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Query: UMLS:C0019693 (HIV)
 170,526 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Recently we described an HLA B27-restricted peptide derived from HIV gag p24 protein. In this study we have isolated an HLA B27-restricted peptide from the nucleoprotein (NP) of influenza A virus. The shortest fragment recognized by cytotoxic T lymphocyte (CTL) is eight amino acids long, residues 384-391. Comparison of the sequence of these two HLA B27 restricted peptides reveals homologies which can be aligned from one peptide to the other. Of the eight residues, two are identical: tryptophan and isoleucine. Both peptides have a positively charged residue at the N terminus, lysine at position 265 of gag and arginine at position 384 of NP. Using modified peptides we have shown that lysine or arginine is crucial for the interaction with HLA B27. The wild-type gag peptide blocked CTL recognition of NP peptide by influenza-specific CTL, but removal of the lysine prevented inhibition of NP peptide recognition. The importance of these charged residues was confirmed by the observation that truncated NP and gag peptides where the lysine or arginine was removed were not recognized by specific CTL. Further studies showed that the tryptophan residue influenced the association of the gag peptide with HLA B27, because the affinity of the gag peptide for B27 was strongly increased after replacing this residue with a leucine or a tyrosine. However, these peptides were not recognized by gag-specific CTL, suggesting that the tryptophan may interact with both HLA B27 and T cell receptor. These observations should help in the identification of HLA B27-restricted peptides from other viruses or organisms.
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PMID:Structural homologies between two HLA B27-restricted peptides suggest residues important for interaction with HLA B27. 212 95

The reported AIDS cases in the USA and the Federal Republic of Germany are growing almost exponentially. Considering the epidemiological curves for different risk groups (homosexual men, i.v. drug abusers, heterosexual partners etc.) it is extremely surprising, that nearly exactly the same development occurs in all risk groups. One only has to consider a certain time shift for each group. The conformity of the development for all groups is evident by the fact, that the curves representing the reported AIDS cases for different risk groups are straight lines (in a logarithmic scale) running nearly exactly in parallel. This remarkable parallelism can be understood only if the spread of AIDS is independent of the sexual or drug risk in a certain sense. On the other hand, the drastic overrepresentation of the sexually highly active groups and drug abusers in the number of AIDS cases obviously requires that the transmission of AIDS unequivocally depends on the sexual and drug risk. We present a mathematical model that is suitable to reconcile this apparent contradiction in the interpretation of the epidemiological data: the observed parallel time series for the spread of AIDS in groups with different risk of infection can be realized by computer simulation, if one assumes that the outbreak of full-blown AIDS only occurs if HIV and a certain infectious coagent (cofactor) CO are present. Such a situation is not uncommon, see, e.g. the influenza virus--Staphylococcus aureus system. According to the mathematical model this cofactor would spread independently of the sexual and drug risk--in contrast to HIV. However, due to its analytical properties the simulated cofactor cannot be identified so far with any known infectious agent.
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PMID:On the structure of the epidemic spread of AIDS: the influence of an infectious coagent. 219 86

Knowledge of the pathogenesis of viruses which are less virulent than human immunodeficiency virus (HIV) may provide valuable insights into the pathogenesis of HIV infection. Influenza virus, an enveloped RNA virus, infects monocyte-macrophages, although the infection is brief and abortive. Isolated purified lymphocytes are completely resistant to infection. In contrast, mixtures of lymphocytes and macrophages can synthesize all virus proteins. Infection requires physical association of monocyte-macrophages and lymphocytes in "clusters." These studies with influenza virus suggest that the pathogenesis of virus infections in mixed cell cultures may be very different from that observed in purified cell populations, and they suggest that similar studies should be performed with HIV.
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PMID:Role of the monocyte-macrophage in influenza virus infection of lymphocytes: implications for HIV infection. 222 42

