Antibodies Are Not Required For Immunity

It is very important to understand that when the scientific community and the MSM talk about antibodies, they are speaking about particles never proven to exist. Like “viruses,” antibodies have never been purified/isolated directly from humans nor have they been EM imaged from completely purified samples where these tiny proteins are separated from everything else. They are assumed to be 10 nm in size which is much smaller than most “viruses.” For comparison, “SARS-COV-2” is said to range anywhere from 50 to 200 nm. Indirect methods such as complement fixation, neutralization assays, immunoprecipitation assays, ELISA tests, etc. are chemical reactions used to “detect” the unseen antibodies in order to claim these particles are present yet there are no methods of direct detection. Contrary to the claims, there is zero direct evidence as to whether or not these particles exist.

It is also uncertain as to what their form and function truly are. This is because antibodies are entirely theoretical. These assumed particles have been given form and function without ever being directly observed. In fact, over the many decades that these particles were “studied,” numerous theories developed attempting to explain what antibodies are, what they do, how they look, how they are created, etc. Technically, these unseen proteins have many different proposed forms and functions. These theories can be broken down as such:

  1. Instructive Theories
    a. Direct Template Theory
    b. Indirect Template Theory
  2. Selective Theories
    a. Natural Selection Theory
    b. Side Chain Theory
    c. Clonal Selection Theory
    d. Immune Network Theory

That is quite a few competing theories for something spoken about today as if it has any actual significance or meaning.

Perhaps this is why we see quotes such as this in articles currently discussing antibodies:

Why do we develop lifelong immunity to some diseases, but not others?

“Scientists still aren’t sure why we maintain our antibody responses longer for some diseases compared with others. It’s possible that some of these more common diseases, such as chickenpox and mono, actually are reinfecting us more frequently than we realize, but that the antibodies we do have crush the infection before we notice, Jenkins said. And in those cases, the immune system would be at full capacity again and again because of the reinfections. “It keeps our immunity vigilant,” he noted. In contrast, “with tetanus, we’re probably very rarely getting exposed, we’re not stepping on a [dirty] nail very often.”

Other scientists point out that the human immune system is trained to target pathogens that “look” a certain way, Slifka said. Bacteria and viruses tend to be symmetrical with a repetitive pattern of proteins across their surfaces. (Think about COVID-19 — it’s a ball with evenly spaced spikes all over it.) One theory suggests that we mount a larger and longer-lasting immune response to more repetitive-looking pathogens. For example, the antibodies we produce against variola, the highly repetitively-structured smallpox virus, last a lifetime. Tetanus, however, isn’t repetitive at all. It’s the toxin produced by tetanus bacteria, not the bacteria itself, that makes us sick. Based on this theory, it’s possible that our bodies aren’t as well-trained to target this single, asymmetrical protein, Slifka said.”

https://www.livescience.com/why-lifelong-immunity.html

Obviously, it’s very hard to understand theoretical concepts when they require other theories in order to attempt to explain them. It is also difficult to gain an understanding when studies come out which completely contradict the existing theories. This happened in 2012 when the results of a study researching VSV infection in mice turned the theory that antibodies are required for survival and immunity from “viruses” completely upside down by showing that antibodies are, in fact, not required at all.

Knowing what we know about the lack of proof regarding these unseen hypothetical/theoretical particles, it shouldn’t come as any surprise that results such as these eventually came about. It is very similar to what Merrill Chase “dicovered” in 1942 when his findings broke immunity into the Innate (Cellular) system and the Adaptive (Antibody) system. However, whereas Chase theorized that antibodies still played a role in survival/immunity, newer findings are showing that this is not the case. Here are some excerpts from the ScienceDaily press release on these findings from 2012:

Antibodies are not required for immunity against some viruses

“A new study turns the well established theory that antibodies are required for antiviral immunity upside down and reveals that an unexpected partnership between the specific and non-specific divisions of the immune system is critical for fighting some types of viral infections. The research may lead to a new understanding of the best way to help protect those exposed to potentially lethal viruses, such as the rabies virus.”

“The research team studied VSV infection in mice that had B cells but did not produce antibodies. Unexpectedly, although the B cells themselves were essential, survival after VSV exposure did not require antibodies or other aspects of traditional adaptive immunity. “We determined that the B cells produced a chemical needed to maintain innate immune cells called macrophages. The macrophages produced type I interferons, which were required to prevent fatal VSV invasion,” says co-author Dr. Matteo Iannacone.

