PubMed · 1458347
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P R Crawford. 1992. Magic disillusion.. https://pubmed.ncbi.nlm.nih.gov/1458347/
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We report the first results of a comparison between the Italian Registry on AIDS (RAIDS) and 13 population-based cancer registries (about 8 million population in 1991) with respect to the notification of Kaposi's sarcoma and non-Hodgkin's lymphoma. Routine indicators of data quality and completeness have been found in both types of registry, consistent with the best international standards. A linkage process was carried out on about 339,000 cancer notifications and 3,134 AIDS notifications and was herein restricted to individuals under the age of 50. Out of 243 Kaposi's sarcomas at either type of registry, 90 (37%) were reported as such by both; 68% of individuals with Kaposi's sarcoma at cancer registries could be identified at the AIDS registry, including AIDS-defining illnesses other than Kaposi's sarcoma; 62% of individuals with Kaposi's sarcoma at RAIDS could be found at cancer registries. Of 2,104 non-Hodgkin's lymphomas at either type of registry, 55 were reported as such by both; 65% of individuals reported as having non-Hodgkin's lymphoma at the AIDS registry were found at cancer registries. Our present results indicate the scope for improving cancer assessment in individuals with HIV infection and AIDS and the potential of AIDS and cancer registries for such a purpose.
The efficacy of triple drug therapy for HIV-1 infection encourages its early use to prevent damage to the immune system. We monitored the effects of such therapy on 12 patients with 14-75-mo histories of minimal disease, i.e., CD4+ counts constantly >500/microl and little or no lymph node enlargement. In this way, we could first determine the extent of viral replication and immunoarchitectural changes in unenlarged nodes early in disease, and second follow the response to triple therapy in plasma and lymphoid tissue in tandem. As is known for lymph nodes with more advanced disease, the germinal centers showed productively infected T cells, i.e., CD4+CD1a-CD68- cells labeling intensely for HIV-1 RNA after in situ hybridization. The unenlarged nodes also showed extensive HIV-1 RNA retention on a well-preserved, follicular dendritic cell (FDC) network, and the follicles were abnormal. There were numerous CD8+ cells, many expressing TIA-1 granule antigen. Also, in contrast to normal follicles, CD4+ T cell proliferation was active, with marked increases in the number of cycling, Ki-67+CD4+CD45R0+ cells. After 28 d and 3 mo of therapy, productively infected T cells decreased dramatically and often were not apparent. The labeling of the FDC network for viral RNA also decreased, but not for gag protein. We conclude that HIV-1 replicates and accumulates in lymphoid organs before damage of the immune system, that at this stage of disease de novo production of T cells occurs in the lymphoid tissue, and that the infection is sensitive to triple drug therapy in both plasma and lymph nodes.
This study was undertaken to determine if prolonged daily subcutaneous administration of ultra low dose IL-2 could influence the constitutive endogenous production of a type 1 (IFN-gamma) cytokine in patients with AIDS or AIDS-associated malignancies. Using a quantitative reverse transcription PCR assay, we demonstrate that daily administration of one type 1 cytokine, IL-2, for 3 mo increases significantly the constitutive endogenous gene expression of another type 1 cytokine, IFN-gamma, in vivo. The predominant source of IFN-gamma appears to be IL-2-expanded natural killer cells and CD8(+) T cells. Moreover, PBMC obtained from these patients during IL-2 therapy showed normalization of a profound deficit in IFN-gamma protein production after stimulation with extracts from infectious agents in vitro. Our data suggest that prolonged exogenous administration of a type 1 cytokine in a nontoxic fashion to patients with AIDS and AIDS-associated malignancies can enhance significantly the endogenous type 1 cytokine profile in vivo. Consequently, ultra low dose IL-2 therapy has the potential to improve the immunodeficient hosts' immune response to infectious pathogens that require IFN-gamma for clearance.