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

Tumor necrosis factor-alpha (TNF-alpha) induces the expression of human immunodeficiency virus type-1 (HIV-1) in vitro in chronically infected cells of T and monocytic origin. The tat protein from the HIV-1 virus has been shown to be essential for HIV replication and in the immunosuppression associated with the virus infection. Previous studies in our laboratory have shown that HIV-1 tat gene induces TNF-beta (lymphotoxin) in human B-lymphoblastoid cells (Sastry et al., 1990, J. Biol. Chem. 265, 20091-20093). In an attempt to characterize further the relationship between the host and HIV-1, we investigated the effect of the functional HIV-1 tat gene on the expression of TNF receptors in a human B lymphoblastoid cell line (Raji). We report here that Raji cells transfected with HIV-1 tat gene express fewer cell surface TNF receptors than control cells. At least a 5-fold decrease in the receptor number without any significant change in receptor affinity was observed. The decrease in TNF receptors in tat-transfected Raji cells (Raji-tat cells) was found not to be due to receptor occupancy by the autocrine production of TNF-beta. The decrease in the cell surface expression of TNF receptors in Raji-tat cells was also found to be not due to a decrease in the gene expression of the receptor. The kinetics, amount of TNF binding and its internalization were temperature dependent, and it was different in Raji-tat cells than in the control cells.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Down-modulation of cell surface expression of p80 form of the tumor necrosis factor receptor by human immunodeficiency virus-1 tat gene. 133 62

Strains of human immunodeficiency virus (HIV) differ greatly in their ability to replicate in T4 cells. Fast-replicating strains are observed during the early and late stages of HIV infection, while slow-replicating strains prevail during the intermediate, latent, stage. The prevalence of slow-replicating strains has been attributed to these strains' ability to escape the immune response. However, how these strains are able to avoid being eliminated by an immune response for several years has not been explained. Recent experiments indicate that HIV may be selectively transferred from infected macrophages to T4 cells specific for HIV antigens. Thus, HIV may preferentially infect those T4 cells necessary for generating a protective immune response. To determine the conditions under which an HIV-specific immune response can be blocked, we developed a mathematical model incorporating the process of viral transfer from infected macrophages to HIV-specific T4 cells along with the known processes of macrophage-T4 interaction, immune stimulation, and viral infection of T4 cells and macrophages. Our model shows that the mechanism of viral transfer to HIV-specific T4 cells can allow slow-replicating strains of HIV to escape immune response under conditions in which an immune response occurs against fast-replicating strains. The model also suggests that in addition to slow replication, the ability to reduce or block T-cell activation may be an important characteristic of escape mutants.
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PMID:A mechanism of immune escape by slow-replicating HIV strains. 134 34

In recent years, the antiviral armamentarium has expanded considerably. Currently available agents are virustatic, inhibiting specific steps in the process of viral replication. No agent is active against nonreplicating or latent viruses. Acyclovir is useful in the treatment of genital herpes, herpes simplex encephalitis, mucocutaneous herpetic infection, varicella infection in the immunosuppressed host, and herpes zoster infection in the normal and the immunosuppressed host. It can also be used for prevention of herpesvirus infection in immunocompromised patients. Ganciclovir is indicated for the treatment of cytomegalovirus retinitis in patients with acquired immunodeficiency syndrome (AIDS) and is effective in the management of organ-specific cytomegalovirus infection in other immunocompromised patients. Chronic hepatitis C and condyloma acuminatum due to human papillomavirus respond to therapy with interferon alfa-2b. Patients with human immunodeficiency virus infection and CD4 lymphocyte counts of less than 500 cells/mm3 should be treated with zidovudine. Amantadine is useful in a therapeutic and prophylactic role in the management of influenza A virus infection. With the expanded use of and indications for antiviral therapy, clinically significant resistance to these agents has been encountered with increasing frequency.
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PMID:Antiviral agents. 134 78

