Antibody dependent enhancement. Medical search

Enhancement of viral infectivity caused by non-neutralizing antibodies. There are at least two mechanisms known to account for this: mediation by Fc receptors (RECEPTORS, FC) or by complement receptors (RECEPTORS, COMPLEMENT). Either the virus is complexed with antiviral IMMUNOGLOBULIN G and binds to Fc receptors, or virus is coated with antiviral IMMUNOGLOBULIN M and binds to complement receptors.

The phenomenon of antibody-mediated target cell destruction by non-sensitized effector cells. The identity of the target cell varies, but it must possess surface IMMUNOGLOBULIN G whose Fc portion is intact. The effector cell is a "killer" cell possessing Fc receptors. It may be a lymphocyte lacking conventional B- or T-cell markers, or a monocyte, macrophage, or polynuclear leukocyte, depending on the identity of the target cell. The reaction is complement-independent.

Antibodies produced by a single clone of cells.

Immunoglobulin molecules having a specific amino acid sequence by virtue of which they interact only with the ANTIGEN (or a very similar shape) that induced their synthesis in cells of the lymphoid series (especially PLASMA CELLS).

The major immunoglobulin isotype class in normal human serum. There are several isotype subclasses of IgG, for example, IgG1, IgG2A, and IgG2B.

Bone marrow-derived lymphocytes that possess cytotoxic properties, classically directed against transformed and virus-infected cells. Unlike T CELLS; and B CELLS; NK CELLS are not antigen specific. The cytotoxicity of natural killer cells is determined by the collective signaling of an array of inhibitory and stimulatory CELL SURFACE RECEPTORS. A subset of T-LYMPHOCYTES referred to as NATURAL KILLER T CELLS shares some of the properties of this cell type.

The phenomenon of target cell destruction by immunologically active effector cells. It may be brought about directly by sensitized T-lymphocytes or by lymphoid or myeloid "killer" cells, or it may be mediated by cytotoxic antibody, cytotoxic factor released by lymphoid cells, or complement.

The property of antibodies which enables them to react with some ANTIGENIC DETERMINANTS and not with others. Specificity is dependent on chemical composition, physical forces, and molecular structure at the binding site.

In vitro antibody-dependent enhancement assays are insensitive indicators of in vivo vaccine enhancement of equine infectious anemia virus. (1/83)

We have previously demonstrated a high propensity for enhancement of virus replication and disease resulting from experimental immunization of ponies with a baculovirus recombinant envelope (rgp90) vaccine from equine infectious anemia virus (EIAV). The current studies were undertaken to examine the correlation between the observed in vivo vaccine enhancement and in vitro assays for antibody-dependent enhancement (ADE) of EIAV replication. Toward this goal an optimized EIAV in vitro enhancement assay was developed using primary equine macrophage cells and used to evaluate the enhancement properties of immune serum taken from rgp90 immunized ponies that displayed various levels of vaccine enhancement after experimental challenge with EIAV. For comparison, we analyzed in parallel immune serum samples from a group of ponies immunized with a viral envelope subunit vaccine (LL-gp) that produced sterile protection from EIAV challenge. The results of these assays demonstrated that the rgp90 immune serum had a greater propensity for in vitro enhancement of EIAV replication than serum from the protected LL-gp immunized ponies; in vitro enhancement levels for the rgp90 immune sera averaged about 1.5, with a maximum enhancement value of about 2.0. While distinguishing between immune serum produced by the rgp90 and LL-gp immunizations, the in vitro enhancement assay failed to reliably correlate with the severity of in vivo enhancement observed among the rgp90 vaccine recipients. Vaccinated ponies that experienced moderate to no disease signs displayed levels of in vitro enhancement similar to those of ponies that experienced severe and fatal enhancement of disease after viral challenge. The observed in vitro enhancement was demonstrated to be dependent on serum immunoglobulin, but independent of complement. These studies demonstrate in the EIAV system that in vitro ADE assays appear to be relatively insensitive indicators of the severity of in vivo enhancement and that relatively low levels of in vitro ADE can be associated with severe to fatal enhancement of virus replication and disease in vivo. These observations suggest that relatively low levels of serum ADE observed in other lentivirus systems, including HIV-1, may have more profound effects on in vivo virus replication and disease than previously recognized. (+info)

Infection of human cells by dengue virus is modulated by different cell types and viral strains. (2/83)

Although prior studies have investigated cellular infection by dengue virus (DV), many have used highly passaged strains. We have reassessed cellular infection by DV type 2 (DV2) using prototype and low-passage isolates representing genotypes from different geographic areas. We observed marked variation in the susceptibility to infection among cell types by different DV2 strains. HepG2 hepatoma cells were susceptible to infection by all DV2 strains assayed. Although the prototype strain generated higher titers of secreted virus than the low-passage isolates, this difference did not correspond to positive- or negative-strand viral RNA levels and thus may reflect variation in efficiency among DV2 isolates to translate viral proteins or package and/or secrete virus. In contrast, human foreskin fibroblasts were susceptible to the prototype and low-passage Thai isolates but not to five Nicaraguan strains tested, as reflected by the absence of accumulation of negative-strand viral RNA, viral antigen, and infectious virus. A similar pattern was observed with the antibody-dependent pathway of infection. U937 and THP-1 myeloid cells and peripheral blood monocytes were infected in the presence of enhancing antibodies by the prototype strain but not by low-passage Nicaraguan isolates. Again, the barrier appeared to be prior to negative-strand accumulation. Thus, depending on the cell type and viral isolate, blocks that limit the production of infectious virus in vitro may occur at distinct steps in the pathway of cellular infection. (+info)

Specific ablation of antiviral gene expression in macrophages by antibody-dependent enhancement of Ross River virus infection. (3/83)

