This article reviews current knowledge on the etiology modes of transmission immunologic aspects clinical outcome and prevention of acquired immunodeficiency syndrome (AIDS). The isolation of a human retrovirus as the etiologic agent has facilitated clearer understanding of the natural history of AIDS. Antibodies to human T-lymphotropic virus type III (HTLV-III) have been found in over 90% of AIDS patients 80-100% of those with related conditions such as unexplained persistent generalized lymphadenopathy but only 1% of people outside the defined risk groups. 4-7 weeks seems to be the latency period for the development of antibodies in cases of parenteral exposure whereas the amount of time required for seroconversion after sexual transmission is unknown. HTLV-III has been isolated from lymphocytes in peripheral blood bone marrow cells spinal fluid and brain tissue lymph nodes cell free plasma saliva semen and tears. The risk of infection seems to depend most on the route of exposure i.e. blood and blood products sexual contact parenteral drug use and prostitution perinatal transmission. Full blown AIDS is associated with the depression or aberration of most measurable cellular and humoral immune responses. Among those seropositive to HTLV-III but without clinical signs of AIDS the viral interaction with the immune system is not well understood. Even minor reductions in the rate with which HTLV-III is spread will have a large impact on the total number of infected persons a few years from now suggesting the importance of preventive education and counseling. Promiscuity and anonymous sex should be discouraged. Blood organ and sperm donors should be tested for antibodies. Screening should be offered to women in high risk groups who are considering pregnancy and those who are antibody positive should be advised not to become pregnant at least until more knowledge is available.

The natural history of human T lymphotropic virus-III infection: the cause of AIDS.

Immune status of human immunodeficiency virus seropositive and seronegative hemophiliacs infused for 3.5 years with recombinant factor VIII

Effect on lymphocyte subsets of clotting factor therapy in human immunodeficiency virus-1-negative congenital clotting disorders. The Transfusion Safety Study Group.

Stool samples of 134 subjectively and apparently healthy male homosexual volunteers were studied, and in 86 men (64.2%) 190 parasite infestations, up to 6 per host, were identified. The most frequent species were Endolimax nana (40), Entamoeba coli (38), Entamoeba histolytica (34), Entamoeba hartmanni (32), and Iodamoeba butschlii (22); Cryptosporidium was not found. All 11 isolates of Entamoeba histolytica analysed belonged to a noninvasive zymodeme: 10 were of zymodeme I and I of zymodeme III. In 172 healthy control adults 6 parasite infestations were found. In the homosexual men, a negative tuberculin test was more frequent in the presence than in the absence of parasites. Entamoeba histolytica (p = 0.005) Entamoeba coli (p = 0.013) and Iodamoeba butschlii (p = 0.004) were associated with the anergy.

Coincidence of deficient delayed hypersensitivity and intestinal protozoa in homosexual men.

Defective T Suppressor-Inducer Cell Function in Human Immune Deficiency Virus-Seropositive Hemophilia Patients

Twenty-nine heterosexual patients with hemophilia were investigated with histories, physical examinations, laboratory evaluations of immune function, delayed hypersensitivity skin tests, and assays for antibody to human T-cell lymphotropic virus type III (HTLV-III). Sixteen patients were HTLV-III antibody positive and 13 were HTLV-III antibody negative. No patient had the acquired immune deficiency syndrome (AIDS). Patients who had antibody to HTLV-III had received significantly more units and lots of factor concentrates in the preceding 5 years than those who did not have antibody. HTLV-III antibody-positive patients had significantly fewer total T cells (Leu-1 positive) and significantly fewer helper T cells (Leu-3 positive) than HTLV-III negative patients. Antibody-positive patients also had increased amounts of IgG and decreased thymidine incorporation in response to concanavalin Ain vitro. There were no differences inin vitro lymphocyte responses to phytohemagglutinin (PHA), pokeweed mitogen,Candida, tetanus, or purified protein derivative (PPD), no significant impairments of gamma interferon or interleukin-2 (IL-2) production, and no anergy. Ten patients with antibody to HTLV-III had immunologic studies repeated 1 year after the original evaluation. A significant increase was seen in suppressor (Leu-2-positive) T cells but not in total T-cell or helper T-cell numbers, helper/suppressor ratios, or T-cell functional assays. We conclude that the immune abnormalities in hemophiliacs are the result of contact with HTLV-III but that these abnormalities may remain stable over prolonged periods.

Charles H. Kirkpatrick

Papers

Altered immunity in hemophilia correlates with the presence of antibody to human T-cell lymphotropic virus type III (HTLV-III)