Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0021051 (immunodeficiency)
 71,517 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Anti-lymphocyte (ALA) antibodies were investigated by using both microcytotoxicity and immunofluorescence analyses in 87 subjects with different clinical features of human immunodeficiency virus (HIV) infection. A similar mean percentage of killing in microcytotoxicity assays using heterologous lymphocytes as cellular target was recorded in four groups of patients, including 36 HIV-seropositive asymptomatic subjects, 34 patients with HIV-induced lymphadenopathy syndrome (LAS), 13 with acquired immunodeficiency syndrome (AIDS)-related complex (ARC), and 4 patients with the full-blown AIDS. Conversely, an increasing percentage of ALA-positive subjects paralleled the evolution of the HIV infection. The majority of ALA were IgM isotype with a significant reactivity against T cells. This specificity was indifferently directed to CD3+, CD4+, and CD8+ lymphocytes. In additional experiments employing enzymatic digestion of lymphocyte membrane antigens, we demonstrated that CD4 and CD8 receptors were digested by the pronase, whereas CD3 molecules were highly resistant. Subsequent flow cytometry analyses using these pronase-digested T cells showed that reactivity of ALA for their target was unchanged. Our data suggest that antigenic specificities of ALA in HIV infection are resistant to pronase treatment and are not related to CD4 and CD8 molecules.
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PMID:Isotype, distribution and target analysis of lymphocyte reactive antibodies in patients with human immunodeficiency virus infection. 257 36

In an effort to develop a useful AIDS vaccine or vaccine component, we have generated a combinatorial library of chimeric viruses in which the sequence IGPGRAFYTTKN from the V3 loop of the MN strain of human immunodeficiency virus type 1 (HIV-1) is displayed in many conformations on the surface of human rhinovirus 14 (HRV14). The V3 loop sequence was inserted into a naturally immunogenic site of the cold-causing HRV14, bridged by linkers consisting of zero to three randomized amino acids on each side. The library of chimeric viruses obtained was subjected to a variety of immunoselection schemes to isolate viruses that provided the most useful presentations of the V3 loop sequence for potential use in a vaccine against HIV. The utility of the presentations was assessed by measures of antigenicity and immunogenicity. Most of the immunoselected chimeras examined were potently neutralized by each of the four different monoclonal anti-V3 loop antibodies tested. Seven of eight chimeric viruses were able to elicit neutralizing antibody responses in guinea pigs against the MN and ALA-1 strains of HIV-1. Three of the chimeras elicited HIV neutralization titers that exceeded those of all but a small number of previously described HIV immunogens. These results indicate that HRV14:HIV-1 chimeras may serve as useful immunogens for stimulating immunity against HIV-1. This method can be used to flexibly reconstruct varied immunogens on the surface of a safe and immunogenic vaccine vehicle.
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PMID:Human rhinovirus type 14:human immunodeficiency virus type 1 (HIV-1) V3 loop chimeras from a combinatorial library induce potent neutralizing antibody responses against HIV-1. 942 Feb 70

The patient, a 30-year-old man with numerous genital condylomata acuminata (CA), has had unsuccessful treatment with liquid nitrogen, 20% podophyllin, and repeated 0.5% podophyllotoxin solution with 5% imiquimod (Figure 1). Before the appearance of CA, he experienced acute orchiepididimitis and a Candida infection. The patient was immunologically examined, and the lower level of lymphocytes, slightly reduced level of IgM, and C4 complement were revealed. Results from a human immunodeficiency virus examination were negative. After the therapeutic failure mentioned above, photodynamic therapy (PDT) was initiated using 20% aminolevulinic acid (5-ALA) in a gel. The photosensitizer was applied to lesions and 10 mm of surrounding skin in a 1-mm-thick layer under occlusive dressing for 3 hours and then removed with saline and nonwoven gauze. The site was immediately irradiated with noncoherent red light with an emission spectrum of 580 to 680 nm wavelength (Medeikonos PDT-Model 200, Medeikonos AB, Sweden). The total light dose was 50 J/cm(2); light intensity ranged from 70 to 90 mW/cm(2). Because of persistent fluorescence during photodynamic therapy, the treatment was repeated 10 times in 2-week intervals with a follow-up of 1, 3, and 6 months after its completion. After the last PDT treatment, the persistent fluorescence disappeared completely. The absence of fluorescence corresponded with a healed clinical finding without scarring and pigmentation (Figure 2). The period from the initiation of PDT to the consolidation of CA was 22 weeks. During PDT treatment, the patient felt only mild burning, which disappeared after the illumination stopped. Six months after the therapy, there were no signs of recurrent disease.
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PMID:Genital warts treated by photodynamic therapy. 1797 55