Taken together, the results show that the essential role of B cells against VSV does not require adaptive mechanisms, but is instead directly linked with the innate immune system. “Our findings contradict the current view that antibodies are absolutely required to survive infection with viruses like VSV, and establish an unexpected function for B cells as custodians of macrophages in antiviral immunity,” concludes Dr. von Andrian. “It will be important to further dissect the role of antibodies and interferons in immunity against similar viruses that attack the nervous system, such as rabies, West Nile virus, and Encephalitis.”

https://www.sciencedaily.com/releases/2012/03/120301143426.htm

Essentially what the researchers did was study mice that had B cells but could not produce antibodies. These mice survived challenges of VSV “virus” by subcutaneous injection. The results not only showed that antibodies are not required for survival, they also showed that B cells are not producers of antibodies as originally proposed. Below are highlights from this 2012 study:

B Cell Maintenance of Subcapsular Sinus Macrophages Protects against a Fatal Viral Infection Independent of Adaptive Immunity

SUMMARY

“Neutralizing antibodies have been thought to be required for protection against acutely cytopathic viruses, such as the neurotropic vesicular stomatitis virus (VSV). Utilizing mice that possess B cells but lack antibodies, we show here that survival upon subcutaneous (s.c.) VSV challenge was independent of neutralizing antibody production or cell-mediated adaptive immunity. However, B cells were absolutely required to provide lymphotoxin (LT) α1β2, which maintained a protective subcapsular sinus (SCS) macrophage phenotype within virus draining lymph nodes (LNs). Macrophages within the SCS of B cell-deficient LNs, or of mice that lack LTα1β2 selectively in B cells, displayed an aberrant phenotype, failed to replicate VSV, and therefore did not produce type I interferons, which were required to prevent fatal VSV invasion of intranodal nerves. Thus, although B cells are essential for survival during VSV infection, their contribution involves the provision of innate differentiation and maintenance signals to macrophages, rather than adaptive immune mechanisms.

INTRODUCTION

Adaptive immunity, especially neutralizing antibody production, is thought to play a critical role in controlling cytopathic viral infections in mammals (Hangartner et al., 2006). However, external barrier breach by rapidly replicating viruses can place a host at risk long before adaptive immune components can be mobilized. Indeed, mice infected with VSV, an acutely cytopathic neurotropic rhabdovirus, can suffer fatal neuroinvasion despite high neutralizing antibody titers (Iannacone et al., 2010). This observation led us to revisit the contribution of humoral immune responses to survival after VSV infection.

Intravenous (i.v.) infection of mice with VSV elicits neutralizing T cell-independent IgM and T cell-dependent IgG responses that become detectable by days 4 and 7 postinfection, respectively (Bachmann et al., 19941996Charan and Zinkernagel, 1986Karrer et al., 1997Thomsen et al., 1997). Because B cell-deficient or CD4+ T cell-deficient mice die after i.v. VSV infection, it had been thought that neutralizing T cell-dependent antibodies were absolutely required for survival (Bründler et al., 1996).”

“We have shown recently that the susceptibility to VSV neuro-invasion upon LN macrophage depletion has a fatal outcome in ~60% of infected mice, with both dying and surviving animals producing similar neutralizing antibody titers (Iannacone et al., 2010). Thus, humoral immunity was apparently not sufficient for most individuals’ survival of s.c. VSV infection, although it remained possible that antibodies afforded viral clearance in the surviving ~40% of mice. To clarify the role of B cells and antibodies and to re-examine the requirements for protection against VSV, we undertook the present study. By utilizing animals that selectively lack antibodies but retain B cells, we found that neither humoral nor cell-mediated adaptive immunity were required for protection against VSV.”

