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Query: UMLS:C0021051 (immunodeficiency)
 71,517 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Incubation of the human T cell lymphotropic virus (HTLV)-IIIB and HTLV-RF strains of human immunodeficiency virus type 1 (HIV-1) with normal seronegative human serum under conditions that allow complement activation resulted in enhancement of infection of the MT2 human T cell line cultured in the presence of low amounts of virus. Infection of MT2 cells was assessed by measuring reverse transcriptase activity in supernatants at day 9 of culture. Complement activation by viral suspensions occurred through the alternative pathway. Opsonization of HTLV-RF viral particles with complement was sufficient to allow a productive infection to occur in cells exposed to suboptimal amounts of virus. Infection of MT2 cells with suboptimal amounts of serum-opsonized HIV-1 was suppressed by blocking the C3dg receptor (CR2, CD21) on MT2 cells with monoclonal anti-CR2 antibody and rabbit F(ab')2 anti-mouse immunoglobulin antibodies. Blocking of the gp120-binding site on CD4 under similar experimental conditions had no inhibitory effect on infection of MT2 cells with opsonized virus. Opsonization of HIV-1 with seronegative serum also resulted in a CR2-mediated enhancement of the infection of normal peripheral blood mononuclear cells and T lymphocytes. These results indicate that complement in the absence of antibody may enhance infection of C3 receptor-bearing T cells with HIV-1, and that the interaction of opsonized virus with the CR2 receptor may result by itself in the infection of target T cells in a CD4- and antibody-independent fashion.
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PMID:Complement mediates human immunodeficiency virus type 1 infection of a human T cell line in a CD4- and antibody-independent fashion. 182 39

A human Epstein-Barr virus-transformed B-cell line (IC.1) was characterized for cell surface antigen profile and permissivity to immunodeficiency virus (HIV) infection. According to cocultivation assay with MT2 cells, P24 release, and immunofluorescence assay, complement-sufficient serum enhanced in vitro infection of IC.1 cells. Enhancement occurs independently of the presence of HIV type 1-specific antibodies, although more efficiently when they are present. Blocking experiments with monoclonal antibodies demonstrated that complement receptor type 2 mediates this phenomenon and that the CD4 molecule is required for infection. Enhancement of in vitro infection on IC.1 cells appears closely related to previously described complement-mediated, antibody-dependent enhancement of HIV infection on the T-lymphoblastoid cell line MT2 (W. E. Robinson, Jr., D. C. Montefiori, and W. M. Mitchell, Lancet i:790-794, 1988).
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PMID:Antibody-dependent and antibody-independent complement-mediated enhancement of human immunodeficiency virus type 1 infection in a human, Epstein-Barr virus-transformed B-lymphocytic cell line. 184 8

The virucidal efficacy of a health care personnel hand wash product containing 0.5% parachlorometaxylenol in a sodium C14-16 olefin sulfonate formula was evaluated in in vitro tests with human immunodeficiency virus type 1 (HIV-1) in the presence of 50% whole human blood. The HTLV-IIIRF strain of HIV-1 was suspended in 50% medium-50% whole human blood and exposed to various dilutions of the hand wash product for 30 or 60 s. Following detoxification, residual infectivity was determined by a lytic cytopathogenic assay in MT2 cell cultures. No infectious HIV could be detected after a 30-s exposure to the hand wash product at dilutions of 1:5 and 1:10 and after a 60-s exposure at dilutions of 1:5, 1:10, 1:20, and 1:30. More than 99.9% of the virus was inactivated at these dilutions and exposure times.
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PMID:Evaluation of an antimicrobial soap formula for virucidal efficacy in vitro against human immunodeficiency virus in a blood-virus mixture. 261 71