Ross River virus (RRV) is an indigenous Australian arthropod-borne alphavirus responsible for epidemic polyarthritis (EPA), myalgia, and lethargy in humans. Macrophages and monocytes have been associated with human RRV disease, and previous studies have shown that RRV is capable of infecting macrophages via both a natural virus receptor and by Fc receptor-mediated antibody-dependent enhancement (ADE). Similar to other viruses, such as human immunodeficiency virus and dengue virus, ADE infection results in dramatic RRV growth increases for in vitro macrophage cultures. This study demonstrates that RRV could resist lipopolysaccharide (LPS)-induced antiviral activity in macrophage cultures when infection was via the ADE pathway. Investigation of this infection pathway found that RRV was able to suppress the transcription and translation of key antiviral genes (tumor necrosis factor and inducible nitric oxide synthase) in LPS-stimulated macrophages by disrupting the transcription into mRNA of the genes coding for the associated transcription factors IRF-1 and NF-kappaB. The transcription of non-antiviral control genes was not perturbed by RRV-ADE infection, and de novo protein synthesis also was not significantly affected in RRV-ADE infected cells. The ADE pathway of infection allowed RRV to specifically target antiviral genes in macrophages, resulting in unrestricted virus replication. As ADE has been observed for several virus families and associated with disease and adverse vaccination outcomes, these findings may have broad relevance to viral disease formation and antiviral vaccination strategies. (+info)

Infectivity-enhancing antibodies to Ebola virus glycoprotein. (4/83)

Ebola virus causes severe hemorrhagic fever in primates, resulting in mortality rates of up to 100%, yet there are no satisfactory biologic explanations for this extreme virulence. Here we show that antisera produced by DNA immunization with a plasmid encoding the surface glycoprotein (GP) of the Zaire strain of Ebola virus enhances the infectivity of vesicular stomatitis virus pseudotyped with the GP. Substantially weaker enhancement was observed with antiserum to the GP of the Reston strain, which is much less pathogenic in humans than the Ebola Zaire and Sudan viruses. The enhancing activity was abolished by heat but was increased in the presence of complement system inhibitors, suggesting that heat-labile factors other than the complement system are required for this effect. We also generated an anti-Zaire GP monoclonal antibody that enhanced viral infectivity and another that neutralized it, indicating the presence of distinct epitopes for these properties. Our findings suggest that antibody-dependent enhancement of infectivity may account for the extreme virulence of the virus. They also raise issues about the development of Ebola virus vaccines and the use of passive prophylaxis or therapy with Ebola virus GP antibodies. (+info)

Enhancement of adenovirus vector entry into CD70-positive B-cell Lines by using a bispecific CD70-adenovirus fiber antibody. (5/83)

Although many recombinant adenovirus vectors (rAd) have been developed, especially by using group C adenoviruses, to transfer and express genes, such rAd do not readily infect B-cell lines due to the lack of the coxsackievirus-adenovirus receptor. Bispecific antibodies have been used in different cell systems to facilitate entry of rAd into otherwise nonpermissive cells. Bispecific antibody is synthesized by covalently linking two monoclonal antibodies with distinct specificities. It has been shown that lymphoproliferative tumors commonly express the cell surface protein CD70, while this receptor is normally expressed on only a small subset of highly activated B cells and T cells. We therefore investigated whether a bispecific antibody with specificities for the adenovirus fiber protein and CD70 can facilitate rAd entry and subsequent expression of rAd-encoded genes in CD70-positive B cells. We found high CD70 expression on Epstein-Barr virus (EBV)-transformed lymphoblastoid cell lines (LCLs), as well as some, but not all, Burkitt lymphoma (BL) lines. We show here that rAd encoding green fluorescent protein (Ad-GFP) infects EBV-transformed LCLs and a CD70-positive BL line 10- to 20-fold more efficiently in the presence of the CD70-fiber bispecific antibody. In contrast, the bispecific antibody does not enhance Ad-GFP infection in CD70-deficient BL cells. Using the CD70-fiber bispecific antibody, we increased the ability of rAd vectors encoding the EBV immediate-early proteins BZLF1 and BRLF1 to induce the lytic form of EBV infection in LCLs. These results indicate that the CD70-fiber bispecific antibody can enhance rAd infection of CD70-positive B cells and suggest the use of this vector to explore EBV-positive LCLs. (+info)

Antibody-dependent enhancement of coxsackievirus B4 infectivity of human peripheral blood mononuclear cells results in increased interferon-alpha synthesis. (6/83)

IgG devoid of neutralizing activity and isolated from donor plasma by chromatography formed immune complexes with coxsackievirus B4 (CVB4) and significantly increased the infection of peripheral blood mononuclear cells with CVB4. The major host cells for CVB4 infection enhanced with IgG are monocytic CD14+ cells. The roles of CVB and adenovirus receptor and Fcgamma receptor II and III have been shown. Increased viral replication and the release of infectious particles were demonstrated when interferon (IFN)-alpha produced by infected cells was first neutralized by use of antibodies. The CVB4 IgG-induced synthesis of IFN-alpha by monocytes reflected entry and uncoating of CVB4 but not of viral replication and required the presence of CVB4 RNA inside the cells. Thus, CVB4 can infect monocytes by an antibody-dependent mechanism through interactions between the virus, antiviral antibodies, and specific receptors that result in IFN-alpha production. (+info)

Enhancement of coxsackievirus B3 infection by antibody to a different coxsackievirus strain. (7/83)

