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)

Human immunodeficiency virus (HIV) often causes latent infection. Transactivation by some DNA viruses has been implicated in inducing HIV-1 replication and pathogenesis. The transactivator (IE-2) gene of the human cytomegalovirus (CMV) can enhance HIV-2 as well as HIV-1 gene expression in vitro. This inducer can act in concert with the HIV-2 tat gene and T-cell activation in enhancing gene expression in human CD4+ lymphocytes. While the HIV-2 and HIV-1 tat genes and T-cell activators apparently employ independent modes of action, the CMV transactivator in combination with the HIV-2 tat or T-cell activators may employ a gene activation pathway with some common and some distinct components. Both HIV-2 and CMV transactivators enhance HIV-2 gene expression by transcriptional activation involving transcript initiation as well as elongation, with CMV transactivator affecting elongation more than the initiation. A significant proportion of transcripts appear to terminate prematurely in the absence of transactivators. Deletion mutation analysis of the HIV-2 long terminal repeat (LTR) suggests that the element that responds to CMV transactivation in human CD4+ lymphocytes is either a diffuse one or located downstream of the HIV-2 enhancer element.
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PMID:Stimulation of the human immunodeficiency virus type 2 (HIV-2) gene expression by the cytomegalovirus and HIV-2 transactivator gene. 197 89

The human immunodeficiency viruses (HIVs) may include a spectrum of retroviruses with varying potential to infect their host, undergo long periods of latent infection, and induce pathology. Since expression of the viruses is in large part regulated by the sequence elements in their long terminal repeats (LTRs), this study was directed to an analysis of the regulatory elements in the HIV-2 LTR. The HIV-2 LTR was found to contain two enhancers. One of these enhancers is, in part, identical to the HIV-1 enhancer. This enhancer in HIV-1 is the T-cell activation response element; in HIV-2, however, it is the second enhancer that is mainly responsible for activation in response to T-cell activators. The second enhancer interacts with two nuclear binding proteins (85 kD and 27 kD mobility) that appear to be required for optimal enhancer function and activation. Observations such as these encourage the speculation that there may be subtle differences in the regulation of HIV-1 and HIV-2 expression that may be relevant to the possible longer latency and reduced pathogenicity of HIV-2.
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PMID:Human immunodeficiency virus type-2 gene expression: two enhancers and their activation by T-cell activators. 198 44

Individuals who are infected with human immunodeficiency virus (HIV) are at high risk of developing tuberculosis, probably due to the reactivation of latent infection associated with HIV-induced immunosuppression. Tuberculin skin test is the best diagnostic means to assess a previous tuberculous infection, but this test may be falsely negative in HIV seropositive subjects. To assess the validity of a non-reactive tuberculin skin test in asymptomatic HIV seropositive subject, we performed Mantoux test 5 TU, chest x-ray, HIV serologic tests on 141 asymptomatic prisoners. Determination of lymphocyte subsets in HIV seropositive carriers had already been performed. Chest x-ray film showed no pleuro-pulmonary lesion in any subject. We found 101 HIV seronegative subjects (89 men and 12 women; 30 +/- 6 yrs with 18-39 range; 34 Mantoux reactive and 67 non-reactive) and 40 HIV seropositive individuals (30 men and 10 women; 29 +/- 6 yrs with 21-39 range; 7 Mantoux reactive and 33 non-reactive). By subdividing HIV seropositive subjects in two groups (reactive and non-reactive to tuberculin test) a significant decrease of CD 4 lymphocytes and CD 4/CD 8 ratio was found in HIV seropositive/Mantoux non-reactive group, without changes in total lymphocytes and CD 8 subset. We conclude that: 1) a non-reactive tuberculin skin test cannot be confidently explained in asymptomatic HIV seropositive subjects with a T helper lymphocyte count decrease; 2) T helper cells are important to keep alive delayed hypersensitivity reaction.
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PMID:[Mantoux intradermal reaction and lymphocyte populations in asymptomatic HIV-seropositive subjects]. 198 96