In vitro inactivation of cell-free human immunodeficiency virus (CFHIV) was investigated by mixing replication-competent virions with aliquots of a culture medium (RPMI) containing increasing amounts (62.5-500 micrograms/ml) of ascorbic acid (AA) at pH7. Similarly, mixtures of CFHIV and 500 micrograms/ml AA in whole blood (WB) and leukocyte depleted blood (LDB) were made; control mixtures containing either CFHIV or AA alone in each experiment were included. After holding the mixtures for 3 h at 4 degrees C, the tubes containing WB and LDB mixtures were centrifuged to remove the blood cells. The respective supernatants, including the control aliquots, were layered over 0.5 x 10(6) MT2 cells in quadruplicate wells in microtitre plates. After 1 h of incubation at 37 degrees C in an atmosphere of 5.0% carbon dioxide to permit contact of viable virions, the fluid in each well was replaced with RPMI containing 20% fetal bovine serum (FBS). The incubation was then continued at 37 degrees C for 5 days. On the basis of (1) absence of syncytia formation, (2) 100% viability of MT2 cells as compared with the cell controls, (3) absence of p24 antigen in the culture supernates, and (4) absence of HIV DNA in MT2 cells, we conclude that 500 micrograms/ml AA, in (a) RPMI, (b) WB, or (c) LDB, inactivated CFHIV in vitro. Furthermore, we determined that addition of 500 micrograms/ml AA to platelet concentrates did not adversely affect the platelet function tests during 5 days of storage at room temperature. These data warrant further work to evaluate the mechanism of CFHIV inactivation by treatment of blood products with AA.
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PMID:In vitro inactivation of human immunodeficiency virus by ascorbic acid. 761 41

Although there are substantial differences between retroviruses originating from avian and primate species, a comparison of these two different biological systems reveals that interaction of these retroviruses with heterologous hosts involves similar biological principles. Retroviral isolates with high replicative capacity in natural targets (e.g. CD4+ lymphocytes and macrophages for human immunodeficiency viruses (HIVs) can infect other cell types [e.g. CD- astrocytes, follicular dendritic cells (FDC) in vivo and/or CD4+ neoplastic T cells in vitro] as well. These viral isolates may have a potential of infecting heterologous cells in vitro and can enlarge their host-range by establishing infection in other species, distantly related. Strains of avian sarcoma/leukemia viruses (ASLV) originating from their natural hosts, chickens, and infectious for other avian species, ducks, can frequently infect mammals (rodents). Similarly, HIV-1 strains infectious for chimpanzees possess capacity of establishing chronic infection in pig-tailed macaques. The broad host-range of retroviral isolates in both viral systems is accompanied by presence of additional structures in viral envelope. These novel or additional envelope structures may recognize alternate viral receptor(s). Moreover, the enlarged host range of primary HIV-1 isolates is evaluated by infection of neoplastic CD4+ permanent cell line, MT2, and serves as a predictive marker of progression of the viral infection toward AIDS.
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PMID:Interaction of avian sarcoma/leukemia viruses with heterologous hosts: inference for host-range and some pathogenic properties of human immunodeficiency viruses. 762 64

We tested the susceptibility of human purified, normal B lymphocytes to human immunodeficiency virus type 1 (HIV-1) infection, in the presence or absence of complement-sufficient serum and of virus-specific antibodies. Virus replication was detected when cells were infected in the presence of both complement and anti-HIV antibodies (C'-ADE conditions), by day 2 postinfection. Similar results were obtained when B lymphocytes were purified either from peripheral blood (three healthy donors) or from tonsils (four individuals with chronic tonsillitis). HIV infection was shown by polymerase chain reaction (PCR) detection of proviral sequences (gag and pol genes), by p24 antigen synthesis, and by cocultivation assay with MT2 cells. The higher p24 production was obtained when B cells were preactivated for 2 days by phorbol 12-myristate 13-acetate (PMA) before infection and then cultured in the presence of low-molecular weight B-cell growth factor (LMW-BCGF). Expression of virus envelope glycoprotein (gp) 120 could also be detected on a subpopulation of B cells (CD19+, CD22+) by flow cytometry. Blocking experiments with monoclonal antibodies (MoAbs) against CD4, CD21 (complement receptor 2 [CR2]), CD35 (CR1), CD19, and CD5 surface molecules indicated that infection of B cells involves CD4, CD21, and CD35 antigens. Indeed, blocking of CD4 receptor inhibited 10% of p24 production, and blocking of both CD21 and CD35 led to extinction of p24 signal. CR-dependent pathway is thus a major route for C'-ADE of HIV infection in normal B cells. Our results emphasize the importance of studying interactions between HIV and the complement system for better understanding infection mechanisms and the major dysfunctions of B cells in HIV-infected individuals.
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PMID:Complement and virus-specific antibody-dependent infection of normal B lymphocytes by human immunodeficiency virus type 1. 846 67

