Antigen detection in primary HIV infection

Serial blood samples were obtained from 21 homosexuals who had developed symptomatic primary infection with human immunodeficiency virus (HIV) after a median incubation time of 14 days. During the first two weeks after the onset of illness HIV antigen (p24) was detected in the blood by enzyme linked immunosorbent assay (ELISA). During the second and third weeks after the onset of illness p24 antibody was detected by Western blot assay and antigen concentrations rapidly decreased to undetectable values. Dissociation of antigen-antibody complexes showed complexed antigen during the phase of declining concentrations of free antigen. Neither free nor complexed antigen was detected in any serum samples for several months thereafter, which suggested that failure to detect HIV antigen reflected low or absent synthesis of viral protein rather than masking of antigen by antibodies. Reappearance of HIV antigen with a fall in p24 antibody concentration was observed in a few patients six months or more after the onset of disease.The combined use of antigen and antibody assays made it possible to obtain evidence of infection with HIV in all of the 95 serum samples tested, illustrating the usefulness of these assays for diagnosing infection with HIV in its early stages.     

The Vancouver Lymphadenopathy-AIDS Study: 7. Clinical and laboratory features of 87 cases of primary HIV infection.

In an ongoing prospective study of homosexual men conducted in Vancouver since November 1982, 87 cases of human immunodeficiency virus (HIV) seroconversion have been documented to date. Comparison of laboratory results obtained a mean of 4.9 months before and 5.4 months after the estimated date of seroconversion revealed that a significant increase in the serum IgG level (from 1149 to 1335 mg/dl on average) and in C1q binding (from 8.8% to 14.2% on average) was associated with early HIV infection (p less than 0.001). A marginally significant decrease in the ratio of helper to suppressor (CD4 to CD8) cells (from 1.55 to 1.29 on average) was also noted (p = 0.025). A marked decrease in absolute number of CD4 cells was not seen with seroconversion, which suggests that profound loss of these cells may be a long-term effect of HIV infection. The occurrence of symptoms (including fatigue, fever, night sweats, unintentional weight loss, diarrhea, joint pains, cough unrelated to smoking, shortness of breath, oral thrush, herpes zoster and rash) did not increase with seroconversion. This finding suggests that most cases of HIV seroconversion may be asymptomatic or associated with relatively minor symptoms. On the other hand, generalized lymphadenopathy was found to develop after HIV seroconversion in about 50% of cases.     

Extramedullary plasmacytoma presenting as a primary mass in the breast. A case report

BACKGROUND: Extramedullary plasmacytoma (EMP) of the breast is extremely rare, especially that not associated with multiple myeloma. CASE: A case of plasmacytoma of the breast in a 73-year-old man was diagnosed by fine needle aspiration cytology (FNAC). Aspiration smears revealed a dispersed population of plasmacytoid cells at various stages of maturation. The tumor was excised, and the histologic sections confirmed the cytologic diagnosis. CONCLUSION: FNAC diagnosis of plasmacytoma of the breast offers the opportunity to distinguish these neoplasms from primary mammary tumors and avoid unnecessary surgery.     

A condition for successful escape of a mutant after primary HIV infection

Cytotoxic T lymphocytes (CTLs) vigorously restrict primary human immunodeficiency virus (HIV) infection. However, the frequently erroneous process of viral replication favors the creation of mutants not recognizable by primary CTLs. Variants that tolerate the mutations may have selective advantage and may increase in abundance, until the immune system reacts against them. Therefore, such variants represent a way of propagating the viremia. With the aid of a simple mathematical model, here we estimate the intensity of CTL cross-reactivity against different strains of HIV in a typical progressor. We show that below a critical intensity of cross-reactivity, the concentration of a mutant created at primary peak grows and causes a secondary peak in viremia. Above this critical intensity, such a mutant strain is prevented from reaching a detectable level. We speculate about how this result may contribute to the design of an anti-HIV vaccine.     

Immunopathogenesis of HIV infection.

The ultimate consequence of infection with HIV is profound immunosuppression that is the result of both quantitative and qualitative abnormalities of the helper/inducer subset of T lymphocytes. The initial pathogenic event in HIV infection is binding of the envelope glycoprotein of HIV to the CD4 receptor molecule present on the surface of CD4+ T lymphocytes and monocyte/macrophages. In vivo the reservoir for HIV infection in the peripheral blood is the CD4+ T cell, whereas in other tissues the monocyte/macrophage may play a substantial role. As disease progresses in HIV-infected individuals, the viral burden in the peripheral blood CD4+ T cells increases. An understanding of the mechanisms involved in the transition from an initially low viral burden during the asymptomatic phase of HIV infection to the higher levels of virus expression detected in late stage disease is being investigated intensively. A number of potential agents that may influence regulation of HIV expression have been identified including mitogens, antigens, heterologous viruses, cytokines, and physical factors. The pathogenic mechanisms of HIV-induced neurologic abnormalities and the potential role of HIV in a number of other clinical manifestations of HIV infection are also discussed.