How vaccines work ?

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A query of minds, this ppt focus on how vaccines induces protective response with help of B cell & T cell. The slides giving notes and detail r hidden

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  • The articles and short videos below show why vaccines do not protect and do cause damage and death to the vaccinated some are physiologically expressed as in Autism, ADD, ADHD, MS, SIDS, Guillain-Barre syndrome (GBS), Allergies and autoimmune diseases and others hidden beneath the surface by ways of creating a weaker immune system. Read the articles so you will understand that what is written in this power point is very incomplete and erroneous.
    It is very important to understand the immune system before you decide to bypass natures and GOD's natural defenses, the mucosa of the lungs, throat and nose, the stomach, and the skin with an assault on the immune system and body with untested chemicals, neurotoxins, DNA from caterpillars, DNA from dog Kidneys, DNA from aborted fetus tissue, additional contaminating viruses, live viruses that shed for up to 28 days causing others to become ill, protein from peanuts that are used as an excipient plays a major role in contributing to the serious peanut allergy epidemic in America and much, much more for you to learn and be aware of before you can say that you are fully informed.

    First of all, vaccine damage and death is much more common than 1:1,000,000 as you are told.
    A. http://articles.mercola.com/sites/articles/archive/2014/04/26/vaccines-adverse-reaction.aspx
    B. An article in JAMA estimated that 1:4000 will experience an adverse reaction, a lot more than the one in a million that is quoted or written.
    Reference: JAMA, June 19, 1999 vol. 281, no.21, pg.2132
    C. How Vaccines Harm Child Brain Development - Dr Russell Blaylock MD (neurosurgeon, researcher)
    http://www.youtube.com/watch?v=7QBcMYqlaDs#t=417 88 minutes
    D. How the studies that doctors site as evidence are skewed (lied about) in the pharmaceuticals favor and how vitamin D3 is much more effective against the Flu and Influenza like illness (ILI) than the Flu vaccine.
    http://www.youtube.com/watch?v=h-3yrrgkcLY&feature=youtube 8 minutes
    I go into 3 other ways that the pharmaceuticals twist and distort the truth in my power point below.

    It is very important to understand how the immune system works and why vaccines do not protect us and that the reasons for the massive decline of disease is due to sanitation, improved nutrition, clean drinking water, and washing hands. All these that we take for granted in the modern world the third world countries do not have and is the reason why disease persists on a larger scale. The billions we spend on vaccination will be much better served in sanitation, clean drinking water and food sustainability like culturing spirulina as is being done in Africa https://www.youtube.com/watch?v=CxSA5iiGgiY
    A. http://www.vaccinationcouncil.org/2011/06/10/basics-of-the-human-immune-system-prior-to-introduction-of-vaccines-are-vaccines-turning-our-children%E2%80%99s-immune-systems-inside-out/
    B. http://www.vaccinationcouncil.org/2011/06/21/risks-damage-basics-of-the-human-immune-system-prior-to-introduction-of-vaccines-are-vaccines-turning-our-childrens-immune-systems-inside-out-part-2/
    C. http://pathwaystofamilywellness.org/Informed-Choice/how-do-vaccines-work-immune-mechanisms-and-consequences.html
    D. http://www.vaccineriskawareness.com/Your-Immune-System-How-It-Works-And-How-Vaccines-Damage-It


    The 3 driving forces of vaccination are listed below with fear as a common denominator to vaccinate.

    1. The belief that polio and smallpox were eradicated is a major force in peoples belief system to subject themselves to vaccine damage and death. Listen to Dr.Suzanne Humphries presentation on
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  • Polio and how it was never eradicated but the diagnostics was changed with the stroke of a pen and was reclassified as transverse myelitis (which there are over 1,000 cases every year just of this one disease) and many other diseases. The horrible photos of the iron lung were replaced with the modern day ventilator and the ECMO http://www.dellchildrens.net/services_and_programs/ecmo/what_is_ecmo/how_does_ecmo The ventilator and ECMO do not stand out as much as the iron lung but they perform the same function, to aid the Pt (Patient) in breathing or to breath for the Pt.
    A. http://www.vaccinationcouncil.org/2013/02/15/dr-suzanne-humphries-discusses-vaccines-and-polio-video/
    B. Purchase “Dissolving Illusions, Disease,, Vaccination and the Forgotten History” 2013, for the most accurate history on vaccination by Dr. Suzanne Humphries. Great details on the history of Polio and other diseases and the lies that are the foundation of vaccination.
    http://www.vaccinationcouncil.org/books-and-media/
    C. Jabs, Jenner and Juggernauts: a Look at Vaccination By Jennifer Craig
    The lies behind small pox and Edward Jenners work
    http://www.vaccinationcouncil.org/books-and-media/
    D. Jenner and Vaccination: A Strange Chapter of Medical History By Charles Creighton
    http://www.vaccinationcouncil.org/books-and-media/

