Appeared in Spring/Summer 1996, Vol. XXII, Nos. 1, 2

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I. Introduction

Recent developments in vaccine technology, and biotechnology in general, have advanced a new version of abortion under the semblance of birth control. Funded by various international agencies (particularly the World Health Organization), research over the past 20 years is coming close to the development and marketing of several types of vaccine technology whose sole purpose is to terminate a pregnancy (i.e.induce an abortion). Abortifacient vaccines (also termed antifertility vaccines, or contragestational vaccines) are defined as vaccines that act to sensitize the maternal immune system to terminate a pregnancy either by blocking a mechanism of pregnancy (i.e. human chorionic gonadotropin) or by the immune system attacking and killing the embryo (usually prior to nidation). The end result is a very early stage first trimester abortion.

This paper explores abortifacient vaccine technology and the repercussions on abortion, the vaccine recipient, and the pro-life movement. This paper strongly urges that the Church and the pro-life movement prepare clear teachings on the evils of this technology, the resultant abortion effects, and the health hazards involved with this technology.


II. Types of Abortifacient Vaccines

A. Human Chorionic Gonadotropin (HCG) Vaccine

Several variations of the abortifacient vaccine are under development: the hCG vaccine and the TBA vaccine.

The first generation vaccine research led by Dr. Vernon C. Stevenslat Ohio State University and by Dr. G.P. Talwar2at the National Institute of Immunology, New Delhi, India, have brought closer the dawn of a new form of abortion.

Since the 1970’s, under support from the World Health Organization (WHO), research has been directed at immunologically blocking conception or the immunological termination of a pregnancy. One key target has been the hormone, human Chorionic Gonadotropin (hCG). This hormone created by the developing embryo signals the maintenance of the corpus luteum which provides progesterone and estrogen to maintain the vascularization of the uterine endometrium during the first few months of pregnancy. Should hCG levels drop in the first critical 6 to 10 weeks, the uterine vascularization would break down resulting in the death of the developing embryo while the uterine endometrium sloughs off the uterine wall. HCG is similar in structure and chemistry to other glycosylated peptide hormones   (e.g.Thyroid Stimulating Hormone (TSH), Luteinizing Hormone (LH),and Follicle Stimulating Hormone (FSH)); beingcomposed of two glycosylated peptide chains (alpha and beta). While the hCG alpha chain is nearly identical to other glycosylated peptide hormones, the hCG beta chain is more distinct biochemically.

Early studies to develop a vaccine against hCG were hampered by immunogenic cross reactivity with FSH, TSH, or LH, due to nearly identical alpha peptide chain sequences. Research focused on the hCG beta chain, but it shares 85 per cent sequence commonality for the first 110 amino acids with LH. Therefore, the focus shifted to the last 35 amino acid sequence of hCG which is sufficiently different from LH. This subunit of the hCG beta chain, now referred to as the hCG beta peptide fragment, has served as the focal immunogen in the development of a hCG vaccine. Further versions have included linking the hCG beta peptide fragment to various carrier molecules (e.g.tetanus or diphtheria toxoids) to enhance immune responses to the hCG peptide.

Recent research has begun to bear fruit at various facilities across the globe. Phase II studies for the Stevens vaccine are still in progress,3but Talwar’s group reports4that early Phase II studies indicate that sexually active women sustained high antibody titers to hCG and were prevented from getting pregnant.


World Health Orginization

No major side effects were reported in either the Phase 15 or early Phase II trials.6 Furthermore, Phase I trials detected no significant changes in the peptide or steroid endocrine parameters.7Presumably, the high levels of antibodies acted to remove hCG molecules from the blood. This would cause any developing embryo to fail uterine implantation (AKA nidation) and pass out during menstruation.

As no disruption of the ovulatory cycle or menstrual cycle was reported, it could be presumed that the embryo passed from the Fallopian tube into the uterus and never achieved complete endometrial implantation. Stevens reports that it is possible that the vaccine might not merely encourage humoral (antibodybased) immunity, but may cause cellular (lymphocyte-based) immunity. Since the trophoblast layer of the embryo produces and secretes hCG, Stevens states that it is possible that sensitized lymphocytes may attack and destroy the trophoblastic cells of the peri- implantation blastocyst (embryo).

Talwar and Stevens’ work suggests that this vaccine could last beyond the initial six months that Phase I studies describe. Further improvements in the vaccine, including those based on monkey trials which used delayed release biodegradable microspheres to achieve active immunization lasting 2 years,8indicate that a long lasting hCG