PubMed · 2881114
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C Kenny, J Parkin, G Underhill, N Shah, B Burnell, E Osborne, D J Jeffries. 1987-03-07. HIV antigen testing.. https://doi.org/10.1016/s0140-6736(87)90210-8
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BACKGROUND: Although pericardial effusion is known to be common among patients infected with HIV, the incidence of pericardial effusion and its relation to survival have never been described. METHODS AND RESULTS: To evaluate the incidence of pericardial effusion and its relation to mortality in HIV-positive subjects, 601 echocardiograms were performed on 231 subjects recruited over a 5-year period (inception cohort: 59 subjects with asymptomatic HIV, 62 subjects with AIDS-related complex, and 74 subjects with AIDS; 21 HIV-negative healthy gay men; and 15 subjects with non-HIV end-stage medical illness). Echocardiograms were performed every 3 to 6 months (82% had follow-up studies). Sixteen subjects were diagnosed with effusions (prevalence of effusion for AIDS subjects entering the study was 5%). Thirteen subjects developed effusions during follow-up; 12 of these were subjects with AIDS (incidence, 11%/y). The majority of effusions (80%) were small and asymptomatic. The survival of AIDS subjects with effusions was significantly shorter (36% at 6 months) than survival for AIDS subjects without effusions (93% at 6 months). This shortened survival remained significant (relative risk, 2.2, P = .01) after adjustment for lead time bias and was independent of CD4 count and albumin level. CONCLUSIONS: There is a high incidence of pericardial effusion in patients with AIDS, and the presence of an effusion is associated with shortened survival. The development of an effusion in the setting of HIV infection suggests end-stage HIV disease (AIDS).
The present study was performed with the aim of better defining the possible role of Epstein-Barr-virus (EBV)-infected cells in the pathogenesis of HIV-related lymphadenopathy syndrome (LAS). In addition, since LAS has been considered as a pre-lymphomatous lesion, we also wished to elucidate the possible contribution of EBV-carrying cells present in LAS tissues to the development of HIV-associated malignant lymphomas. To this end, we have characterized EBV-infected cells in LAS lymph nodes in terms of EBV DNA prevalence, tissue distribution in relation to HIV-carrying cells, virus sub-type, expression of latent and replicative antigens, and presence of clonal EBV episomes. When compared with HIV-unrelated lymphadenopathies (4/10, 40%), LAS showed a higher prevalence of EBV DNA (14/20, 70%). Comparable values of EBV prevalence were detected in LAS with follicular hyperplasia (12/16, 75%) and with follicular involution (4/4, 100%). All EBV+ non-neoplastic lymph nodes from HIV-seronegative patients carried type-I EBV, whereas LAS specimens showed almost equivalent distribution of the 2 EBV sub-types. Of the 14 EBV-carrying LAS, 4 (29%) were positive by Southern-blot analysis for the BamHI-W region of the virus genome but negative for the presence of monoclonal EBV episomes. In situ hybridization revealed a remarkably higher load of EBV-infected cells in LAS than in HIV-unrelated lymphadenopathies. In LAS lymph nodes, EBV-carrying cells were identified as isolated, cytologically normal elements, sometimes with immunoblastic morphology, usually scattered throughout the interfollicular areas. By contrast, the expression of HIV p24 was restricted to germinal center cells. All the EBV+ LAS samples were negative for the expression of EBV-encoded latent (LMP-1 and EBNA-2) and replicative proteins (BZLF-1, BHLF-1, EA-D, EA-R and VCA). In addition, amplification of the immunoglobulin heavy-chain genes using 2 different polymerase-chain-reaction protocols showed evidence of B-cell clonal expansion in 2/20 (10%) LAS, one EBV- case, and one sample with low numbers of EBV-infected cells. These results suggest that (i) EBV-carrying cells are probably not involved in the development of LAS, either directly or indirectly; (ii) type-2-EBV-infected cells are present in LAS lymph nodes from the early phases of HIV infection; (iii) EBV-carrying LAS per se probably does not constitute a lesion at high risk for subsequent development of EBV+ lymphomas; (iv) it is unlikely that a high viral load or strong EBV-mediated antigenic stimulation plays a contributory role in the development of EBV-unrelated lymphomas of HIV-seropositive individuals.
To assess the safety, pharmacokinetics, and antiviral effects of intravenous recombinant CD4 immunoglobulin G (CD4-IgG), a 12-week Phase One study with an optional maintenance phase was performed. Twenty-two subjects with advanced human immunodeficiency virus (HIV) infection were enrolled; 15 subjects completed the initial 12 weeks. CD4-IgG doses were 30, 100, or 300 micrograms/kg weekly; 1,000 micrograms/kg once, twice, or three times per week; or 3,000 micrograms/kg twice weekly. Serum concentrations of CD4-IgG increased linearly with dose, with average peak serum concentrations of 22 micrograms/ml with 1,000 micrograms/kg. CD4-IgG was well tolerated; one patient had self-limited tachycardia and flushing associated with CD4-IgG therapy. No changes were seen in CD4 cell counts, hematologic or coagulation studies, serum chemistries, HIV p24 antigen titers, or plasma HIV titers. No subject developed anti-CD4 antibodies. HIV isolates from five patients had IC90 values that were higher than the peak concentrations of CD4-IgG achieved in those patients. Additional studies that achieve higher CD4-IgG concentrations are necessary to evaluate the antiviral activity of this compound.