The central nervous system (CNS) of 221 adults and 31 infants or children with the acquired immunodeficiency syndrome (AIDS) was examined with immunocytochemistry for infectious agents and for human immunodeficiency virus-1 (HIV-1) antigen (gp41). Since the major risk factor in this population was intravenous drug abuse, there were more female and pediatric patients than in other neuropathology autopsy series. Although children had a different spectrum of pathologic changes, including less frequent opportunistic infections, women did not differ from men in terms of types or incidence of opportunistic infections, vascular disease, neoplasia, and subacute AIDS encephalitis (SAE). Subacute AIDS encephalitis was detected in 26% of adult and 48% of pediatric brains. Immunocytochemical analysis of 100 adult and 20 pediatric brains revealed gp41 immunoreactivity in 78% and 40%, respectively. Virtually all adult brains with SAE had gp41 immunoreactivity in macrophages and microglia. Even brains with no significant pathology had frequent gp41 immunoreactivity, especially in the basal ganglia. In pediatric brains, including cases with SAE, gp41 immunoreactivity was less abundant, suggesting the possibility of latent infection or viral clearance. Spinal cords with vacuolar myelopathy or corticospinal tract degeneration had only rare gp41-positive cells. Brains from 16 aborted fetuses from HIV-1-seropositive women were all negative for gp41 immunoreactivity, but 12 brains were positive for HIV-1 by the polymerase chain reaction. These results may indicate that HIV-1 infection in fetal brains is below the limits of detection of immunocytochemistry. The differences noted between adults and children suggest that adults more often have productive CNS HIV-1 infection.
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PMID:Human immunodeficiency virus-1 infection of the nervous system: an autopsy study of 268 adult, pediatric, and fetal brains. 207 Nov 14

Antibodies that augment human immunodeficiency virus (HIV) infectivity of monocytes through Fc receptor (FcR) type III for IgG have been found in the blood of sero-positive patients and immunized chimpanzees. This study investigated the effect of acute and chronic HIV infection, as well as protein kinase C activators capable of up-regulating latent HIV, on the expression of these receptors. In addition, the frequency of this antibody-dependent enhancement (ADE) phenomenon was estimated using purified IgG from HIV-1 seropositive individuals at various clinical stages of infection. The existence of an FcR-dependent pathway for ADE of HIV-1 infection in peripheral blood monocytes and promonocytic U937 cells was confirmed in sera from a small subset of patients, and the phenomenon extended to FcR types I and II. The level of ADE activity was minimal, however, and no relationship between the presence or magnitude of the ADE phenomenon and clinical stage was uncovered. Finally, perturbations which activate a latent HIV infection were shown to concomitantly up-regulate FcR on infected and uninfected cells. This suggests a positive feedback loop linking up-regulation of latent infection, enhanced expression of low affinity HIV receptors such as FcR, and viral spread.
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PMID:Human immunodeficiency virus infection of monocytes: relationship to Fc-gamma receptors and antibody-dependent viral enhancement. 214 69

Histologic studies supplemented by in situ hybridization for human immunodeficiency virus type 1 (HIV-1), Epstein-Barr virus, cytomegalovirus, and human herpesvirus type 6 were performed on tissues obtained from the autopsy of six patients who died either by homicide or suicide shortly after learning of their seroconversion. Except for mild nonspecific lymphoid tissue reactions, no lesions were noted that would indicate HIV-1 infection. DNA from all viruses was detected in some lymphoid cells. The amount of DNA for Epstein-Barr virus, cytomegalovirus, and human herpesvirus type 6 corresponded to that observed for clinically occult latent infection. Lymphoid cells carrying HIV-1 DNA were even less frequent. Cells positive for HIV-1 were noted in the lamina propria of the large intestine in three male homosexuals and in one female prostitute. The cells were arranged similar to antigen-presenting cells. The present findings are consistent with current theories regarding the pathogenesis of HIV-1-associated disease.
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PMID:Search for early lesions following human immunodeficiency virus type 1 infection. A study of six individuals who died a violent death after seroconversion. 215 81