We examined the relationship between the amino acid sequences of the V2 and V3 regions of the envelope protein and the biological properties of ten human immunodeficiency virus type 1 (HIV-1) primary isolates. The infectivity, cytopathic effect (CPE), and syncytium forming activity of these primary isolates were tested against three T cell lines (CEM, MT2, and MOLT4/CL.8 cells), CD8-depleted peripheral blood mononuclear cells (PBMC), and primary monocyte-derived macrophages (MDM) from seronegative donors. In addition to the viral groups which had the syncytium inducing/T-cell line tropic (SI/TT) phenotype or non-syncytium inducing/non-T cell line tropic (NSI/NT) phenotype (including the NSI/macrophage tropic (NSI/MT) phenotype), there was a group of viruses that infected one or two T cell lines and PBMC but could not mediate syncytium formation. We therefore classified this group of viruses as a non-syncytium inducing/partial T-cell line tropic (NSI/pTT) virus. To investigate the relationship between these viral phenotypes and the sequence variability of the V2 and V3 regions of the envelope, we cloned the viral gene segment and sequenced the individual isolates. The sequence data suggested that the SI/TT type changes in the V3 sequence alone mediate a partial T cell line tropism and mild cytopathic effect and that an isolate became more virulent (SI/TT phenotype) if there were additional changes in the V2 or other regions. On the other hand, sequence changes in the V2 region alone could not mediate phenotypic changes but some additional changes in the other variable regions (for example, V3) might be required for the phenotypic changes in combination with changes in V2. These findings also suggested that amino acid changes in both the V2 and V3 region are required for the development of virulent variants of HIV-1 that outgrow during advanced stages of the disease.
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PMID:Relationship of HIV-1 envelope V2 and V3 sequences of the primary isolates to the viral phenotype. 870 63

We sought to determine the clinical significance of macrophage tropic and non-syncytium inducing isolates of human immunodeficiency virus type 1 (HIV-1) in the cerebrospinal fluid (CSF) of patients with and without AIDS dementia complex (ADC). HIV-1 was isolated from the CSF of 31 patients with and without ADC. The isolates were then characterised as to the degree of macrophage tropism by quantitation of p24 production and the presence of syncytium inducing (SI) or non-syncytium inducing (NSI) isolates by MT2 assay and SupT1 coculture. The degree of macrophage tropism varied according to the donor macrophage that was used except in strongly macrophage tropic isolates. Moderate and severe ADC (stage > or = 2) was associated with the presence of highly macrophage tropic isolates in the CSF (P = 0.01). The sensitivity and specificity values of a highly macrophage tropic isolate in the CSF for ADC stage > or = 2 were 82% and 66% respectively while the predictive value was 64%. Three of four asymptomatic patients with such highly macrophage tropic isolates in the CSF subsequently developed ADC after an average of 4 months. Twenty-eight isolates from the CSF and 23 from the blood were NSI regardless of the presence or absence of ADC. The predictive value of an SI isolate in the blood reflecting an SI isolate in the CSF was 37.5% while the predictive value of an NSI isolate in the blood reflecting an NSI in the CSF was 100%. These data suggest that host factors are essential in determining the degree of macrophage tropism in HIV-1 and that such tropism is important for the presence and possibly subsequent development of ADC. The CSF usually has NSI isolates regardless of the presence of ADC and irrespective of the presence of such isolates in the blood thereby suggesting that the CSF is behaving virologically as a separate compartment to the blood.
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PMID:The relationship between AIDS dementia complex and the presence of macrophage tropic and non-syncytium inducing isolates of human immunodeficiency virus type 1 in the cerebrospinal fluid. 879 7