Group B coxsackieviruses (CVBs) are a major cause of viral myocarditis and pancreatitis in humans and produce a similar pattern of disease in inbred strains of mice. As there are six strains of CVBs, individuals can be infected with multiple serotypes. This raises the possibility of antibody enhancement of infectivity (AEI) by cross-reactive but non-neutralizing antibody to a different strain from a prior infection. To determine whether AEI plays a role in coxsackievirus pathogenesis, an in vitro system using the murine macrophage cell line J774.1 was tested for enhanced infection when incubated with CVB3 plus anti-CVB2 antibody. Yields of virus were found to increase by 10-50-fold and the percentage of infected cells increased proportionately. The effect was Fc-mediated as F(ab')2 fragments of the antibody could not mediate the effect. To determine whether AEI could also be demonstrated in vivo CVB3 was injected into 5-week-old mice together with mouse polyclonal anti-CVB2. Controls included mice injected with PBS or CVB3 alone. Results showed that the titres of virus in tissues of animals injected with virus plus antibody were 1-2 logs higher than when virus was injected alone. This was accompanied by greater histopathological damage, particularly in the heart. These results have implications for human disease as infection with multiple strains likely occurs during the lifetime of an individual. (+info)

Complement-mediated enhancement of antibody function for neutralization of pseudotype virus containing hepatitis C virus E2 chimeric glycoprotein. (8/83)

We previously reported a number of features of hepatitis C virus (HCV) chimeric glycoproteins related to pseudotype virus entry into mammalian cells. In this study, pseudotype virus was neutralized by HCV E2 glycoprotein-specific antibodies and infected human sera. Neutralization (50% reduction of pseudotype virus plaque formation) was observed with two human immunoglobulin G1 monoclonal antibodies (MAbs) at concentrations of between 2.5 and 10 microg/ml. A hyperimmune rabbit antiserum to an E2 hypervariable region 1 (HVR1) mimotope also exhibited an HCV E2 pseudotype virus neutralization titer of approximately 1/50. An E1 pseudotype virus used as a negative control was not neutralized to a significant level (<1/10) by these MAbs or rabbit antiserum to E2 HVR1. Since HCV probably has a lipid envelope, the role of complement in antibody-mediated virus neutralization was examined. Significant increases in the neutralization titers of the human MAbs (approximately 60- to 160-fold higher) and rabbit antiserum to HVR1 mimotopes (approximately 10-fold higher) were observed upon addition of guinea pig complement. Further, these studies suggested that complement activation occurred primarily by the classical pathway, since a deficiency in the C4 component led to a significant decrease in the level of virus neutralization. This same decrease was not observed with factor B-deficient complement. We also determined that 9 of 56 HCV-infected patient sera (16%) had detectable pseudotype virus neutralization activity at serum dilutions of between 1/20 and 1/50 and that complement addition enhanced the neutralization activity of some of the HCV-infected human sera. Taken together, these results suggest that during infection, HCV E2 glycoprotein induces a weak neutralizing antibody response, that those antibodies can be measured in vitro by the surrogate pseudotype virus plaque reduction assay, and that neutralization function can be augmented by complement. (+info)

Antibody-Dependent Enhancement (ADE) is a phenomenon in which the presence of antibodies against a particular virus actually enhances the ability of the virus to infect and replicate within host cells, leading to increased severity of infection. This occurs when the antibodies bind to the virus but do not neutralize it, instead facilitating uptake of the virus into immune cells expressing Fc receptors, such as macrophages. The virus can then use these cells as a site for replication and evasion of the host's immune response. ADE has been observed in various viral infections, including dengue fever and respiratory syncytial virus (RSV) infection. It is a concern in the development of vaccines against these viruses, as non-neutralizing antibodies induced by vaccination could potentially enhance subsequent infection with a heterologous strain of the virus.

Antibody-Dependent Cell Cytotoxicity (ADCC) is a type of immune response in which the effector cells of the immune system, such as natural killer (NK) cells, cytotoxic T-cells or macrophages, recognize and destroy virus-infected or cancer cells that are coated with antibodies.

In this process, an antibody produced by B-cells binds specifically to an antigen on the surface of a target cell. The other end of the antibody then interacts with Fc receptors found on the surface of effector cells. This interaction triggers the effector cells to release cytotoxic substances, such as perforins and granzymes, which create pores in the target cell membrane and induce apoptosis (programmed cell death).

ADCC plays an important role in the immune defense against viral infections and cancer. It is also a mechanism of action for some monoclonal antibody therapies used in cancer treatment.

Monoclonal antibodies are a type of antibody that are identical because they are produced by a single clone of cells. They are laboratory-produced molecules that act like human antibodies in the immune system. They can be designed to attach to specific proteins found on the surface of cancer cells, making them useful for targeting and treating cancer. Monoclonal antibodies can also be used as a therapy for other diseases, such as autoimmune disorders and inflammatory conditions.

Monoclonal antibodies are produced by fusing a single type of immune cell, called a B cell, with a tumor cell to create a hybrid cell, or hybridoma. This hybrid cell is then able to replicate indefinitely, producing a large number of identical copies of the original antibody. These antibodies can be further modified and engineered to enhance their ability to bind to specific targets, increase their stability, and improve their effectiveness as therapeutic agents.

Monoclonal antibodies have several mechanisms of action in cancer therapy. They can directly kill cancer cells by binding to them and triggering an immune response. They can also block the signals that promote cancer growth and survival. Additionally, monoclonal antibodies can be used to deliver drugs or radiation directly to cancer cells, increasing the effectiveness of these treatments while minimizing their side effects on healthy tissues.

Monoclonal antibodies have become an important tool in modern medicine, with several approved for use in cancer therapy and other diseases. They are continuing to be studied and developed as a promising approach to treating a wide range of medical conditions.