The mechanisms of human immunodeficiency virus (HIV-1) entry into CD4+ cells and HIV-1 inactivation by sCD4 were studied by analyzing the kinetics of inhibition of viral infection by sCD4 and the kinetics of fusion of CD4+ cells with intact virions labeled with the lipid fluorophore octadecylrhodamine (R18). sCD4 inhibited HIV-1 infection much more effectively when preincubated with virus prior to interaction with CD4+ cells than when mixed simultaneously with virions and cells. The kinetics of inhibition of infection was much slower at 4 degrees and at low sCD4 concentrations than at 37 degrees and at high sCD4 concentrations. In the absence of sCD4, attachment of virus to cells leading to productive infection occurred within 10-30 min. Fusion of the virions with cells started after a 1-2 min lag time and was complete within 15 min. In high-density cell suspensions (5 x 10(7) cells/ml), even very high sCD4 concentrations (100 micrograms/ml) failed to block viral infection during simultaneous mixing of cells, sCD4 and HIV-1. We conclude that the kinetics of sCD4-virus interaction and the competition of sCD4 with the cell surface associated CD4 for the virus are crucial factors in the inhibition of HIV-1 infection by sCD4. These results provide insight into mechanisms of viral penetration into cells and should be considered when designing new approaches for AIDS therapy.
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PMID:Kinetics of HIV-1 interactions with sCD4 and CD4+ cells: implications for inhibition of virus infection and initial steps of virus entry into cells. 134 67

Compounds with medium relative molecular masses active against human immunodeficiency virus (HIV) were synthesized. Sulfated alkyl oligosaccharides such as sulfated octadecyl maltohexaoside, sulfated dodecyl laminaripentaoside and sulfated dodecyl laminari-oligomer caused 50% inhibition of virus infection in the EC50 range of 0.4-0.7 microgram/mL in vitro using the MT-4 cell line and HIV-1HTLV-IIIB virus isolate, though sulfated oligosaccharides without alkyl groups showed low anti-HIV activities. This anti-HIV activity was close to the EC50 of 0.43 microgram/mL for a highly active sulfated polysaccharide curdlan sulfate which was reported to inhibit completely the HIV infection at a concentration as low as 3.3 micrograms/mL. These compounds were also active against HIV-2 and a clinically isolated HIV-1 with reduced AZT sensitivity. For such sulfated alkyl oligosaccharides, the mechanism of inhibition of HIV infection was assumed to be the inhibition of HIV binding to the cell and to some extent the interaction of the alkyl portion with the lipid bilayer of the virus.
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PMID:Sulfated alkyl oligosaccharides with potent inhibitory effects on human immunodeficiency virus infection. 135 27

Infection by the human immunodeficiency virus is associated with polyclonal B cell activation and increased levels of serum IgA. In order to characterize the molecular species of serum IgA, we have measured total IgA, IgA1, and IgA2 in sera from 60 HIV-1-infected patients and 40 healthy controls. In addition, secretory IgA (S-IgA), secretory IgM (S-IgM), free immunoreactive secretory component (SC), and the distribution of monomeric and polymeric IgA were determined. The data confirm the elevation of total serum IgA levels in HIV-1-infected patients, and both IgA1 and IgA2 concentrations are elevated. Furthermore, the data show a substantial increase in serum levels of both monomeric and polymeric IgA. Serum S-IgA levels were significantly increased in CDC group II patients versus controls and more frequently elevated in CDC group IV patients. The highest S-IgA levels were found among patients with the lowest blood CD4+ cell counts. Serum S-IgA levels were not correlated with serum levels of either total IgA or polymeric IgA. Serum S-IgM levels were also increased in HIV-1-infected patients and positively correlated with serum S-IgA levels. Conversely, serum levels of free SC were not altered. An increase in serum S-IgA was not related to human hepatitis B virus infection and/or to hepatic dysfunction or to diarrhea or overt intestinal infection. The data indicate that secretory Ig (S-IgM and S-IgA), which are likely to be produced at mucosal sites, increase in the serum of HIV-1-infected patients.
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PMID:Secretory immunoglobulins in serum from human immunodeficiency virus (HIV)-infected patients. 135 13