    2. The second driving force of vaccination is the myth of herd immunity and it is morally and ethically wrong not to vaccinate because of others weakened immune system. Herd immunity is only achieved by a community acquiring the disease naturally and passing on the antibodies in breast milk. Benefits are a lifelong immunity and a stronger immune system, two benefits that can not be achieved with vaccination.
    A. http://www.vaccinationcouncil.org/2012/07/05/herd-immunity-the-flawed-science-and-failures-of-mass-vaccination-suzanne-humphries-md-3/
    B. http://www.vaccinationcouncil.org/2012/02/18/the-deadly-impossibility-of-herd-immunity-through-vaccination-by-dr-russell-blaylock/

    3. The third driving force is the belief that vaccines will prevent the disease the Pt was vaccinated against.
    Short videos and articles of outbreaks within the the vaccinated (not protected as advertised) and caused by the vaccinated.
    A. http://experimentalvaccines.org/2014/03/31/new-york-measles-outbreak-90-vaccinated/
    B. http://experimentalvaccines.org/2014/04/03/ohio-mumps-outbreak-97-vaccinated/
    C. http://experimentalvaccines.org/2014/03/25/mumps-outbreak-involves-highly-vaccinated-students/
    D. http://experimentalvaccines.org/2014/01/31/cfr-council-on-fake-realities-vaccine-created-outbreaks-map/
    E. http://experimentalvaccines.org/2014/04/04/fda-vaccine-insert-lists-autism-as-adverse-reaction/
    F. http://experimentalvaccines.org/2013/10/09/91-fully-vaccinated-involved-in-pertussis-outbreak/

    G, 17 more vaccine failures
    http://vactruth.com/2013/02/23/17-examples-of-vaccine-failure/

    H. http://www.collective-evolution.com/2014/04/23/measles-outbreak-traced-to-fully-vaccinated-patient-for-first-time/

    After over 1,000 hours of research on my own I was compelled to create a source of factual information for those who want to learn more about the who, what, where, why and how of vaccination
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  • and become fully informed with a purpose to encourage independent research and critical thinking and not parrot what someone has heard all of their lives.
    A. I have many recommended books, DVD's, Documentaries and websites that you can learn from in my power point
    http://www.slideshare.net/db61/exposing-the-myth-of-vaccination-essential-information-you-need-to-know-to-be-fully-informed-30978670?qid=144d3297-fe17-4eb8-bd7d-d92656e9c477&v=default&b=&from_search=1
    B. A great place to start is at this website composed of physicians, read the articles and listen to their presentations
    http://www.vaccinationcouncil.org/start-here-2/
    C. Recommended Books and media
    http://www.vaccinationcouncil.org/books-and-media/