Antibodies are proteins produced by the immune system in response to the presence of a foreign substance, such as a bacterium or virus. They are capable of identifying and binding to specific antigens (foreign substances) on the surface of these invaders, marking them for destruction by other immune cells. Antibodies are also known as immunoglobulins and come in several different types, including IgA, IgD, IgE, IgG, and IgM, each with a unique function in the immune response. They are composed of four polypeptide chains, two heavy chains and two light chains, that are held together by disulfide bonds. The variable regions of the heavy and light chains form the antigen-binding site, which is specific to a particular antigen.

Immunoglobulin G (IgG) is a type of antibody, which is a protective protein produced by the immune system in response to foreign substances like bacteria or viruses. IgG is the most abundant type of antibody in human blood, making up about 75-80% of all antibodies. It is found in all body fluids and plays a crucial role in fighting infections caused by bacteria, viruses, and toxins.

IgG has several important functions:

1. Neutralization: IgG can bind to the surface of bacteria or viruses, preventing them from attaching to and infecting human cells.
2. Opsonization: IgG coats the surface of pathogens, making them more recognizable and easier for immune cells like neutrophils and macrophages to phagocytose (engulf and destroy) them.
3. Complement activation: IgG can activate the complement system, a group of proteins that work together to help eliminate pathogens from the body. Activation of the complement system leads to the formation of the membrane attack complex, which creates holes in the cell membranes of bacteria, leading to their lysis (destruction).
4. Antibody-dependent cellular cytotoxicity (ADCC): IgG can bind to immune cells like natural killer (NK) cells and trigger them to release substances that cause target cells (such as virus-infected or cancerous cells) to undergo apoptosis (programmed cell death).
5. Immune complex formation: IgG can form immune complexes with antigens, which can then be removed from the body through various mechanisms, such as phagocytosis by immune cells or excretion in urine.

IgG is a critical component of adaptive immunity and provides long-lasting protection against reinfection with many pathogens. It has four subclasses (IgG1, IgG2, IgG3, and IgG4) that differ in their structure, function, and distribution in the body.

Natural Killer (NK) cells are a type of lymphocyte, which are large granular innate immune cells that play a crucial role in the host's defense against viral infections and malignant transformations. They do not require prior sensitization to target and destroy abnormal cells, such as virus-infected cells or tumor cells. NK cells recognize their targets through an array of germline-encoded activating and inhibitory receptors that detect the alterations in the cell surface molecules of potential targets. Upon activation, NK cells release cytotoxic granules containing perforins and granzymes to induce target cell apoptosis, and they also produce a variety of cytokines and chemokines to modulate immune responses. Overall, natural killer cells serve as a critical component of the innate immune system, providing rapid and effective responses against infected or malignant cells.

Immunologic cytotoxicity refers to the damage or destruction of cells that occurs as a result of an immune response. This process involves the activation of immune cells, such as cytotoxic T cells and natural killer (NK) cells, which release toxic substances, such as perforins and granzymes, that can kill target cells.

In addition, antibodies produced by B cells can also contribute to immunologic cytotoxicity by binding to antigens on the surface of target cells and triggering complement-mediated lysis or antibody-dependent cellular cytotoxicity (ADCC) by activating immune effector cells.

Immunologic cytotoxicity plays an important role in the body's defense against viral infections, cancer cells, and other foreign substances. However, it can also contribute to tissue damage and autoimmune diseases if the immune system mistakenly targets healthy cells or tissues.

Antibody specificity refers to the ability of an antibody to bind to a specific epitope or antigenic determinant on an antigen. Each antibody has a unique structure that allows it to recognize and bind to a specific region of an antigen, typically a small portion of the antigen's surface made up of amino acids or sugar residues. This highly specific binding is mediated by the variable regions of the antibody's heavy and light chains, which form a pocket that recognizes and binds to the epitope.

The specificity of an antibody is determined by its unique complementarity-determining regions (CDRs), which are loops of amino acids located in the variable domains of both the heavy and light chains. The CDRs form a binding site that recognizes and interacts with the epitope on the antigen. The precise fit between the antibody's binding site and the epitope is critical for specificity, as even small changes in the structure of either can prevent binding.

Antibody specificity is important in immune responses because it allows the immune system to distinguish between self and non-self antigens. This helps to prevent autoimmune reactions where the immune system attacks the body's own cells and tissues. Antibody specificity also plays a crucial role in diagnostic tests, such as ELISA assays, where antibodies are used to detect the presence of specific antigens in biological samples.