Antiretroviral therapy with zidovudine is indicated in patients with CD4 cell counts below 500 per mm3 (500 x 10(6) per L). Patients intolerant of zidovudine and those with advanced human immunodeficiency virus infection may benefit from newer antiretroviral agents, such as didanosine (ddl) or zalcitabine (ddC). Prophylactic therapy for Pneumocystis carinii pneumonia is indicated in patients with CD4 cell counts below 200 per mm3 (200 x 10(6) per L), in patients with CD4 cell counts less than 20 percent of the total lymphocytes and in patients with a prior history of P. carinii infection. In addition, prophylaxis is often initiated if thrush is present, even when CD4 cell counts are above 200. Trimethoprim-sulfamethoxazole is the drug of choice for Pneumocystis prophylaxis; aerosolized pentamidine is reserved for patients unable to tolerate trimethoprim-sulfamethoxazole. Oral candidiasis is treated with nystatin suspension, clotrimazole troches, ketoconazole or fluconazole, with fluconazole used for resistant or more invasive infection. Finally, acyclovir is used to treat herpes zoster or herpes simplex virus infection.
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PMID:Update on drug therapy for HIV and related infections in adults. 835 31

The low copy number of human immunodeficiency virus 1 (HIV-1) DNA infected cells precludes routine detection by in situ hybridization. The inability to detect cells latently infected by HIV-1 makes difficult the study of factors that induce viral transcription, an essential factor in the development of the acquired immune deficiency syndrome (AIDS). A sensitive and rapid technique to detect HIV-1 DNA could be used as a diagnostic test for AIDS and to differentiate latent versus active viral infection. We describe a 3-h technique whereby HIV-1 DNA is amplified by hot start polymerase chain reaction (PCR) and detected directly in infected cells. The specificity of the assay was demonstrated by double labeling the positive cells with CD4. Using a CR10 HIV-1-infected cell line, the 90% of cells that were HIV-1 DNA positive could be distinguished from the 10% that were actively expressing HIV-1 RNA. The PCR in situ technique should allow for the direct localization of DNA sequences in cells that would otherwise be undetectable by conventional in situ analysis.
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PMID:Rapid in situ detection of PCR-amplified HIV-1 DNA. 136 73

Although virus infections have been classically studied with "cell-free" virion preparations, many animal viruses are able to spread both in vitro and in vivo by inducing cell-cell fusion. An efficient system to monitor the cell-to-cell spread of HIV-1 has been developed employing chronically infected H9 donor cells. Under appropriate conditions of cocultivation with uninfected cells, the synthesis of unintegrated viral DNA, monitored by Southern blot hybridization, occurred between 2 and 4 hr following infection; viral proteins were detected 8 to 12 hr following cocultivation and progeny virions were released into the medium by 16 hr. The use of metabolic inhibitors or specific envelope/receptor antibodies revealed that the cell-to-cell spread of HIV required: (1) gp120-CD4 interaction and (2) reverse transcription. Light and electron microscopy, fluorescent dye redistribution, and soluble CD4 competition experiments all demonstrated that the HIV-induced cell-cell fusion began within 10 to 30 min of cocultivation. Surprisingly, the electron microscopic analyses also suggested that budding or mature virus particles did not participate in this process. Thus the virus-induced cell-cell fusion observed is very likely the result of gp120/gp41 proteins, on the surface of infected cells, interacting with CD4 molecules on uninfected cells. These findings are of immediate importance in understanding the mechanism(s) of HIV-1 transmission in vivo and for the design of effective vaccines and antiviral agents.
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PMID:Cell-to-cell spread of HIV-1 occurs within minutes and may not involve the participation of virus particles. 137 Jul 39

Cytological smears (CS), taken from the lateral border of the tongue of HIV-seropositive patients (HIV+) (n = 34) and of seronegative controls (HIV-) (n = 16), were examined by means of immunocytochemistry (APAAP) for the distribution patterns of different cytokeratins and MHC class II antigens. Compared with HIV- patients in CS of HIV-infected patients cornification associated cytokeratins 10/11 were increased, while the number of keratinocytes positive for cytokeratins 13/16 was comparable in both groups. Expression of simple epithelial cytokeratins 19, rarely observed in CS of HIV- patients, was a frequent findings in CS of HIV+ patients. Keratinocytes positive for MHC class II antigens were observed in CS of 12/34 HIV+, while all control CS were negative. In the group of HIV+ patients no correlation was found between the clinical presence of HL and the expression of cytokeratins or class II antigens. The altered distribution of cytokeratins may reflect local responses to proliferative stimuli or local inflammation due to the presence of microbial antigens or may occur as a general unspecific reaction in the setting of systemic viral infection. This non-invasive technique seems to be a valuable tool to determine the proliferation rate of oral epithelial cells.
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PMID:Distribution of cytokeratins in oral cytological smears of HIV-infected patients. 137 35


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