RESULTS

Antibodies, but Not B Cells, Are Dispensable for Protection against Subcutaneous VSV Infection

Previous studies have shown that B cell-deficient mice are highly susceptible to acutely cytopathic viruses, including VSV (Bachmann et al., 1995Bründler et al., 1996Gobet et al., 1988Hangartner et al., 2006). Although this finding was interpreted as evidence that antibodies are absolutely required, it must be considered that B cell-deficient mice not only lack antibodies but also display abnormal lymphoid architecture (Kitamura et al., 1991). Therefore, we sought to re-evaluate the relative contribution of antibody-dependent and -independent functions of B cells to protective immunity against VSV. We took advantage of a recently generated mouse strain, DHLMP2A, in which the JH segment of the IgH locus was replaced by the Epstein-Barr virus-derived LMP2A protein (Casola et al., 2004). Because LMP2A provides tonic survival signals, B cells develop without a B cell receptor; therefore, DHLMP2A mice retain B cells and normal lymphoid tissue architecture, yet are devoid of surface-expressed and secreted antibodies.

Consistent with previous studies (Bründler et al., 1996), B cell-deficient (μMT) mice died within 10 days of i.v. infection, whereas WT mice survived the viral challenge (Figure 1A). DHLMP2A mice were also susceptible to death after i.v. VSV infection, with a clinical course and mortality rate that were indistinguishable from those of μMT mice (Figure 1A). However, when mice were challenged s.c. (the natural transmission route for arboviruses, such as VSV [Mead et al., 1999]), ~60% of μMT mice died after developing ascending paralysis. In contrast, DHLMP2A mice, like WT mice, were protected (Figure 1B), even though (as expected) they were incapable of mounting a neutralizing antibody response to VSV (Figure 1C).”

“Although our results after i.v. viral challenge support an antibody requirement for survival of acutely cytopathic viral infection (Bachmann et al., 1997Bründler et al., 1996), our findings in the s.c. infection model are not compatible with this antibody-centric paradigm. Rather, our findings in DHLMP2A mice imply that B cells may have an additional innate role in antiviral immunity that must be antibody independent.”

Adaptive Immunity Is Dispensable during Primary Subcutaneous VSV Infection

“Most macrophage-depleted WT mice died when challenged s.c. with VSV even though they possessed neutralizing antibody titers that were much higher than in macrophage-sufficient animals (Iannacone et al., 2010). In fact, antibody titers were indistinguishable between macrophage-depleted WT mice that succumbed to VSV infection and those that remained asymptomatic (Figure S4C). Although the mechanism by which CLL-induced macrophage depletion leads to increased antibody titers in this model remains to be determined, these data, together with our findings in DHLMP2A mice, firmly establish that antibodies are neither required nor sufficient for survival of a primary s.c. infection with VSV.

This observation raised the question whether adaptive immunity mediated by other lymphocytes is required for protection against peripheral VSV infection. Indeed, both T cells (Kündig et al., 1996Zinkernagel et al., 1978) and a subset of Thy1+ natural killer cells (Paust et al., 2010) can mount virus-specific effector and memory responses against VSV. To address this question, DHLMP2A mice were depleted of these adaptive lymphocytes by administration of Thy1 antibodies, which resulted in greater than 95% loss of circulating T cells (Figures S4D and S4E). Remarkably, despite the complete lack of both humoral and cellular adaptive immunity, all anti-Thy1-treated DHLMP2A mice survived VSV infection (Figure 7B). This indicates that the innate immune system, particularly the presence of fully differentiated SCS macrophages, provides sufficient protection to clear this acutely cytopathic viral infection without the need for adaptive immunity.

DISCUSSION

The results presented here contradict the current view that B cell-derived neutralizing antibodies are absolutely required to survive a primary cytopathic viral infection, such as that caused by VSV. This paradigm arose originally from experiments in B cell-deficient mice (Bachmann et al., 19941997Bründler et al., 1996Gobet et al., 1988), which lack antibodies, but also have abnormal lymphoid tissue architecture and altered macrophage phenotype. Our experiments in mice that lack antibodies but possess B cells and normal lymphoid tissues confirm that both B cells and antibodies are critical to survive a systemic infection after i.v. bolus administration of VSV. However, only B cells are essential when VSV is encountered via the more “natural” s.c. route, whereas antibodies are neither needed nor sufficient for protection. Our data collectively indicate that immunity to s.c. VSV infection relies on B cell-derived LTα1β2, rendering SCS macrophages capable of replicating VSV and producing neuroprotective IFN-I.