    D. Dr. Sherrie Tenpenny's Vaccine Research Library is a one-of-a-kind collection of over 6,000 medical and scientific studies revealing truth about vaccine dangers. The information has been amassed by sifting through tens of thousands of medical abstracts and full text articles hosted in Pubmed, Scholar, Quertle, Biomed Central and more. Complex information has been extracted from scientific journals such as Nature and Science, and from releases by the CDC, FDA, NIH, HHS, and Pharmcast. The evidence has been examined and categorized. The Vaccine Research Library is a no-nonsense, sobering collection of the actual clinical studies and papers telling “The Other Side of the Story.”
    http://tenpennyimc.com/2012/03/04/announcing-the-vaccine-research-library/
    D. Conflicts of interest. This is just the tip of the ice burg on this subject.
    http://www.cbsnews.com/news/how-independent-are-vaccine-defenders/
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  • Well presented, Dr Vikram.Thanks.
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  • My topic is Immunology – How Vaccines Work ? Immunology of Vaccination ?
  • So we will discuss how do vaccines work? Which are the main effectors of vaccine responses? We will also see how Vaccine responses are elicited ,supported, maintained and reactivated by vaccine antigens
  • Innate immunity comes into play within hours of the entry of an infective agent. The components of the innate immune system comprise of epithelial and mucosal barriers, the antibacterial chemicals in these barriers, phagocytes (neutrophils, macrophages and NK cells) as well as complement. It is not very specific as it is trigerred by structures shared by different microbes instead of specific microbial antigens. There is no immune memory. It plays a very important role as it is the first line of defense. It also is the effector pathway of adaptive immunity.   Adaptive immunity is trigerred by antigen presentation by the cells of the innate immune system. It takes time to develop. The two arms of adaptive immunity humoral immunity ( B lymphocyte mediated) and cell mediated immunity (T lymphocyte mediated). It has intense diversity and is capable of responding to millions of antigens and possesses immune memory. Innate immunity comes into play within hours of the entry of an infective agent. The components of the innate immune system comprise of epithelial and mucosal barriers, the antibacterial chemicals in these barriers, phagocytes (neutrophils, macrophages and NK cells) as well as complement. It is not very specific as it is trigerred by structures shared by different microbes instead of specific microbial antigens. There is no immune memory. It plays a very important role as it is the first line of defense. It also is the effector pathway of adaptive immunity.   Adaptive immunity is trigerred by antigen presentation by the cells of the innate immune system. It takes time to develop. The two arms of adaptive immunity humoral immunity ( B lymphocyte mediated) and cell mediated immunity (T lymphocyte mediated). It has intense diversity and is capable of responding to millions of antigens and possesses immune memory.   Innate and adaptive immunity are interlinked. The immune response to microbes stimulates the adaptive response and the adaptive response strengthens the innate immune response. Some of the effecter pathways of the adaptive immune response are components of the innate response eg complement. Characteristics Innate immunity Adaptive immunity Onset Immediate (hrs) Delayed (days) Specificity Structures shared by groups of microbes Microbial and non microbial antigens Diversity Limited Very large Memory None Yes Components Skin and epithelia Complement Neutrophils, macrophages, NK cells Lymphocytes Antibodies
  • Most of the currently available vaccines provide protection through induction of B cells and production of antigen-specific antibodies . This is known as humoral immunity. Antibodies either neutralize the antigen or promote opsonophagocytosis which results in early reduction of pathogen load and clearance of extracellular pathogens. Another way vaccine provides protection is by induction of T cells which is known as cell mediated immunity.The role of cell mediated immunity in currently used vaccines (that have T cell dependent antigens) is mainly by supporting antibody protection. Other less common mechanisms by which cell mediated immunity works is by are cytotoxic CD8+ T lymphocytes* (CTL) that may limit the spread of infectious agents by recognizing and killing infected cells or secreting specific antiviral cytokines. Cellular immunity is essential for clearance of intracellular pathogens. BCG is the only currently used human vaccine for which there is conclusive evidence that T cells are the main effectors. However, there is indirect evidence that vaccine-induced T