The suboptimal antibodies can result from natural infection or from vaccination. (wikipedia.org)
In ADE, antiviral antibodies promote viral infection of target immune cells by exploiting the phagocytic FcγR or complement pathway. (wikipedia.org)
The process of phagocytosis is accompanied by virus degradation, but if the virus is not neutralized (either due to low affinity binding or targeting to a non-neutralizing epitope), antibody binding may result in virus escape and, therefore, more severe infection. (wikipedia.org)
Natural infection and the attenuated vaccine induce antibodies that enhance the update of the homologous virus and H1N1 virus isolated several years later, demonstrating that a primary influenza A virus infection results in the induction of infection enhancing antibodies. (wikipedia.org)
Infection induces the production of neutralizing homotypic immunoglobulin G (IgG) antibodies that provide lifelong immunity against the infecting serotype. (wikipedia.org)
Antibodies are of several kinds (IgG, IgM, IgA, IgE and IgD) depending on when and where they are produced in the body post infection. (tigs.res.in)
Although all of them have Fab capable of binding to various parts of the virion, only a subset of these antibodies are able to block the infection. (tigs.res.in)
The beneficial roles of antibodies are well known, however, sometimes the invading viruses are able to exploit these antibodies to facilitate their own entry into cells and hence result in enhanced infection. (tigs.res.in)
Such a situation typically arises when antibodies are produced against a particular virus during a primary infection event followed by a secondary infection later, by similar viruses sharing partially similar epitopes (e.g different serotypes of a given virus) or other viruses having similar epitopes. (tigs.res.in)
Observations of increased disease severity hint at the possibility of antibody dependent enhancement of infection (ADE). (cwu.edu)
One of those is the phenomenon of antibody-dependent enhancement (ADE), where vaccines may apart from blocking the actual infection process enhance the disease course. (pharmcourse.com)
As a result, the infection aggravates and the antiviral antibodies formed after vaccination may contribute to the viral load increase to an extent [4]. (pharmcourse.com)
Data correlating clinical outcomes with laboratory markers of cell-mediated immunity, not only with antibody response, after SARS-CoV-2 natural infection and vaccines may prove critically valuable if protective immunity fades or if new patterns of disease emerge. (nih.gov)
This occurs when non-neutralizing antibodies generated by past infection or vaccination fail to shut down the pathogen upon re-exposure. (expose-news.com)
Case counts are based on infections confirmed by laboratory detection of Zika virus in the body using a method called RT-PCR (used to confirm symptomatic cases at the time of infection), and an algorithm developed to serologically classify -- a process that involves examining antibodies in blood samples -- cases not confirmed by RT-PCR (primarily clinically inapparent cases). (sciencedaily.com)
Background It is to be determined whether people infected with SARS-CoV-2 will develop long-term immunity against SARS-CoV-2 and retain long-lasting protective antibodies after the infection is resolved. (researchgate.net)
After SARS-CoV-2 infection, people are unlikely to produce long-lasting protective antibodies against this virus. (researchgate.net)
This information is in contrast to a study in Wuhan, China that found 10% of patients lost SARS-CoV-2 antibodies within weeks of infection (12) , although different serology tests were used in this case. (researchgate.net)
We propose that additional investigation into the role of ADCP in protective viral responses, the specific virus epitopes targeted by ADCP antibodies, and the types of phagocytes and Fc receptors involved in ADCP at sites of virus infection will provide insight into strategies to successfully leverage this important immune response for improved antiviral immunity through rational vaccine design. (frontiersin.org)
and monoclonal recombinant antibodies are also currently being pursued for prevention of HIV-1 infection in large Phase IIb clinical trials (NTC02716675 and NCT02568215). (frontiersin.org)
ADE occurs when the antibodies generated during an immune response recognize and bind to a pathogen, but they are unable to prevent infection. (deepcapture.com)
After an infection with one DENV serotype, antibodies induced are type specific and cross-react with other DENV serotypes ( 4 ). (cdc.gov)
In many countries in Asia where this disease is endemic, outbreaks occur in cycles of 3 to 5 years due, perhaps, to enhanced infection with one serotype caused by cross-reactive antibody produced in response to an earlier infection with a second serotype ( 4 ), rather than to climatic effects ( 5 ). (cdc.gov)

Monoclonal antibodies are complex and expensive to produce, meaning poor countries might be priced out. (natureasia.com)
The serotype of the virus was determined by performing indirect immunofluorescence ( 23 ) on cells from the cultures of C6-36 cells used for virus isolation with flavivirus-, dengue-, or serotype-specific monoclonal antibodies ( 23 , 24 ). (cdc.gov)

ADE may occur because of the non-neutralizing characteristic of an antibody, which binds viral epitopes other than those involved in host-cell attachment and entry. (wikipedia.org)
It may also happen when antibodies are present at sub-neutralizing concentrations (yielding occupancies on viral epitopes below the threshold for neutralization), or when the strength of antibody-antigen interaction is below a certain threshold. (wikipedia.org)
Plasma cells produce several antibodies targeted against multiple viral epitopes. (tigs.res.in)

However, of the information collated by Pfizer so far in the ongoing study they have conducted, it is clear to see that they were fully aware in February 2021 that antibody-dependent enhancement was a possible consequence of their Covid-19 injection, and it appears they also knew by April 2021 that the phenomenon was killing people. (expose-news.com)

However, fourteen vaccinated children died after encountering dengue virus in the community as they had developed antibody responses that were not capable of neutralizing the natural virus circulating in the community. (expose-news.com)

Later, in the 1970s, role of ADE phenomenon was confirmed within severe forms of Dengue hemorrhagic fever, when in mild cases occurrence of specific antiviral antibodies led to severe course of the disease when infected with another serotype of the virus. (pharmcourse.com)

This is reminiscent of the ADE (antibody dependent enhancement) phenomenon that has been seen for other vaccine and that has been expressed as a point of concern among many scientists for the COVID vaccines," Stephanie Seneff, a senior researcher at the Massachusetts Institute of Technology's Computer Science and Artificial Intelligence Laboratory told LifeSiteNews. (lifesitenews.com)
Intensive research conducted by health experts throughout the years has brought to light increasing concerns about "Antibody-Dependent Enhancement" (ADE), a phenomenon where vaccines make the disease far worse by priming the immune system for a potentially deadly overreaction. (expose-news.com)

The core of ADE phenomenon is as follows: antigen-specific antiviral antibodies produced during vaccination form an unstable "virus-antibody" complex, this complex interacts with the Fc receptor and the complement receptor on the surface of phagocytic macrophages. (pharmcourse.com)

What are the roles of antibodies versus a durable, high quality T-cell response in protective immunity against SARS-CoV-2? (nih.gov)

She successfully used swiss cohort to show vaccination of Tick borne encephalitis was successful and due to which cross-reactive antibodies were formed in the subjects we were given to study. (upes.ac.in)

To study the antibody response to Zika and another flavivirus, Esswein and Bjorkman looked at several antibodies from the blood of patients from Mexico and Brazil. (news-medical.net)