Although VSV infections are typically self-limiting in mammals, rabies virus, a close relative, is responsible for >55,000 human deaths every year. Neutralizing antibodies are also believed to be required to survive rabies infections, as shown by the fact that passive antibody transfer and active vaccination to elicit humoral immunity are standard of care. Although neutralizing antibodies are undoubtedly effective prophylaxis against rhabdoviruses, our findings indicate that antibody therapy may be insufficient to treat existing rhabdoviral infections in nonimmune subjects, at least in the case of VSV. It is unclear whether this caveat applies also to rabies virus infection, but failures of both passive and active vaccination after exposure to rabies are known to occur (Anonymous, 1988). Thus, it will be important to further dissect the role of antibodies and interferon in this disease. In addition, recent years have seen the emergence and/or spread of other arthropod-borne neurotropic viral infections, such as West Nile virus, Japanese encephalitis virus, and Eastern and Western equine encephalitis virus, to name a few (Weaver and Barrett, 2004). It remains to be determined whether the cellular and molecular immunological events that occur upon inoculation of these pathogens in the skin are similar to the ones identified here.”

In contrast to the likely benefit of adaptive immunity during reinfection, our results demonstrate that during a primary s.c. infection, recognition of viral epitopes by either antibody or TCR is neither necessary nor sufficient to prevent fatal VSV neuroinvasion. This observation runs counter to the commonly held view that during viral infections, innate immunity must orchestrate the induction of antiviral adaptive responses to achieve sterilizing immunity. Given the rapid replication of some viruses, a proliferating pathogen may overwhelm its host before adaptive immune countermeasures can be mobilized. Innate defenses like complement, type I interferon, and others are believed to provide stopgap measures, lowering pathogen burden and buying time for adaptive immune responses to develop. Although this concept may apply to other viral infections, our findings with VSV turn this view upside down, indicating that during a primary infection with this cytopathic virus, innate immunity can be sterilizing without adaptive immune contributions. 

In summary, we demonstrate that naive mice can survive a s.c. VSV challenge without requiring antigen-specific adaptive immunity. Efficient protection against VSV is provided by SCS macrophages in the draining LNs that rely on contact with follicular B cells expressing LTα1β2 on their surface. The constant exposure to LTα1β2 induces and maintains the protective SCS macrophage phenotype. Consequently, SCS macrophages in B cell-deficient mice or in mice that lack B cell-expressed LTα1β2 display an altered phenotype that resembles that of medullary macrophages, which are not protective in VSV infection. Like medullary macrophages, SCS macrophages that are deprived of LTα1β2 capture lymph-borne VSV but fail to replicate it. Without replication, SCS macrophages do not produce IFN-I that is required to prevent VSV invasion of intranodal nerves. These findings establish a critical innate function for B cells in antiviral immunity. This setting requires B cells not as a source of antibodies, but as providers of an anatomically restricted maintenance signal and as the day-to-day custodians of macrophage differentiation.”

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3359130/

The 2012 findings that antibodies are not required for immunity were later backed up in a different study from 2016 involving the Dengue “virus.” In this case, researchers showed that antibodies injected into mice did not confer any protection whatsoever to the naive mice. The researchers point to other vaccination studies which also failed to show protective abilities from induced antibodies in high titers. Highlights from this paper below:

Antibodies are not required to a protective immune response against dengue virus elicited in a mouse encephalitis model

“Generating neutralizing antibodies have been considered a prerequisite to control dengue virus (DENV) infection. However, T lymphocytes have also been shown to be important in a protective immune state. In order to investigate the contribution of both humoral and cellular immune responses in DENV immunity, we used an experimental model in which a non-lethal DENV2 strain (ACS46) is used to intracranially prime Balb/C mice which develop protective immunity against a lethal DENV2 strain (JHA1). Primed mice generated envelope-specific antibodies and CD8+ T cell responses targeting mainly non-structural proteins. Immune sera from protected mice did not confer passive protection to naïve mice challenged with the JHA1 strain.”

