischild-2020-rcpch.504.

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Wilson, David. "PL10.1 The global HIV response at 40." In Abstracts for the STI & HIV World Congress (Joint Meeting of the 23rd ISSTDR and 20th IUSTI), July 14–17, 2019, Vancouver, Canada. BMJ Publishing Group Ltd, 2019. http://dx.doi.org/10.1136/sextrans-2019-sti.13.

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Reports on the topic "Antibody response to HIV"

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Serão, Nick V. L., Bob Kemp, Benny Mote, Philip Willson, John Harding, Steve Bishop, Graham Plastow, and Jack C. M. Dekkers. Accuracy of Genomic Prediction for PRRS Antibody Response. Ames (Iowa): Iowa State University, January 2015. http://dx.doi.org/10.31274/ans_air-180814-1361.

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Banks, H. T., M. Davidian, Shuhua Hu, Grace M. Kepler, and E. S. Rosenberg. Modeling HIV Immune Response and Validation with Clinical Data. Fort Belvoir, VA: Defense Technical Information Center, March 2007. http://dx.doi.org/10.21236/ada465194.

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Serão, Nick V. L., Oswald Matika, Steve Bishop, Bob Kemp, John Harding, Graham Plastow, and Jack C. M. Dekkers. Genetic Analysis of Reproductive Traits and Antibody Response in PRRS Infected Sows. Ames (Iowa): Iowa State University, January 2014. http://dx.doi.org/10.31274/ans_air-180814-1362.

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Kalibala, Sam, and Drosin Mulenga. Situation assessment of the HIV response among young people in Zambia. Population Council, 2011. http://dx.doi.org/10.31899/hiv2.1002.

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Little, S. F., W. M. Webster, S. L. Norris, and G. P. Andrews. Evaluation of an Anti-rPA IgG ELISA for Measuring the Antibody Response in Mice. Fort Belvoir, VA: Defense Technical Information Center, January 2004. http://dx.doi.org/10.21236/ada428618.

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Ciraci, Ceren, Michael G. Kaiser, and Susan J. Lamont. Chicken Antibody Response to Salmonella enteritidis Vaccine in Advanced Intercross Lines and Parental Lines. Ames (Iowa): Iowa State University, January 2009. http://dx.doi.org/10.31274/ans_air-180814-8.

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Ishimaru, Hitoshi. Predictions of Intentions of College Students to Take an HIV Antibody Test and Their Preferences for a Testing Procedure. Portland State University Library, January 2000. http://dx.doi.org/10.15760/etd.7222.

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Mackey, Katherine, Irina Arkhipova-Jenkins, Charlotte Armstrong, Emily Gean, Johanna Anderson, Robin A. Paynter, and Mark Helfand. Antibody Response Following SARS-CoV-2 Infection and Implications for Immunity: A Rapid Living Review. Agency for Healthcare Research and Quality (AHRQ), March 2021. http://dx.doi.org/10.23970/ahrqepccovidimmunity.

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 Evidence suggests that the majority of adults develop detectable levels of immunoglobulin M (IgM) and immunoglobulin G (IgG) antibodies following infection with SARS-CoV-2 (moderate strength of evidence* [SoE]).  IgM levels peak approximately 20 days after symptom onset or RT-PCR diagnosis and subsequently decline. IgG levels peak approximately 25 days after symptom onset or RT-PCR diagnosis and may remain detectable for at least 120 days (moderate SoE*).  Almost all adults develop neutralizing antibodies in response to SARS-CoV-2 infection, and these antibodies may remain detectable for at least 152 days (low SoE*).  A small percentage of people do not develop antibodies in response to SARS-CoV-2 infection for reasons that are largely unclear but may be related to less severe disease or absence of symptoms.  Antibody prevalence does not appear to vary by age or sex, but older age may be associated with higher antibody levels (low SoE*). Non-White race may be associated with higher antibody prevalence and levels (low SoE*). COVID-19 severity and presence of symptoms may also be associated with higher antibody prevalence or levels (low SoE*). More evidence is needed to draw stronger conclusions regarding how the antibody response varies by patient characteristics and disease factors.  Studies to date have not established the relationship between the development of antibodies after RT-PCR-diagnosed SARS-CoV-2 infection and the risk of reinfection. Studies based on index serologic testing suggest that the presence of antibodies is associated with a lower risk of a subsequent positive SARS-CoV-2 RT-PCR test.
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Hess, Andrew S., Benjamin Trible, Nicholas J. Boddicker, Raymond Rowland, Joan Lunney, Susan L. Carpenter, and Jack C. M. Dekkers. Factors Associated with Neutralizing Antibody Response in Piglets Experimentally Infected with Porcine Reproductive and Respiratory Virus. Ames (Iowa): Iowa State University, January 2013. http://dx.doi.org/10.31274/ans_air-180814-1246.

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Basu, Sayani. Monoclonal Antibody Therapy: A New Hope in Cancer Treatment. Natur Library, November 2020. http://dx.doi.org/10.47496/nl.blog.14.

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The remarkable specificity, high efficacy and the ability to elicit an antitumor response indicate that monoclonal antibody therapy offers promise in the treatment of malignancy and appears to be clinically relevant
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