To make purified antigens highly immunogenic, they have to be presented in several copies in the form of a microscopic or submicroscopic particle. This is the case, regardless of whether the antigens are obtained by isolation from conventional microorganisms, or from gene-manipulated cells, or synthesized. In the iscom, the antigens are attached as multimers to a 40-nm cage-like particle with a built-in adjuvant. The antigens in iscoms are rapidly transported from the injection site to the draining lymphatic organ. Iscom-borne antigens induced a 10-fold higher antibody response than the same amount of antigen in micelle form. One intranasal immunization with influenza virus iscoms induced protection to intranasal challenge infection in mice. Besides a strong antibody response in all Ig classes and isotypes, cytotoxic T cells were induced. With iscoms containing gp160 of HIV-1, cytotoxic T cells (CD8+ CD4-) were induced under restriction of class I MHC antigen. Iscoms containing the fusion protein of measles virus induced T cell clones in mice whereof one, after adoptive transfer, protected mice against intracerebral challenge infection. Protective immunity against Epstein-Barr virus (EBV)-induced tumor formation by iscoms containing gp350 of EBV has been elicited in cotton-top Tamerin monkeys. Protective immunity has also been induced against several virus infections including feline leukemia virus and against parasites, i.e., Trypanosoma cruzi, in mice.
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PMID:The iscom: an immunostimulating system. 228 59

Acute exanthema occurs in patients who are human immunodeficiency virus (HIV) positive before they become seropositive. The patients have influenza like symptoms and a macular skin rash on the upper trunk. Histopathological investigation of skin punch biopsy specimens from four patients with acute HIV exanthema showed a normal epidermis and a sparse dermal, mainly perivascular, lymphocytic/histiocytic infiltrate around vessels of the superficial plexus. Histopathological changes of the exanthema of acute HIV infection are non-specific and resemble those of other acute viral exanthema, but when both the histopathological features and the clinical picture are suggestive, the clinician should take into consideration the possibility of HIV infection.
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PMID:Histopathology of acute human immunodeficiency virus exanthema. 233 16

The HIV/ARC/AIDS story continues to unfold. It is both the old, sadly familiar experience of plague and disease, of lepers isolated as unclean, of smallpox decimating the American Indians, of a Black Death sweeping medieval Europe, of the 1918 influenza. It is also a new story, one in which medical scientists rather quickly identified the causative infectious agent but, as yet, have been unable to cure the infection, although some amelioration of the basic course of the illness appear possible if treatment with AZT is begun relatively early. The ethical problems are numerous and constantly change as the understanding of the disease and its potency evolves. The social answers have, after initial delay, received positive action on an official level. On the more personal level of the average American there remains animosity, prejudice, and a deeply rooted fear, the ancient fear of the leper, of the plague victim. The health professionals have also officially responded well to the challenge of AIDS. Personally, as in society generally, there has been a mixed response. We believe that the ethical concerns enumerated in this article will be resolved in favor of persons with AIDS. Nevertheless, the personal, spiritual, emotional, and economic isolation experienced by persons with AIDS and their families challenge us about what kind of society we wish to be. We will ultimately be measured as a civilization by the way in which we treated the least fortunate. America's track record in this regard has been mixed. AIDS presents us with a chance to change.
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PMID:Ethical concerns about AIDS. 233 79

beta-Interferon (IFN-beta) was evaluated prospectively for its antiviral activities in early stage human immunodeficiency virus (HIV) infection. Ten patients with hemophilia and HIV infection [8 asymptomatic carriers (AC) and 2 AIDS-related complex (ARC)] were intravenously injected with 1 million IU of IFN-beta twice a week for 6 months. For comparison, seven patients (six AC and one ARC) with hemophilia and HIV infection were observed for the same time period without any drugs. One episode of localized herpes zoster each occurred during the trial in the IFN group and in the control group. There were no significant differences in the absolute number of CD4+ lymphocytes and ratios of CD4+/CD8+ lymphocytes between the two groups. Recipients had flu-like symptoms but no serious toxicities. No clinical and immunological benefits to patients with early stage HIV infection were observed during the 6 months of treatment.
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PMID:Beta-interferon and early stage HIV infection. 249 47