“Severity of symptoms displayed by a DENV infection is highly associated with viremia titers (Horstick et al., 2015Murgue et al., 2000Vaughn et al., 2000). Historically, antibodies capable of preventing virus of infecting susceptible cells have been thought to represent the main and, perhaps, the sole protection correlate (Guzman and Harris, 2014Guzman et al., 2010SABIN, 1952Whitehead et al., 2007). Such antibodies were extensively demonstrated to be capable of preventing infection of the host cells in vitro (Blaney et al., 2005Chiang et al., 2012Guzman et al., 2010Roehrig et al., 2008Whitehead et al., 2007Zhang et al., 2007), either by blocking the binding step of viral particles or by preventing conformational changes in the protein required for membranes fusion in endosome (Teoh et al., 2012), or by inducing a structural disruption of the viral envelope (Cockburn et al., 2012Lok et al., 2008Pierson and Kuhn, 2012). This rational was reinforced by reports of in vivo protection mediated by neutralizing antibodies in non-human primate model (Guirakhoo et al., 2004Guirakhoo et al., 2001Guirakhoo et al., 2000Guy et al., 2010), and was adopted in the development of presently tested anti-dengue vaccine formulations which are based on chimeric or live-attenuated viruses which induce neutralizing antibodies to the four serotypes of DENV (Whitehead et al., 2007). In particular, chimeric live attenuated viruses between DENV and yellow fever virus (YFV) were constructed with the aim of inducing high titers of neutralizing antibodies against DENV envelope proteins (Guirakhoo et al., 2001). In clinical trials considerable titers of neutralizing antibodies were induced in vaccinees volunteers (Sabchareon et al., 2012Villar et al., 2014). Unfortunately, especially for DENV2, the vaccine formulation based on those chimeric viruses did not achieve the expected protective efficacy in a phase III clinical trials in different parts of the world (Sabchareon et al., 2012Villar et al., 2014).

“In this study we used a mouse encephalitis model to further evaluate the contribution of antibodies and T cells on the generation of a protective immunological status for DENV infection. Based on two different DENV2 strains: the ACS46, unable to cause any harm to mice, and the neurovirulent JHA1 strain, capable to cause encephalitis and kill immunocompetent adult mice; we observed that Balb/C mice intracranially inoculated with ACS46 developed a protective immunity to a subsequent, otherwise lethal, challenge with the JHA1 strain. We found that antibodies generated in mice inoculated with the ACS46 strain, although capable of neutralizing the virus in vitro, were not capable to confer passive protection in the encephalitis model. In contrast, depletion of CD4+ and CD8+ T lymphocytes drastically reduced the protection of ACS46-inoculated mice challenged with the neurovirulent DENV2 strain. Collectively, our results clearly show that cellular immune responses, particularly those targeting non-structural proteins, are specifically involved in the control of DENV infection in the mouse encephalitis model.”

Contribution of humoral and cellular immune responses in the protective immunity elicited in Balb/C mice inoculated with the ACS46 DENV2 strain

“Aiming to access the specific contribution of the humoral immune response to the protection induced by the ACS46 strain, we carried out in vivo serum transfer experiments. First, envelope-specific IgG titers were determined by ELISA in both serum and brain macerate from mice which were protected from the lethal challenge with the JHA1 strain. We found that envelope-specific antibodies were not present in brain macerate but only in sera (Fig. 4A). Thus, sera from protected mice were administered to naive mice in one, two or three doses. The transfer regimen with three doses resulted in in vivo envelope-specific IgG titers statistically indistinguishable from those found in donor animals (Fig. 4B). Although sera from protected mice showed a minimum PRNT50 titer of 1:40, we observed that its transfer in one, two or three doses did not confer neither protection from nor exacerbation of infection under a lethal challenge with 100 PFU of the JHA1 strain (Fig. 4C). The lethality curves of animals treated with antibodies from mock or ACS46-primed mice were indistinguishable.

On the other hand, IFN-γ-secreting CD8+ T lymphocytes specific to NS1, NS3H and NS5 DENV2 proteins were significantly increased in ACS46-primed mice (Fig. 5A and B). Moreover, when CD4+, CD8+ or both populations of T lymphocytes were depleted from ACS46-primed mice the protective immunity was significantly reduced or completely abrogated (Figs. 5C and 6). These results indicate that anti-envelope antibodies induced in the mouse encephalitis model do not contribute to protection, but T lymphocytes specific responses, particularly those for non-structural proteins, play major roles in controlling virus replication and prevention of encephalitis.”

Antibodies may not protect because they do not exist.

