Abstract
 
          Intravenous injections of donor sperm may possibly be of
          value to AIDS patients. The immunological basis for this
          proposal is reviewed in detail. Donor sperm introduced into
          the blood of a healthy patient produces anti-sperm
          antibodies which may become attached to the T-cells and
          cause their depletion. Reintroduction of donor sperm into
          the blood of an AIDS patient may reverse the pathogenesis by
          the donor sperm combining with anti-sperm antibodies so
          allowing the T-cells to recover. HIV is just the common
          among the occupational viral infections of AIDS patients. A
          clinical trial is proposed.
 
          Primary AIDS infection
 
          The heterogenous clinical manifestations of primary AIDS
          infection reflect an immunological response. Subjects
          typically present with an illness of acute onset
          characterized by fever, lethargy, malaise, myalgias,
          headaches, retro-orbital pain, photophobia, sore throat,
          lymphadenopathy and maculopapular rash. Meningoencephalitis
          may also occur. Lymphadenopathy occurs in approximately 70%
          of people with primary AIDS infection (1). An erythematous
          maculopapular rash is common during primary HIV infection.
          The rash generally resolves within 1 week. Immunohistology
          reveals a predominantly CD4+ cell infiltrate around the
          superficial dermal vessels in the presence of a normal
          epidermal layer. These cells might present p24 antigen to
          CD4+ lymphocytes, eliciting a delayed-type hypersensitivity
          reaction (2). The lymphopenia that occurs during the first 2
          weeks of primary AIDS infection (3) affects both the CD4+
          and cd8+ subsets, and the level of CD4+ cells can be as low
          as that seen in people with AIDS (4). The interval between
          infection and development of AIDS has been estimated to have
          a median duration of approximately 10 years (5). Changes in
          the immune system mark the period before AIDS, as measured
          by laboratory markers as well as by clinical findings and
          symptoms (6).
 
          AIDS virus
 
          One of the major obstacles to understanding the pathology of
          HIV infection in humans is that we do not know precisely how
          the presence of the HIV genome in only a minority of CD4+
          T-cells leads to the gradual destruction of the immune
          system. CD4 has two identified roles on T-cells: it acts
          like an adhesion molecule in the class II-target cell
          interaction (7), and it has been proposed to have a signal
          transduction capacity in a transient complex with the T-cell
          receptor (8). The immune system of individuals infected with
          HIV is affected by loss of CD4+ cells (9) and by loss of
          T-helper-cell function (10). The loss of T-helper cell
          function is independent of the decline in CD4+ cell counts.
          The loss of such function precedes a significant reduction
          in CD4+ cells counts (11).
          Soluble CD4 proteins can bind to HIV and HIV-infected cells
          and release gp120 from free virus and virus-infected cells
          (12). Recombinant CD4-IgG fusion protein can prevent HIV
          infection in chimpanzees (13). Duesberg (14) claimed that
          AIDS virus is just the most common among the occupational
          viral infections of AIDS patients and those at risk for
          AIDS, rather than the cause of AIDS. Other viral infections
          of AIDS patients and those at risk for AIDS include
          Epstein-Barr and cytomegalovirus in 80-90% (15), and herpes
          virus in 75-100% (14). In addition, hepatitis B virus is
          found in 90% of drug addicts positive for antibody to AIDS
          virus (16). Gottlieb et al. (17), who described the first 4
          patients with AIDS in the literature, commented that they
          "acknowledge the possibility that cytomegalovirus infection
          was a result rather than a cause of the T-cell defect, and
          that some other exposure to an undetected micro-organism,
          drug, or toxin made these patients susceptible to infection
          with opportunistic organisms, including cytomegalovirus".
          Bisset (18) suggested a possible role for mycoplasma as a
          "superantigen cofactor" to the ongoing process of HIV
          infection.
 