We have tested the T helper cell (TH) potential of asymptomatic, HIV seropositive (HIV+) patients, using an in vitro assay for IL-2 production. Peripheral blood leukocytes (PBL) from 74 HIV+ patients and 70 HIV- control donors were tested for TH function when stimulated with influenza A virus (FLU), tetanus toxoid (TET), HLA alloantigens (ALLO), or PHA. Of the HIV+ patients, four different response patterns were observed: (a) patients who responded to all four stimuli (16%); (b) patients who were selectively unresponsive to FLU and TET, but responded to ALLO and PHA (54%); (c) patients who were unresponsive to FLU, TET, or ALLO, but responsive to PHA (16%); and (d) patients who failed to respond to any of these stimuli (14%). Our results indicate a time-dependent progression from a stage responsive to all four stimuli to a stage unresponsive to any of the stimuli tested, progressing in the order outlined above. The earliest TH defect is the loss of responses to FLU and TET, indicating a selective defect in CD4+ MHC self-restricted TH function. The later loss of ALLO and PHA IL-2 responses suggests more severe TH dysfunction involving both CD4+ and CD8+ T cells. None of these patterns of TH unresponsiveness in asymptomatic HIV+ individuals were correlated with CD4+ cell numbers nor with Walter Reed staging criteria. This study indicates that the in vitro TH assay used can detect multiple stages of immune dysregulation early in the course of HIV infection and raises the possibility that staging of HIV+ patients should include in vitro TH functional analyses of the type described here.
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PMID:Detection of three distinct patterns of T helper cell dysfunction in asymptomatic, human immunodeficiency virus-seropositive patients. Independence of CD4+ cell numbers and clinical staging. 257 88

We studied whether a two-dose regimen of inactivated influenza virus vaccine was more effective than a single dose in inducing protective hemagglutination-inhibition antibody responses in patients infected with human immunodeficiency virus (HIV). Participants included subjects with acquired immunodeficiency syndrome, subjects with acquired immunodeficiency syndrome-related complex, and HIV-seropositive individuals with either lymphadenopathy only or no symptoms. Control subjects were HIV-seronegative heterosexuals and HIV-seronegative homosexuals. Two doses of inactivated influenza vaccine containing 15 micrograms of the hemagglutinin of influenza A/Taiwan/1/86(H1N1), A/Leningrad/360/86(H3N2), and B/Ann Arbor/1/86 were administered intramuscularly in the deltoid region 1 month apart. The second dose of vaccine did not significantly increase the frequency or magnitude of antibody responses of either HIV-seropositive or HIV-seronegative subjects over that achieved by a single dose. The two-dose regimen induced a protective level (greater than or equal to 1:64) of hemagglutination-inhibition antibody to influenza A(H1N1) or (H3N2) virus less often in subjects with symptomatic HIV infection than in uninfected control subjects (39% vs 87% or 46% vs 97%, respectively). Our results suggest that a substantial proportion of individuals with symptomatic HIV infection might remain unprotected from influenza, even after immunization with a two-dose regimen.
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PMID:The influence of HIV infection on antibody responses to a two-dose regimen of influenza vaccine. 278 16

We studied 6 patients from 6 different geographic areas who presented with acute flu-like illnesses. The patients developed persistent fevers, lymphadenopathy or diarrhea, pneumonia, and/or heart, liver, or adrenal failure. They died in 1-7 weeks. These patients had no serological evidence of HIV infection and could not be classified as AIDS patients according to CDC criteria. The clinical signs as well as laboratory and pathological studies of these patients suggested an active infectious process, although no etiological agent was found despite extensive infectious disease work-ups during their hospitalization. Post-mortem examinations showed histopathological lesions of fulminant necrosis involving the lymph nodes, spleen, lungs, liver, adrenal glands, heart, and/or brain. No viral inclusion cells, bacteria, fungi, or parasites could be identified in these tissues using special tissue stains. We report that immunohistochemistry using rabbit antiserum raised against VLIA, the virus-like infectious agent previously identified in patients with AIDS and shown to cause fatal systemic infection in primates, revealed VLIA antigens in these necrotizing lesions. In situ hybridization using an 35S labeled VLIA-specific DNA probe also detected VLIA genetic material in the areas of necrosis. Furthermore, virus-like particles closely resembling VLIA were identified ultrastructurally in these histopathological lesions. VLIA was associated with the systemic necrotizing lesions in these previously healthy non-AIDS patients with an acute fatal disease.
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PMID:Association of the virus-like infectious agent originally reported in patients with AIDS with acute fatal disease in previously healthy non-AIDS patients. 280 22


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