Acquired Immunodeficiency Syndrome, Opportunistic Infections, and Malignancies in Male Homosexuals

Sonnabend, Joseph; Witkin, Steven S.; Purtilo, David T.

doi:10.1001/jama.1983.03330410056028

Cited by 164 publications

(15 citation statements)

References 27 publications

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“…In the first year after infection, many patients develop hypergammaglobulinemia (11)(12)(13), characterized by increased levels of serum antibodies reactive with self antigens (such as T cells and nuclear determinants; foreign antigens such as trinitrophenyl (TNP)l and sheep red blood cells; and HIV viral proteins, including gp160 and p24 [14][15][16][17][18][19][20][21][22]). …”

Section: Introductionmentioning

confidence: 99%

Human immunodeficiency virus infection induces both polyclonal and virus-specific B cell activation.

Shirai¹,

Cosentino²,

et al. 1992

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Peripheral blood lymphocytes (PBL) were obtained from HIV-1-infected patients at different stages of disease. The absolute number of IgM-, IgG-, and IgA-producing lymphocytes per 106 PBL was increased 2.8-, 3.4-, and 1.9-fold, respectively, compared with normal controls. 2-17% of IgG-secreting patient cells reacted with the gpl60 envelope glycoprotein of HIV-1 (a 737-fold increase over background), while 1-9% reacted with p24 (140-fold over background). In addition to this HIV-specific B cell activation, the number of lymphocytes reactive with nonviral antigens such as DNA, myosin, actin, trinitrophenylated keyhole limpet hemocyanin, and ovalbumin was increased by a mean of 17.9-fold. Evidence suggests that the latter changes reflect an HIV-induced polyclonal B cell activation unrelated to the production of anti-HIV antibodies. For example, the proportion of IgG anti-gpl6O-and anti-p24-secreting lymphocytes declined in patients with advanced disease, whereas the number of B cells producing antibodies to non-HIV antigens rose. Moreover, CD4 cell count and T4/T8 ratio showed a significant inverse correlation with the degree of polyclonal activation but not with anti-HIV responsiveness. These observations demonstrate that both quantitative and qualitative changes in B cell activation accompany (and may be predictive of) disease progression in HIV-infected individuals. (J. Clin.

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Section: Introductionmentioning

confidence: 99%

Human immunodeficiency virus infection induces both polyclonal and virus-specific B cell activation.

Shirai¹,

Cosentino²,

et al. 1992

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“…They state further that failure of the immune system to control these viruses is "instrumental in the occurrence of some B-cell lymphomas, Kaposi's sarcoma, and squamous cell and hepatocellular carcinomas. " Sonnabend and associates [35] have made a very complete survey of this subject. They are also much impressed with the role of viruses in malignancies in AIDS and make the statement that "evidence is mounting that Kaposi's sarcoma is caused by cytomegalovirus (CMV), and that Epstein-Barr virus is responsible for the B-cell lymphomas in those patients. "…”

Section: Malignancy In Patients Immunosuppressed Following Transplantmentioning

confidence: 99%

The increase in immunosuppression and its role in the development of malignant lesions

Cole

1985

Journal of Surgical Oncology

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The first evidence that a major operation results in immunosuppression appeared in 1957. A few years later, numerous articles appeared in the medical literature showing that the same effect took place in the human being. When kidney transplantation was begun, it was soon learned that immunosuppression was necessary to obtain good results. Soon after suppression was adopted it was noted that malignancies were being encountered. The same was true with cardiac transplantation. Within the many types of immunodeficiencies, malignant lesions are significantly encountered in only one-AIDS, KEY WORDS: immunologic functions, immunoglobulins, immunosuppression immunodeficiency disease, suppressive agents and procedures, malignancy, organ transplants 1NTRODUCTION:TYPES OF IMMUNOLOGIC FUNCTIONKnowledge of our immunologic protection against cancer is increasing rapidly but is still meager. There are two types, cellular and humoral. The important cells of the immune system are lymphocytes, plasma cells, and macrophages. The most active lymphocytes are the B cells and T cells.B cells represent 12-15 % of the peripheral blood lymphocytes, 50% of the splenic lymphocytes, and perhaps 75% of the lymphocytes in the bone marrow of the normal human being [I]. The chief function of these cells is the production of antibodies. They carry immunoglobulins, perhaps the most important of which is IgM. It is thought that one lymphocyte can carry antibody for only one immunoglobulin class [4] have indicated that these are able to mediate antibodydependent cellular cytotoxicity. They are not of thymic origin and must have a receptor for the Fc portion of immunoglobulin. They are not phagocytic; their lethal effect is not dependent on complement. Rayer et al [5] have reported that killer cells are activated when incubated with "fresh peripheral blood lymphocytes in inter-*Unaware of the preparation of the issue in his honor, Dr. Cole, manifesting once again his support of the Journd of Surgicd Oncology, submitted a manuscript which arrived before we went to press. It was felt to be uniquely fitting to publish it in this special issue. -G.P.M.

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“…However, CMV is a major cause of morbidity and mortality in immunocompromised individuals such as recipients of renal or bone marrow transplants (Ho, 1977) or patients with the aquired immunodeficiency syndrome (Sonnabend et al, 1983). The foetus is also at high risk from congenital CMV infection which occurs in 0.3 ~ to 2~ of all neonates with approximately 20~ of those infected developing disease during childhood (Stagno et al, 1983).…”

Section: Introductionmentioning

confidence: 99%

Cytomegalovirus Strain AD169 Binds beta2 Microglobulin in Vitro after Release from Cells

Grundy

McKeating

Griffiths

1987

Journal of General Virology

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SUMMARYWe previously reported that a host protein, f12 microglobulin (fl2m) inhibited the detection of human cytomegalovirus (CMV) in urine specimens by enzyme immunoassay and postulated that fl2m bound to the virus particle and masked the viral antigenic determinants. We report here that CMV strain AD169 grown in cell culture bound human fl2m when this protein was added to cell culture fluids or when the virus was added to urine. Such binding was not seen with herpes simplex virus. CMV could also bind bovine fl2m from foetal calf serum in cell culture fluids. The use of radiolabelled flzm in other experiments showed that CMV bound fl2m after release from cells and that the bound fl2m did not represent acquisition of class I HLA molecules during budding from host cell membranes. Immunoprecipitation studies showed that fl2m was bound by two viral envelope proteins fl2m BP1 (fl2m-binding protein 1) and fl2m BP2 of molecular masses 36 000 and 65 000 daltons respectively, fl2mcould not bind to separated viral proteins under reducing or non-reducing conditions. We propose that interaction of these two proteins on the viral surface is required to enable CMV to bind fl2m.

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Acquired Immunodeficiency Syndrome, Opportunistic Infections, and Malignancies in Male Homosexuals

Cited by 164 publications

References 27 publications

Human immunodeficiency virus infection induces both polyclonal and virus-specific B cell activation.

Human immunodeficiency virus infection induces both polyclonal and virus-specific B cell activation.

The increase in immunosuppression and its role in the development of malignant lesions

Cytomegalovirus Strain AD169 Binds beta2 Microglobulin in Vitro after Release from Cells

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