Discussion

A very large number of people are infected by any of the DENV serotypes per year and a significant portion of them develop severe forms of dengue. Despite the significant epidemiological effect of this disease, there is not an effective anti-DENV vaccine formulation approved for use in humans. Relevantly, an important vaccine formulation designed to induce generation of neutralizing antibodies did not achieve the expected protective efficacy in a phase III clinical trial, especially against serotype 2 (Sabchareon et al., 2012Villar et al., 2014). In other words, the correlate of protection proposed seven decades ago for DENV infection seems to be incomplete, and the need to reformulate it is clear. In this study we found antibodies generated in a protective immunity induced in a Balb/C encephalitis model are not capable to control in vivo encephalitis caused by DENV2. However, CD4+ and CD8+ T lymphocytes are crucial in our experimental model. In addition, CD8+/IFN+ T lymphocytes targeting non-structural proteins are present in significantly increased levels in animals capable to control infection and play major roles in controlling encephalitis. Together, results presented in this study show that antibodies are not capable alone to establish protective immunity to DENV2 in the Balb/C mouse encephalitis model.”

Another study has investigated the role of humoral versus cellular responses induced by a protective anti-DENV vaccine (Zellweger et al., 2013). In this study the humoral component by itself was shown to be unable to control the infection of immune deficient mice (AG129) with a DENV2 strain after intravenous administration. On the other hand, and in contrast to our results, only cellular immune responses involving CD8+ T cells were shown to be required for the reduction of viral load (Zellweger et al., 2013). In humans, both CD8+ and CD4+ T cell populations have been shown to contribute to the control of DENV infection (Weiskopf et al., 2015bWeiskopf et al., 2015a). Specifically for CD4+ T cells cytotoxic functions have been associated with the protective immunity state (Weiskopf et al., 2015b). As we showed in this study using an immunocompetent mouse model based on DENV-induced encephalitis, CD4+ and CD8+ T cells, mainly those targeting non-structural proteins, are crucial in the control of DENV infection. Even though this experimental infection model does not resemble the context of the infection seen in humans, it represents another clear evidence that the control of DENV infection requires the involvement of T cell responses, particularly to non-structural proteins. Results presented in this study further reinforce the need to reevaluate the role of antibodies as the unique parameter involved in DENV infection. Also, our results show that the use of only DENV envelope proteins as vaccine targets does not seem to be the best strategy for vaccine development. Such conclusion might be considered in the context of the recombinant chimeric vaccine presently being tested at different countries.”

“Notably, these two subsets of T lymphocytes were shown to control infection without requirement of antibodies, which again recall data generated with i.m. immunization, in which envelope-specific antibodies are not capable to control encephalitis. Thus, the protective immune response observed in our model and headed by T lymphocytes does not seem to require the triggering of viral envelope antigens, at least with regard to induction of antibody responses. In conclusion, results presented in this study further support the view that activation of T cells targeting non-structural proteins represents a promising way to follow in the search of an effective vaccine against dengue.”

https://www.sciencedirect.com/science/article/pii/S004268221500433X

In Summary:

  • Antibodies are unseen and unproven particles explained by numerous theories:
    1. Instructive Theories
      • a. Direct Template Theory
      • b. Indirect Template Theory
    2. Selective Theories
      • a. Natural Selection Theory
      • b. Side Chain Theory
      • c. Clonal Selection Theory
      • d. Immune Network Theory
  • Scientists still aren’t sure why we maintain antibody responses longer for some diseases compared with others
  • One theory suggests that we mount a larger and longer-lasting immune response to more repetitive-looking pathogens
  • Based on this theory, it’s possible that our bodies aren’t as well-trained to target single, asymmetrical proteins
  • A 2012 study turned the well established theory that antibodies are required for antiviral immunity upside down
  • The research team studied VSV infection in mice that had B cells but did not produce antibodies
  • Survival after VSV exposure did not require antibodies or other aspects of traditional adaptive immunity
  • “Our findings contradict the current view that antibodies are absolutely required to survive infection with viruses like VSV, and establish an unexpected function for B cells as custodians of macrophages in antiviral immunity,” concluded Dr. von Andrian
  • Neutralizing antibodies have been thought to be required for protection against acutely cytopathic “viruses”
  • Utilizing mice that possess B cells but lack antibodies, the researchers showed that survival upon subcutaneous (s.c.) VSV challenge was independent of neutralizing antibody production or cell-mediated adaptive immunity
  • Mice infected with VSV, an acutely cytopathic neurotropic “rhabdovirus,” can suffer fatal neuroinvasion despite high neutralizing antibody titers
  • Dying and surviving animals produced similar neutralizing antibody titers
  • Humoral immunity was apparently not sufficient for most individuals’ survival of s.c. VSV infection
  • They found that neither humoral nor cell-mediated adaptive immunity were required for protection against VSV
  • Previous studies have shown that B cell-deficient mice are highly susceptible to acutely cytopathic “viruses,” including VSV
  • Although this finding was interpreted as evidence that antibodies are absolutely required, it must be considered that B cell-deficient mice not only lack antibodies but also display abnormal lymphoid architecture
  • DHLMP2A mice challenged with “virus,” like WT mice, were protected even though (as expected) they were incapable of mounting a neutralizing antibody response to VSV
  • Although they state that their results after i.v. “viral” challenge support an antibody requirement for survival of acutely cytopathic “viral” infection, their findings in the s.c. infection model are not compatible with this antibody-centric paradigm
  • Most macrophage-depleted WT mice died when challenged s.c. with VSV even though they possessed neutralizing antibody titers that were much higher than in macrophage-sufficient animals
  • Antibody titers were indistinguishable between macrophage-depleted WT mice that succumbed to VSV infection and those that remained asymptomatic
  • They state that their findings firmly establish that antibodies are neither required nor sufficient for survival of a primary s.c. infection with VSV
  • Despite the complete lack of both humoral and cellular adaptive immunity, all anti-Thy1-treated DHLMP2A mice survived VSV infection
  • This indicated that the innate immune system provided sufficient protection to clear this acutely cytopathic “viral” infection without the need for adaptive (i.e. antibody) immunity
  • The results presented here contradict the current view that B cell-derived neutralizing antibodies are absolutely required to survive a primary cytopathic “viral” infection
  • They claim only B cells are essential when VSV is encountered via the more “natural” s.c. route, whereas antibodies are neither needed nor sufficient for protection
  • Neutralizing antibodies are also believed to be required to survive rabies infections, however, their findings indicate that antibody therapy may be insufficient to treat existing rhabdoviral infections in nonimmune subjects and failures of both passive and active vaccination after exposure to rabies are known to occur
  • In contrast to the likely benefit of adaptive immunity during reinfection, their results demonstrate that during a primary s.c. infection, recognition of “viral” epitopes by either antibody or TCR is neither necessary nor sufficient to prevent fatal VSV neuroinvasion
  • This observation runs counter to the commonly held view that during “viral” infections, innate (i.e. natural) immunity must orchestrate the induction of antiviral adaptive (i.e. antibody) responses to achieve sterilizing immunity
  • Innate defenses like complement, type I interferon, and others are believed to provide stopgap measures, lowering pathogen burden and buying time for adaptive immune responses to develop
  • Although this concept may apply to other “viral” infections, their findings with VSV turn this view upside down, indicating that during a primary infection with this cytopathic “virus,” innate (natural) immunity can be sterilizing without adaptive (antibody) immune contributions
  • The researchers conclude that they demonstrated that naive mice can survive a s.c. VSV challenge without requiring antigen-specific adaptive immunity
  • These findings establish a critical innate function for B cells in “antiviral” immunity
  • This setting requires B cells not as a source of antibodies, but as providers of an anatomically restricted maintenance signal and as the day-to-day custodians of macrophage differentiation
  • Generating neutralizing antibodies have been considered a prerequisite to control dengue “virus” infection
  • Immune sera from protected mice did not confer passive protection to naïve mice challenged with the JHA1 strain
  • Historically, antibodies capable of preventing “virus” of infecting susceptible cells have been thought to represent the main and, perhaps, the sole protection correlate
  • In clinical trials considerable titers of neutralizing antibodies were induced in vaccinees volunteers yet the vaccine formulation based on those chimeric “viruses” did not achieve the expected protective efficacy in a phase III clinical trials in different parts of the world
  • The researchers found that antibodies generated in mice inoculated with the ACS46 strain, although capable of neutralizing the “virus” in vitro, were not capable to confer passive protection in the encephalitis model
  • Although sera from protected mice showed a minimum PRNT50 titer of 1:40, they observed that its transfer in one, two or three doses did not confer neither protection from nor exacerbation of infection under a lethal challenge with 100 PFU of the JHA1 strain
  • The lethality curves of animals treated with antibodies from mock or ACS46-primed mice were indistinguishable
  • These results indicate that anti-envelope antibodies induced in the mouse encephalitis model do not contribute to protection
  • An important vaccine formulation designed to induce generation of neutralizing antibodies did not achieve the expected protective efficacy in a phase III clinical trial, especially against serotype 2
  • In other words, the correlate of protection (i.e. how many antibodies are required for protection) proposed seven decades ago for DENV infection seems to be incomplete, and the need to reformulate it is clear
  • In this study the rearchers found antibodies generated in a protective immunity induced in a Balb/C encephalitis model are not capable to control in vivo encephalitis caused by DENV2
  • Results presented in this study show that antibodies are not capable alone to establish protective immunity to DENV2 in the Balb/C mouse encephalitis model
  • In a separate study, the humoral (antibody-mediated) component by itself was shown to be unable to control the infection of immune deficient mice (AG129) with a DENV2 strain after intravenous administration
  • Even though this experimental infection model does not resemble the context of the infection seen in humans, it represents another clear evidence that the control of DENV infection requires the involvement of T cell responses, particularly to non-structural proteins
  • The researchers state that the results presented in their study further reinforce the need to reevaluate the role of antibodies as the unique parameter involved in DENV infection
  • Two subsets of T lymphocytes were shown to control infection without requirement of antibodies, which again recall data generated with i.m. immunization, in which envelope-specific antibodies are not capable to control encephalitis
  • The protective immune response observed in their model and headed by T lymphocytes does not seem to require the triggering of “viral” envelope antigens, at least with regard to induction of antibody responses