9-[2-(phosphonomethoxy)ethyl]adenine (PMEA), an acyclic nucleoside phosphonate analog, is active against several retroviruses and herpesviruses and has shown anti-human immunodeficiency virus (HIV) activity in clinical trials. Serial passage of HIV type 1 (strain IIIb, in MT2 cells in increasing concentrations of PMEA resulted in viruses with > 12-fold increases in their 50% inhibitory concentrations of PMEA compared with that for strain IIIb. Sequence analyses of these PMEA-selected viruses demonstrated the presence of a novel lysine-to-glutamic acid mutation at amino acid 70 (K70E) in HIV reverse transcriptase. A recombinant virus carrying the K70E mutation was constructed and showed a 10-fold increase in its 50% inhibitory concentrations of PMEA and 2',3'-dideoxy-3'-thiacytidine but showed wild-type susceptibility levels to 2',3'-dideoxycytosine, 2',3'-dideoxyinosine,2',3'-didehydro-2'3'-dideoxythymidine, 3'-azido-3'-deoxythymidine, foscarnet, and two additional phosphonates, 9-[(R)-2-(phosphonomethoxy)propyl]adenine and 9-[2,5-dihydro-5-(phosphonomethoxy)-2-furanyl]adenine. Additionally, the K70E recombinant showed a minor reduction in growth kinetics compared with those of the wild-type virus in vitro.
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PMID:Novel mutation (K70E) in human immunodeficiency virus type 1 reverse transcriptase confers decreased susceptibility to 9-[2-(phosphonomethoxy)ethyl]adenine in vitro. 887 11

The mechanism of in vitro inactivation of cell-free human immunodeficiency virus (CFHIV) with ascorbic acid (M) or Congo red (CR) was investigated with specific regard to the impact of an excess of magnesium ions on the viral inactivation. Quadruplicate reaction mixtures containing CFHIV were mixed with a virus-inactivating dose of 500 micrograms/ml ascorbic acid in RPMI medium devoid of fetal bovine serum and incubated for 3 h at 4 degrees C in two parallel sets of experiments. AA-free CFHIV and virion-free AA were included in each experiment as the positive and negative controls, respectively. After adding 10(6) MT2 cells to capture the surviving virons, the mixtures were incubated for 1 h at 37 degrees C. The cells from the first set were washed three times with Hanks balanced salt solution (HBSS) only, and those from the second set were washed with HBSS fortified with MgCl2 (1.0 mg/ml). Similarly, inactivation of CFHIV by increasing amounts of CR ranging between 12.5-100 micrograms/ml was also tested for the effect of MgCl2, except that (i) the assay was performed in subdued light, (ii) CFHIV-CR mixtures were incubated at 37 degrees C for 1 h in the dark and (iii) H9 cells were used instead of the MT-2 cells to capture the surviving virions in the test mixtures. The cells were cultured in RPMI with 20% FBS for 5 days at 37 degrees C. The absence of p24 antigen in the culture supernatant of MT2 or H9 cells indicated HIV inactivation by AA or CR, respectively. Remarkably, the cultured cells that were washed with HBSS + MgCl2 consistently expressed p24 antigen at levels comparable with those from the untreated virus control. Therefore, the apparent in vitro inactivation of CFHIV by either AA or CR was reversible as validated by washing of the cells with HBSS + MgCl2 following capture of the virions from CFHIV-AA or CFHIV-CR inactivation mixtures. These observations underscore the need for including extra magnesium ions as a control in validating various protocols used for assessing the in vitro virucidal activity of reverse transcriptase inhibitors, membrane binding dyes, or other candidate chemical agents.
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PMID:Magnesium-mediated reversal of the apparent virucidal effect of ascorbic acid or congo red reacted in vitro with the human immunodeficiency virus. 888 57


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