Antibody-dependent enhancement (ADE), sometimes less precisely called immune enhancement or disease enhancement, is a phenomenon in which binding of a virus to suboptimal antibodies enhances its entry into host cells, followed by its replication. (wikipedia.org)
This phenomenon is referred to as "Antibody Dependent Enhancement" (ADE) or simply "Immune Enhancement", and was proposed early in the 1960s by Dr. Scott Halstead. (tigs.res.in)
Antibody dependent enhancement is a phenomenon observed in flaviviruses esp. (upes.ac.in)

As demonstrated in Table 3, there was no significant correlation between days of symptom onset to collection of serum and antibody index/ratio to suggest waning of antibodies during the time period tested. (researchgate.net)
Based on our "know-how", a 3-in-1 dengue test (Dengue Day 1) has been developed by an Indian company for simultaneous point-of-care detection of Dengue NS1 Antigen & differential detection of IgM & IgG antibodies in Human Serum/ Plasma. (icgeb.org)
The type and screen are the first pretransfusion compatibility tests performed and are used to identify the patient's ABO group and Rh type and to detect expected and unexpected antibodies in the patient's serum, respectively. (medscape.com)
It serves 2 purposes: (1) to serve as a final check of ABO compatibility between donor RBCs (RBCs) and patient plasma or serum and (2) to detect clinically significant antibodies that may have been missed by the antibody screening test. (medscape.com)
In an antiglobulin crossmatch performed using the column agglutination system, the donor RBCs, suspended in a hypotonic buffered saline solution, are mixed with the recipient's serum or plasma to allow antigen-antibody interaction in the upper chamber of the microtube. (medscape.com)
The antibody in the recipient's serum or plasma is detected when the sensitized donor RBCs react with the anti-immunoglobulin G (IgG) in the microtube during centrifugation. (medscape.com)

In dot blots, we could successfully detect rabbit IgG against firefly luciferases, Limpet Haemocyanin, and SARS-CoV-2 Nucleoprotein (1-250 ng), as well as the antigen bound antibodies using either CCD imaging , and even photography using smartphones . (chagghana.org)
Antiviral activities of antibodies may either be dependent only on interactions between the antibody and cognate antigen, as in binding and neutralization of an infectious virion, or instead may require interactions between antibody-antigen immune complexes and immunoproteins or Fc receptor expressing immune effector cells. (frontiersin.org)
The Fc receptor-dependent function of antibody-dependent cellular phagocytosis (ADCP) provides mechanisms for clearance of virus and virus-infected cells, as well as for stimulation of downstream adaptive immune responses by facilitating antigen presentation, or by stimulating the secretion of inflammatory mediators. (frontiersin.org)
Fc receptor-dependent antibody functions are also involved in activation of downstream adaptive immune responses by facilitating antigen presentation or by stimulating the secretion of inflammatory mediators ( 12 , 13 ). (frontiersin.org)
According to the concept of RNA-based injections, the antigen (here, the spike protein of SARS-CoV-2) is synthesized by our cells and presented at the cell surfaces, where it serves as a target for the generation of neutralizing antibodies. (newstarget.com)

It is conceivable to me that the laser-beam specificity of the induced antibodies is offset by a general weakening of innate immunity," Seneff said. (lifesitenews.com)
One of the major defence arms (humoral immunity) of the body comprises of special proteins called antibodies or immunoglobulins. (tigs.res.in)
The first SARS-CoV-2 vaccine(s) will likely be licensed based on neutralizing antibodies in Phase 2 trials, but there are significant concerns about using antibody response in coronavirus infections as a sole metric of protective immunity. (nih.gov)

After interaction with a virus, the antibodies bind Fc receptors (FcR) expressed on certain immune cells or complement proteins. (wikipedia.org)
Evidence strongly suggests the body may produce a second round of antibodies that mistakenly attack healthy cells or bind to ACE2 receptors, leading to heart rate fluctuations and blood pressure issues. (expose-news.com)
In this review, we discuss the properties of Fc receptors, antibodies, and effector cells that influence ADCP. (frontiersin.org)

Indeed, it is unclear whether antibody production is protective or pathogenic in coronavirus infections. (nih.gov)
Antibodies can exert their protective functions via a multitude of mechanisms. (frontiersin.org)
Previous studies have shown the envelope domain III is an important target of protective antibodies that fight flavivirus infections. (news-medical.net)

Enhancement of antibody-dependent cellular cytotoxicity is associated with treatment response to extracorporeal photopheresis in Sézary syndrome. (chuv.ch)

The donor unit is deemed incompatible for transfusion, and the antibody responsible for the reaction should be identified. (medscape.com)

With a linear mixed model, neutralizing antibody titer was shown to peak between week 5 and week 8 after onset and to decline thereafter, with a half-life of 6.4 weeks. (cdc.gov)

Unlike skin, which is also a primary defence mechanism that can defend us against all kinds of pathogens, antibodies are specifically produced against a given epitope and hence are specific to a particular pathogen, more like a lock and key. (tigs.res.in)
Instead, these antibodies act as a 'Trojan horse,' allowing the pathogen to get into cells and exacerbate the immune response. (deepcapture.com)
To protect against these and other pathogens, 'we have the ability to make a huge diversity of antibodies, and if we get infected or vaccinated, those antibodies recognize the pathogen,' Esswein said. (news-medical.net)

ADE allows endocytosis of virus-antibody complexes into the host's immune cells, which include macrophages, causing a weakening of the immune system. (newstarget.com)

Fc receptor-dependent antibody functions are important components of the immune response that provide mechanisms for clearance of infected host cells, immune complexes, or opsonized pathogens. (frontiersin.org)

Antibody response plays a crucial role during viral infections. (tigs.res.in)
Antibodies can neutralize viral infections in a number of ways. (tigs.res.in)
That hijacking, called antibody-dependent enhancement, happens in viral infections that are similar to COVID-19, like SARS and MERS, as well as Zika and Dengue. (rochester.edu)