cells contribute to the protection conferred by other vaccines. Example is that of measles immunization in 6- month-old infants. These infants fail to raise antibody responses because of immune immaturity and/or the residual presence of inhibitory maternal antibodies, but generate significant IFN-γ producing CD4+ T cells.These children remain susceptible to measles infection, but are protected against severe disease and death, presumably because of the viral clearance capacity of their vaccine-induced T cell effectors. Thus, prevention of infection may only be achieved by vaccine-induced antibodies, whereas disease attenuation and protection against complications may be supported by T cells even in the absence of specific antibodies .
  • Following injection (1), the vaccine antigens attract local and systemic dendritic cells, monocytes and neutrophils (2). These activated monocytes and dendritic cells (3) change their surface receptors and migrate along lymphatic vessels (4), to the draining lymph nodes (5) where the activation of T and B lymphocytes will take place.
  • So in case of deltoid injection draining lymphnodes will be axillary group and in case of quadriceps it will be inguinal group of lymph nodes.
  • There is no microbial replication at site of injection in case of non-live vaccines so vaccine-induced activation of dendritic cells (DC’s) remains more limited, both in time and space. This limited activation has the following implications The immunogenicity of non live vaccines is limited as compared to live vaccines. Site and route of administration is important. Route of administration for non-live vaccines is decided by number of DCs in the tissue. DCs are numerous in the well-vascularized muscles, which is the preferred route of injection for most vaccines. DCs are fewer in adipose tissues, such that subcutaneous injections may be less effective than intramuscular injections under conditions of limited immunogenicity, such as for adult immunization against hepatitis B. Dendritic cells are in highest number in the skin – this allows a marked reduction (e.g. 10 fold) of the antigen dose in intradermal immunization, an advantage that is applied to the prevention of rabies in many countries. Simultaneous administration of several distinct vaccines may take place without immune interference if vaccines are administered at sites draining into distinct lymph node areas.
  • Conversely live vaccines replicate, disseminate and activate dendritic cells at multiple sites, which migrate towards the corresponding draining lymph nodes and launch multiple foci of T and B cell activation. This widespread activation has the following implications Higher immunogenicity of live versus non-live vaccines . Site and route of injection of live viral vaccines are of minor importance: for example, the immunogenicity and reactogenicity of measles vaccine is similar following intramuscular or subcutaneous injection. Immune interference may occur unless they are given on the same day or if the routes of administration are different (eg OPV with other live vaccines)
  • Now we will see what are the vaccine responses to polysaccharide antigens. This antigen released from the injection site essentially reach the marginal zone of the spleen / lymph nodes.
  • B cells use their specific Ig surface receptors to bind to the repetitive structures of polysaccharides.
  • In the absence of antigen-specific T cell help, B cells are activated, proliferate and differentiate in plasma cells without undergoing affinity maturation in germinal centers.
  • These plasma cells migrate towards the red pulp of the spleen where they survive for a few weeks / months, secreting low levels of low affinity IgM, IgG or IgA antibodies.
  • As PS antigens do not induce germinal centres, bona fide memory B cells are not elicited. Consequently, subsequent re-exposure to the same PS results into a repeat primary response that follows the same kinetics in previously vaccinated as in naïve individuals. Revaccination with certain bacterial PS - of which group C meningococcus is a prototype - may even induce lower antibody responses than the first immunization, a phenomenon referred to as hyporesponsiveness and whose molecular and cellular basis is not yet fully understood.
  • In response to a protein antigen reaching lymph nodes or spleen. Extrafollicular reaction is same as in case of PS antigen , B cells rapidly differentiate in plasma cells that produce low-affinity antibodies (of the IgM +/- IgG/IgA isotypes) that appear at low levels in the serum within a few days after immunization . DC: dendritic cells APC: antigen presenting cells
  • Antigen-specific helper T cells that have been activated by antigen-bearing dendritic cells trigger some antigen-specific B cells to migrate towards follicular dendritic cells (FDCs) , initiating the germinal center (GC) reaction.