The determinants of cytomegalovirus (CMV) infection and disease can now be understood from studies of newborns, recipients of organ or bone marrow transplants, subjects infected with human immunodeficiency virus, and recipients of blood transfusions. CMV is transmitted to the neonate transplacentally, by passage through a contaminated birth canal, or by ingestion of infected breast milk; to the adult by heterosexual and homosexual sex with an infected partner; and to the transplant recipient by infected organs. A major unsolved problem in the study of CMV is the nature of viral latency. Knowledge regarding the requirements for activation of latent infection at the molecular, cellular, or host level is incomplete. Both viral and host factors may contribute to the successful transmission of CMV by latently infected cells in transplanted organs and transfused blood.
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PMID:Epidemiology of cytomegalovirus infections. 217 99

Phagocytic macrophages are known to support noncytopathic, chronic infections of human immunodeficiency virus (HIV). Regulation of viral replication in such cells with either chronic low-grade or latent HIV infection is probably influenced by both viral and cellular factors acting on the viral long terminal repeat (LTR). This study identifies naturally occurring biological response modifiers which are able to affect the HIV-LTR linked to the chloramphenicol acetyl transferase (LTR-CAT) gene in a stable transfection of the human promonocyte cell line, U937, in the absence of other viral proteins. In this model system, endotoxin lipopolysaccharide (LPS) and tumor necrosis factor-alpha (TNF-alpha) are able to independently stimulate expression of LTR-CAT. Granulocyte/macrophage-colony-stimulating factor can enhance the effect of TNF-alpha or LPS, but other cytokines tested had minimal or no effect on LTR-CAT. In addition to effects on cellular susceptibility and immune function, the ability of naturally occurring factors to affect HIV-LTR in its integrated state may have particular relevance to progression of active disease from latent infection.
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PMID:Expression of human immunodeficiency virus long terminal repeat in the human promonocyte cell line U937: effect of endotoxin and cytokines. 220 Jun 14

The link between genital ulcers and transmission of the human immunodeficiency virus highlights the need of prevention and treatment of genital herpes. Although a diversity of specific and unspecific drugs have been tested on effects toward herpes simplex virus types 1 and 2, only one antiviral drug, acyclovir, have proven safe and efficacious on some aspects of the disease. The drug has a marked effect on first episodes of herpes genitalis, but the effect on recurrences are less pronounced because viral replication is of shorter duration. Selection of patients for antiviral treatment involves considerations of immune status, the risk of neonatal transmission for pregnant women, and the severity of local and systemic symptoms, incidence of prodromal symptoms, and most importantly, recurrence rates, because this signals the psychological impact of the disease. The main goals of any herpes treatment--to eradicate latent infection in primary as well as recurrent disease--are not achieved by any known antiviral or immunomodulatory drug.
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PMID:Genital herpes--when and how to treat. 220 9

The protein kinase C (PKC) activator phorbol myristate acetate (PMA) was used to upregulate viral replication in a clone of promonocytic cells chronically infected with human immunodeficiency virus (HIV)-1. Induction of virus could be inhibited by the triphenylethylene anti-estrogen tamoxifen at concentrations that had minimal effects on cellular DNA synthetic responses and cell cycle kinetics. This effect correlated with tamoxifen's ability to block PMA-mediated enhancement of HIV-promoter-driven transactivation in cells of monocyte and CD4+ T-lymphocyte lineages. No interference with a primary infection was noted. Tamoxifen's mechanism of action may relate both to its capacity to inhibit PKC and to consensus sequences for gonadal steroid responsive elements in the HIV long terminal repeat, as it was able to partially inhibit another HIV activator, 5-azacytidine, which does not modulate PKC function. The finding that regulation of HIV in a model for low-level chronic or latent infection is amenable to a nonimmunosuppressive steroid antagonist may suggest approaches to pharmacologic intervention early in HIV infection.
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PMID:Effect of tamoxifen on regulation of viral replication and human immunodeficiency virus (HIV) long terminal repeat-directed transcription in cells chronically infected with HIV-1. 229 71


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