Essentially, the virus "deceives" the process of phagocytosis of immune cells and uses the host's antibodies as a Trojan horse. (wikipedia.org)

In this study, we demonstrated proofs-of-concept for a technology that uses microfluidics and molecular genomics to capture diverse mammalian antibody repertoires as multivalent recombinant drugs. (biorxiv.org)
These "recombinant hyperimmune" drugs comprised thousands to tens of thousands of antibodies and were derived from convalescent human donors, or vaccinated human donors or immunized mice. (biorxiv.org)
We also validated a recombinant hyperimmune for Zika virus disease that abrogates antibody-dependent enhancement (ADE) through Fc engineering. (biorxiv.org)

Some anti-GPCR antibodies exist on the market, but the success rate of development is still poor compared with antibodies targeting soluble or peripherally anchored proteins. (awljournal.org)

and antibody-dependent enhancement of pathology and clinical severity has been described. (nih.gov)

Antibodies may form in response to these antigens, resulting in destruction of donor red blood cells (RBCs), with sequelae leading to clinical manifestations of fever, hypotension, rigors, acute respiratory failure, and acute renal failure. (medscape.com)

Immunoassays are widely used for detection of antibodies against specific antigens in diagnosis, as well as in electrophoretic techniques such as Western Blotting. (chagghana.org)

This is especially important for flaviviruses, because antibodies that protect against one flavivirus may also stick to, but not protect against other flavivirus, increasing the risk of ADE. (news-medical.net)

FcγRs bind antibodies via their fragment crystallizable region (Fc). (wikipedia.org)
ADE is induced in the presence of either 'non-neutralizing' antibodies, which are able to bind to viral particles but not able to cause their destruction, or 'sub-neutralizing' antibodies, which are present in insufficient numbers. (tigs.res.in)
The worry has been that if antibodies are generated to this viral "spike protein" after it has had a chance to bind to human cells (post-fusion conformation), that this would give a better chance for non-neutralizing antibodies to arise (and thus provide a better chance for unwanted inflammation of ADE to develop). (educatetruth.com)

Antibody therapies could be a bridge to a coronavirus vaccine - but will the world benefit? (natureasia.com)
The ability to detect antibodies to severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is currently under investigation with various performance characteristics and indications for use. (researchgate.net)

Given the high rate of occurrence of adverse effects that have been reported to date, as well as the potential for vaccine-driven disease enhancement, Th2-immunopathology, autoimmunity, and immune evasion, there is a need for a better understanding of the benefits and risks of mass vaccination, particularly in groups excluded from clinical trials. (researchgate.net)
This is important because some of the earlier attempts at a SARS vaccine (back in 2002-2004) showed ADE effects (antibody-dependent enhancement with increased immune-mediated inflammation and lung damage following vaccination) in mouse models. (educatetruth.com)

It might also tell us whether SARS-CoV-2 can hijack antibodies - which usually help you fight off viruses - to instead help it infect more of your cells and make you sicker. (rochester.edu)

In addition, antibody detection may provide a complementary perspective, along with RT-qPCR testing, in the diagnosis of COVID-19 (24,25). (researchgate.net)

Patients with a longer illness showed a lower neutralizing antibody response than patients with a shorter illness duration (p = 0.008). (cdc.gov)
However, it has been previously shown that more severe disease produces a stronger antibody response, and thus our mild disease cohort may result in a lower sensitivity (26). (researchgate.net)
These Fc receptor-dependent antibody functions provide a direct link between the innate and adaptive immune systems by combining the potent antiviral activity of innate effector cells with the diversity and specificity of the adaptive humoral response. (frontiersin.org)
In each sample, they will look for antibodies (a crucial part of the immune response) against the virus that causes COVID-19, called SARS-CoV-2, as well as related coronaviruses that cause the common cold, and the SARS-Cov-1 virus that emerged in 2003. (rochester.edu)
There is a concern that antibodies generated in response to a Zika virus vaccine could trigger ADE if someone were to be later infected with dengue or other flaviviruses. (news-medical.net)
Their insights into the antibodies involved in this immune response will help inform vaccine design strategy. (news-medical.net)
The characteristics of this response would include production of neutralizing antibodies, generation of a T-cell response, and avoidance of immune-enhanced disease4. (who.int)

To gain a better insight into the humoral responses in the context of epidemiologic and clinical settings, we analyzed the neutralizing antibody data, along with a variety of epidemiologic elements in the database. (cdc.gov)

Shannon Esswein, a graduate student, and Pamela Bjorkman, a professor, at the California Institute of Technology, have new insights on how the body's antibodies attach to the Zika virus. (news-medical.net)
The researchers studied how those antibodies changed over time as they mature and become better able to stick to the Zika virus, and also how the antibodies cross-react with other flaviviruses, including the four types of dengue viruses. (news-medical.net)
They found that the Zika antibodies also tightly stick to and defend against dengue type 1, and weakly stick to West Nile and dengue types 2 and 4. (news-medical.net)
They also determined structures showing how two antibodies recognize Zika and West Nile envelope domain III. (news-medical.net)
2020) Structural basis for Zika envelope domain III recognition by a germline version of a recurrent neutralizing antibody. (news-medical.net)

Using the Taiwan nationwide laboratory-confirmed severe acute respiratory syndrome (SARS) database, we analyzed neutralizing antibody in relation to clinical outcomes. (cdc.gov)
Plasma-derived polyclonal antibodies are polyvalent drugs used for many important clinical indications that require modulation of multiple drug targets simultaneously, including emerging infectious disease and transplantation. (biorxiv.org)