These two studies show that the theoretical particles claimed to be antibodies are not a requirement for immunity nor protection. The results completely contradict the main theories regarding the function and role of antibodies in supposed immunity. Maybe the fact that these studies were unable to find a protective effect from antibodies goes a ways towards explaining how one can be considered HIV positive if antibodies are detected yet be considered “immune” if they are found as in the case of every other “virus.” Maybe it explains how having too many antibodies can be associated with an overactive immune system while too few antibodies is associated with a weakened immune system. Maybe it helps to explain why a second infection with Dengue fever is worse than the first and that the resulting antibodies are blamed for triggering life-threatening infections. Maybe it just goes to show that they truly have no idea what these unseen hypothetical/theoretical particles are, how they function, or if they even exist to begin with. One thing that is certain is that, when it comes to the theories about antibodies, they are not certain about anthing at all. When nothing is for certain, any contradicting hypothesis or theory will seem possible.

2 comments

  1. I am quite sure that proteins that protect from disease exist but antibody would be the wrong word for them. That name implies that the particles protect by attacking some invading organism (body). Being aware myself that the Germ Theory is false and viruses are a myth, and that toxins are the true cause of disease (or things that induce a toxic state in the body, e.g. malnutrition, radio waves) I would call these proteins anti-toxins instead. One example that springs to mind of an organic compound providing protection from a man-made toxin is the protection that capsaicin (the compound that provides chilli peppers with their pungency) provides to animals challenged with the emulsifier (and common vaccine ingredient) polysorbate 80 as shown in this study: https://pubmed.ncbi.nlm.nih.gov/8880377/

    …here we have a foreign compound providing an antidote-like function due to it having opposing qualities to a class of toxins — whilst emulsifiers push particles apart (keeping them in an emulsion), capsaicin makes them clump together (it promotes clotting). If a foreign compound (from a plant, even) can provide such protection, then surely our own bodies may well be able to make all sorts of anti-toxins in defense of the many toxins, man-made or otherwise that we continue to be exposed to.

    Just like Rockefeller Medicine wrongly labels exosomes as viruses, i’d say they are wrongly naming anti-toxins as anti-bodies.

    Liked by 1 person

    1. It’s definitely possible yet the structures claimed as antibodies are entirely theoretical. There is no proof of their existence nor their function. Virologists infer that these things exist through indirect chemical reactions and then create stories to explain what they think is happening and what these invisible particles do in the body. The problem lies with claiming antibodies exist (at least in the sense we are told) and that the measurement has any meaning. At this point in time, based on the evidence presented, they are purely fictional.

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