          Sperm cells with AIDS
 
          Erlander (19) proposed that sperm cells which apparently are
          also capable of complexing with HLA-DR and CD4 receptors,
          could, under certain circumstances, such as a joint
          interaction of HIV and sperm with the same T-cells, induce
          immune reactions to HIV. Anti-sperm antibodies (an allogenic
          immunization) occurred in 19 out of 26 homosexual sperm
          recipients (2). Similar evidence for alloimmunization was
          found also in the female of a heterosexual couple who
          routinely practiced anal intercourse (20).
          Hypogonadism is present in many male patients with AIDS (21)
          and testicular atrophy has been reported as an autopsy
          finding (22). El-Demiry and James (23) examined
          immunocytochemically specimens of human testis, epididymis,
          vas deferens, prostate and seminal vesicles. They found that
          T-lymphocytes are the predominant immunological cell type in
          all these tissues. Of particular interest was the
          preponderance of suppressor-cytotoxic T-cells within the
          epithelium and lamina propria of those tissues where the
          blood-testis barrier is weak or deficient. They suggested
          that these macrophages may provide an ancillary back-up
          protection against the risk of escaped sperm antigens
          following alterations in the integrity of the blood-testis
          barrier.
          Haas et al. (24) showed that washing sperm even 18 times
          does not reduce the sperm antibody level. Using media with
          high level of serum appear to cause a drop in the sperm
          antibodies. However, the sperm antibodies are only masked
          and reappear when the spermatozoa are resuspended in
          serum-free media (25).
          Spermatozoa injected into the bloodstream tend to accumulate
          in the capillaries, eventually to be taken up by the
          reticuloendothelial system (26).
          Spermatozoa are known to be sequestered within the
          seminiferous tubules by a blood-testis barrier formed by
          tight junctions between Sertoli cells and thus prevented
          from being exposed to the immune system. Alternatively, it
          is likely that active immuno-suppression exists within the
          testes (27). Spermatozoa can penetrate somatic cells and
          fuse with their nuclei (28). Such nuclear fusion, other than
          in normal fertilization, can give rise to malignant
          transformation (29). Stein-Werblowsky (30) suggested that
          allogenic ectopic spermatozoa having gained access via anal
          fissures or lacerations of the rectal mucosa may survive in
          the vascular (portal) system and therein impinge on
          endothelial cells, eventually invading them and fusing with
          their nuclei. This may result in an endothelioma, i.e.
          Kaposi`s sarcoma.
          There is a high frequency of antibodies to seminal plasma in
          Kaposi`s sarcoma patients (31). Antibodies to spermatozoa
          and to circulating immune complexes are present in
          apparently healthy homosexuals (32). Human seminal fluid
          also contains components that potentially can suppress the
          immune response (33). Weekly deposition of pooled rabbit
          semen into the rectum in healthy male rabbits resulted in
          the appearance of immune complexes and antibodies to sperm
          and to peripheral lymphocyte antigens (34).
 
          Intravenous injections of donor sperm to AIDS patients
 
          The concept that blood transfusion might not be deleterious
          to graft outcome was proposed in the late 1960s (35). Many
          people did not at first accept the finding that blood
          transfusion actually improved renal allograft survival (36).
          In 1973, Opelz et al. (36) reported that the outcome of
          renal allografts in patients who were never blood transfused
          before transplantation was worse than that of recipients who
          had been transfused. Blood transfusion has been demonstrated
          to induce antibodies against the T-cell alloantigen-specific
          receptors, i.e. anti-idiotypic antibodies (37).
          The preparation of an antiserum against lymphoid cells was
          first described by Metchnikoff in 1899 (38). Antilymphocyte
          globulin was first used clinically in 1966 (39).
          Antilymphocyte globulin was used in vitro to remove
          T-lymphocytes from the bone marrow graft (40).
          Antilymphocyte globulin is prepared by injecting horses,
          rabbits, pigs, or goats with human lymphoid cells in the
          form of buffy coat, thoracic duct lymphocytes, thymus or
          lymphoblastoid cell lines and the polyclonal antiserum which
          results contains a variety of antibodies, some of which have
          organ-specificity, some all-specificity and some
          xeno-specificity.
          Circulating immune complexes are capable of reacting with Fc
          or complement receptors on T- and B-lymphocytes and
          macrophages and thus modulate both cellular and humoral
          immunity. Direct deposition of circulating immune complexes
          in kidneys or arteries may lead, respectively, to
          glomerulonephritis (41) or atherosclerosis (42). Spermatozoa
          and T-lymphocyte share common surface antigens (43). An
          immune response to spermatozoa may therefore lead to the
          production of antibodies that interfere with
          T-lymphocyte-mediated functions. A major mechanism of HIV
          entry into cells is by binding of the HIV envelope gp120 to
          the cell CD4 receptor (44). Soluble CD4 acts by binding HIV
          extracellularly, thereby preventing entry of HIV into CD4+
          cells (45). There is a 5-10-fold greater frequency of
          HIV-infected cells in the primary lymphoid tissues than in
          the blood (46).
 
          Conclusion
 
          Intravenous injections of donor sperm are suggested to be
          given to AIDS patients. It is proposed that the donor sperm
          introduced into the blood of an AIDS patient will attach to
          the anti-sperm antibodies existing there and attacking the
          T-cells. The donor sperm will also take off those antibodies
          from the T-cells, so allow the T-cells to recover. An
          immunological basis for the cause and cure of AIDS is
          proposed.
 
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