Conclusions Very few healthcare providers had IgG antibodies to SARS-CoV-2, though a significant proportion of them had been infected with the virus. (researchgate.net)
This is also the reason for the emphasis on detecting neutralizing antibody titers along the way as well since a high proportion of neutralizing antibodies is a safeguard against the antibody-driven enhancement of disease. (educatetruth.com)

On top of thar, interferon promotes antibodies-immunoglobulins production of various classes within Vimmunity system and plasma cells activation [6]. (pharmcourse.com)

These are the sort of figures you would expect to see if a vaccine was causing Vaccine-Associated Enhanced Disease and antibody-dependent enhancement, and it turns out the latest round of confidential Pfizer documents confirm that both Pfizer and the US Food & Drug Administration knew it was a possibility upon emergency approval of the mRNA jab. (expose-news.com)

The virus, which is loosely bound to the antibody, penetrates into a macrophage, replicates and multiplies in it. (pharmcourse.com)

Antibodies are a key component of the human adaptive immune system, and the elicitation of antibodies has been correlated with vaccine efficacy in many diseases ( 1 ). (frontiersin.org)

In order to prevent ADE when creating a vaccine, it's crucial for scientists to have a detailed understanding of how antibodies stick to a specific virus. (news-medical.net)

Due to these reasons, ADE has been a serious concern in the field of antibody-based drug therapy and vaccine design. (tigs.res.in)

To find antibodies that recognize flaviviruses, they used a piece of the outside of the virus, called the envelope domain III protein. (news-medical.net)

However, almost two years later, the authorities have quietly decided to begin an investigation into Covid-19 vaccine induced Acquired Immunodeficiency Syndrome and Antibody-Dependent Enhancement after scientists around the world, including many from Harvard and Yale, were forced to admit a debilitating suite of problems have been appearing hours, days or weeks after a Covid-19 vaccine has been administered. (expose-news.com)

Antibody memories are stored in special cells called memory B-cells that can last for decades. (tigs.res.in)
Called antibody-dependent enhancement (ADE), this happens when the antibodies stick to the outside of the virus without blocking its ability to infect cells, which can inadvertently help the virus infect more cells by allowing it to enter cells that the antibodies stick to. (news-medical.net)

Further testing is unnecessary if no antibodies are identified with the immediate spin phase. (medscape.com)

The current pipeline for antibody development primarily screens for overall affinity rather than functional epitope recognition. (awljournal.org)
We developed a new strategy utilizing natural ligand affinity to generate a library of antibody variants with an inherent bias toward the active site of the GPCR. (awljournal.org)

Anatomy1

Chemicals and Drugs3

Phenomena and Processes4

In vitro antibody-dependent enhancement assays are insensitive indicators of in vivo vaccine enhancement of equine infectious anemia virus. (1/83)

Infection of human cells by dengue virus is modulated by different cell types and viral strains. (2/83)

Specific ablation of antiviral gene expression in macrophages by antibody-dependent enhancement of Ross River virus infection. (3/83)

Infectivity-enhancing antibodies to Ebola virus glycoprotein. (4/83)

Enhancement of adenovirus vector entry into CD70-positive B-cell Lines by using a bispecific CD70-adenovirus fiber antibody. (5/83)

Antibody-dependent enhancement of coxsackievirus B4 infectivity of human peripheral blood mononuclear cells results in increased interferon-alpha synthesis. (6/83)

Enhancement of coxsackievirus B3 infection by antibody to a different coxsackievirus strain. (7/83)

Complement-mediated enhancement of antibody function for neutralization of pseudotype virus containing hepatitis C virus E2 chimeric glycoprotein. (8/83)

No images available that match "antibody dependent enhancement"

Antibody-Dependent Enhancement

Antibody-Dependent Cell Cytotoxicity

Antibodies, Monoclonal

Antibodies

Immunoglobulin G

Killer Cells, Natural

Cytotoxicity, Immunologic

Antibody Specificity

In vitro antibody-dependent enhancement assays are insensitive indicators of in vivo vaccine enhancement of equine infectious anemia virus. (1/83)

Infection of human cells by dengue virus is modulated by different cell types and viral strains. (2/83)

Specific ablation of antiviral gene expression in macrophages by antibody-dependent enhancement of Ross River virus infection. (3/83)

Infectivity-enhancing antibodies to Ebola virus glycoprotein. (4/83)

Enhancement of adenovirus vector entry into CD70-positive B-cell Lines by using a bispecific CD70-adenovirus fiber antibody. (5/83)

Antibody-dependent enhancement of coxsackievirus B4 infectivity of human peripheral blood mononuclear cells results in increased interferon-alpha synthesis. (6/83)

Enhancement of coxsackievirus B3 infection by antibody to a different coxsackievirus strain. (7/83)

Complement-mediated enhancement of antibody function for neutralization of pseudotype virus containing hepatitis C virus E2 chimeric glycoprotein. (8/83)

Infection23

Monoclonal antibodies2

Epitopes3

20211

Dengue virus1

Serotype1

Vaccines2

Antiviral antibodies1

Roles of antibodies1

Cross-reactive1

Several antibodies1

Phenomenon3

Serum6

Antigen5

Immunity3

Receptors3

Protective3

Cytotoxicity1

Reaction1

Titer1

Pathogen3

Macrophages1

Pathogens1

Viral infections3

Host's1

Recombinant3

Proteins1

Severity1

Respiratory failure1

Antigens1

Flavivirus1

Bind3

Coronavirus2

Vaccination2

Sicker1

Detection1

Response7

Responses1

Zika5

Clinical2

Proportion2

Plasma1

MRNA1

Bound1

Adaptive1

Crucial1

Concern1

Recognize1

Scientists1

Cells2

Phase1

Affinity2

No images available that match "antibody dependent enhancement"