  • In GCs, B cells receive additional signals from follicular T cells (Tfh) and undergo massive clonal proliferation, switch from IgM towards IgG, IgA or IgE, undergo affinity maturation and differentiate into plasma cells secreting large amounts of antigen-specific antibodies.
  • Most of the plasma cells die at the end of germinal centre reaction and thus a decline in antibody production and thus decline in antibody levels is noted 4-8 weeks after vaccination.
  • However a few plasma cells exit nodes/spleen and migrate to survival niches mostly located in the bone marrow, where they survive through signals provided by supporting stromal cells. This results in prolonged production of antibodies and persistence of antibodies in the serum.
  • Memory B cells are generated in response to T-dependent antigens, during the GC reaction, in parallel to plasma cells. At their exit of GCs, these B cells do not differentiate into antibody secreting plasma cells but in memory B cells that transiently migrate through the blood towards the extrafollicular areas of spleen and nodes. They persist there as resting cells until re exposed to their specific antigens. Upon secondary antigen exposure, memory B cells readily proliferate and differentiate into plasma cells secreting large amounts of high-affinity antibodies that may be detected in the serum within a few days after boosting.
  • All protein containing vaccines (T cell dependent vaccines) whether live or non live induce immunologic memory. Non protein containing vaccines (T cell independent vaccines) do not induce memory as explained earlier.
  • Vaccine type o Live vs inactivated- Higher intensity of innate responses, higher antigen content following replication and more prolonged antigen persistence generally result into higher Ab responses to live than inactivated vaccines. o Protein vs polysaccharide Recruitment of T cell help and induction of GCs results into higher Ab responses to protein or glycoconjugate than to PS vaccines o Adjuvants Modulation of antigen delivery and persistence (depot or slow-release formulations) or enhancement of Th responses (immunomodulator) may support or limit Ab response 􀂃Antigen dose. As a rule, higher Ag doses increase the availability of Ag for B / T cell binding and activation, as well as for association with FDCs. 􀂃 Vaccine schedule o Interval between doses A 4 week minimal interval between primary doses avoids competition between successive waves of primary responses. 􀂃 Genetic determinants. 􀂃 Environmental factors. Mostly yet identified. 􀂃 Age at immunization. Early life immune immaturity or age-associated immune senescence.
  • Nature of vaccine plays a crucial role: only live attenuated viral vaccines induce antibody responses that persist for several decades, if not life long in absence of subsequent antigen exposure and reactivation of immune memory. Shortest response are seen with PS vaccines. Vaccine Schedules: Closely spaced (1-2 Weeks) primary vaccine doses may be administered when a rapid induction of protection is desirable e.g. prior to travel,However for better persistence of responses 1-2 months interval is required between primary doses. Antibody responses are shorter at two extremes of ages. Certain disease conditions also modify vaccine responses like malaria .
  • Memory B cells do not produce antibodies unless re-exposed to antigen which drives their differentiation in to antibody producing plasma cells. Read from the slide.
  • When the second exposure with the similar antigen occurs at a short interval from the first dose, it triggers off a second wave of primary response rather than a true boosting response. Due to this the antibody levels attained are not very high.
  • When the second antigenic exposure after a long interval between two doses ( 4 months) then an exuberant booster response is elicited. This is due to affinity maturation of B cells that results in high levels of antibodies of high affinity.
  • Since vaccination induces immunological memory the vaccination schedule need not be started all over again. Only the remaining doses need to be given. For live viral vaccines, they should be either given on the same day or after 4 weeks to prevent immunologic interference. Exceptions are BCG and measles/ MMR should not be given on the same day as measles depresses CMI that interferes with uptake of BCG. OPV may be given at any interval from any live vaccine because the route of administration is different
  • So what are the strategies to overcome these shortcomings during early infancy? We give more doses or give vaccine at later age? It is not possible to give vaccine late as most of these diseases occur at early age. We give more doses of vaccines in comparision to adults and older children. Age for starting vaccination and time interval depends on disease epidemiology.
  • How vaccines work ?

    1. 1. How Vaccines Work ? Dr. Vikram GuptaImmunology ofVaccination
    2. 2. How Vaccines Work? Dr. Vikram Gupta Assistant Professor, Department of Community Medicine,Dayanand Medical College & Hospital, Ludhiana dr_vikramgupta@yahoo.co.in
    3. 3. Agenda• How do vaccines work? Which are the main effectors of vaccine responses?• How Vaccine responses are elicited, supported, maintained and/or reactivated by vaccine antigens
    4. 4. Innate and Adaptive immunity
    5. 5. First steps after immunization
    6. 6. • So in case of deltoid injection draining lymphnodes will be axillary group and in case of quadriceps it will be inguinal group of lymph nodes.
    7. 7. Non-live vaccines• No microbial replication at site of injection so vaccine- induced activation of dendritic cells (DC’s) is limited, both in time and space.• Immunogenicity of non live vaccines is limited• Site and route of administration is important• Simultaneous administration of several distinct vaccines may take place without immune interference.• DCs are numerous in the well-vascularized muscles, which is the preferred route of injection for most vaccines.• Dendritic cells are in highest number in the skin – this allows a marked reduction (e.g. 10 fold) of the antigen dose in intradermal immunization, an advantage that is applied to the prevention of rabies in many countries.
    8. 8. Live vaccines• Replicate, disseminate and activate dendritic cells at multiple sites launching multiple foci of T and B cell activation• Immunogenicity of live vaccines is higher• Site and route of administration is unimportant• Simultaneous administration- Immune interference may occur unless they are given on the same day or if the routes of administration are different (eg OPV with other live vaccines
    9. 9. • These plasma cells migrate towards the red pulp of the spleen where they survive for a few weeks / months, secreting low levels of low affinity IgM, IgG or IgA antibodies.• As PS (polysachharide) antigens do not induce germinal centres, bona fide memory B cells are not elicited. Consequently, subsequent re-exposure to the same PS results into a repeat primary response that follows the same kinetics in previously vaccinated as in naïve individuals.• Revaccination with certain bacterial PS - of which group C meningococcus is a prototype - may even induce lower antibody responses than the first immunization, a phenomenon referred to as hyporesponsiveness and whose molecular and cellular basis is not yet fully understood.
    10. 10. What affects primary vaccine antibody responses?• Vaccine types: Live vs inactivated , Protein vs PS, Adjuvants• Antigen dose: Higher the dose-higher primary response.• Vaccine Schedule: 4 weeks minimum interval between primary doses avoids interference• Genetic, Environmental factors , Age
    11. 11. What controls persistence of Vaccine antibody responses?• Nature of vaccine- only live vaccine induces long lasting antibody resonse, shortest response by PS antigens• Vaccine schedules- Interval between primary doses, Interval before boosting• Age at immunization -shorter at two extremes of age• Disease conditions
    12. 12. Hallmarks of B cell memory responses?• Memory B cells do not protect• Reactivation occurs in response to natural boosters by pathogens or booster immunization• On reactivation antibodies appear in blood very rapidly (4-7 days) as proliferation and differentiation occurs without requiring development of Germinal center• Antibodies are of markedly higher affinity ( they can be only induced when sufficient time has passed after priming)
    13. 13. Immune Memory – implications for immunization programs• Immunization schedule should never be started “all over again” regardless of duration of interruption• Regular boosters are not required to maintain immune memory during low risk periods (Travellers)• Certain immunization schedules may not need boosters if exposure provides regular natural boosters• Booster may not be needed where reactivation of immune memory by offending pathogen is sufficiently rapid and effective to interrupt microbial invasion (Hep B)
    14. 14. Vaccine catch-up rules1. Count the number of vaccine doses that are necessary for protection – separately for each antigen2. Substract doses received = missing doses !3. Do not give more doses than an unimmunized child would receive !4. Choose the optimal intervals between missing doses • Baseline rule : 0 – 1 – 6 months (i.e. 6 month interval) • All missing vaccines may be given on the same day – at distant sites (>2.5cm) ! • All missing vaccines may be given at any interval (days, weeks) … •Except 2 live viral vaccines : 0 or 4 weeks (…)
    15. 15. • Since vaccination induces immunological memory the vaccination schedule need not be started all over again. Only the remaining doses need to be given.• For live viral vaccines, they should be either given on the same day or after 4 weeks to prevent immunologic interference. Exceptions are1.BCG and measles/ MMR should not be given on the same day as measles depresses CMI that interferes with uptake of BCG.2.OPV may be given at any interval from any live vaccine because the route of administration is different
    16. 16. Young Age Immunization1. Young age limits antibody responses to most vaccine antigens: Why ?• Maternal antibodies inhibits antibodies responses but not T-Cell response• Limitation of B cell responses2. Induction of B memory cells is not limited3. Antibody responses elicited in early life are short lasting
    17. 17. Strategies• So what are the strategies to overcome these shortcomings during early infancy?• We give more doses or give vaccine at later age?• It is not possible to give vaccine late as most of these diseases occur at early age.• We give more doses of vaccines in comparison to adults and older children.• Age for starting vaccination and time interval depends on disease epidemiology.
    18. 18. Acknowledgement• This presentation is based on Science of Vaccinology Module of IAP and Advac Course .• International Vaccine Conference was held, by IAP at New Delhi in November 2008 and slides were part of resource material.Reference:1. Siegrist CA : Vaccine Immunology . In:Vaccines.5th edition .Elsevier.2007 ,2,20-34.
    19. 19. THANX….

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