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)

To elucidate the functions of human immunodeficiency virus type 1 (HIV-1) genes in a nonhuman primate model, we have constructed infectious recombinant viruses (chimeras) between the pathogenic molecular clone of simian immunodeficiency virus (SIV) SIVmac239 and molecular clones of HIV-1 that differ in phenotypic properties controlled by the env gene. HIV-1SF33 is a T-cell-line-tropic virus which induces syncytia, and HIV-1SF162 is a macrophage-tropic virus that does not induce syncytia. A DNA fragment encoding tat, rev, and env (gp160) of SIVmac239 has been replaced with the counterpart genetic region of HIV-1SF33 and HIV-1SF162 to derive chimeric recombinant simian/human immunodeficiency virus (SHIV) strains SHIVSF33 and SHIVSF162, respectively. In the acute infection stage, macaques inoculated with SHIVSF33 had levels of viremia similar to macaques infected with SIVmac239, whereas virus loads were 1/10th to 1/100th those in macaques infected with SHIVSF162. Of note is the relatively small amount of virus detected in lymph nodes of SHIVSF162-infected macaques. In the chronic infection stage, macaques infected with SHIVSF33 also showed higher virus loads than macaques infected with SHIVSF162. Virus persists for over 1 year, as demonstrated by PCR for amplification of viral DNA in all animals and by virus isolation in some animals. Antiviral antibodies, including antibodies to the HIV-1 env glycoprotein (gp160), were detected; titers of antiviral antibodies were higher in macaques infected with SHIVSF33 than in macaques infected with SHIVSF162. Although virus has persisted for over 1 year after inoculation, these animals have remained healthy with no signs of immunodeficiency. These findings demonstrate the utility of the SHIV/macaque model for analyzing HIV-1 env gene functions and for evaluating vaccines based on HIV-1 env antigens.
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PMID:Persistent infection of rhesus macaques with T-cell-line-tropic and macrophage-tropic clones of simian/human immunodeficiency viruses (SHIV). 763 18

SCID mice were engrafted with human foetal liver, thymus and lung. Human cells were subsequently detected among peripheral blood leukocytes for 81% of tested animals and in tissue implants for 100% of tested animals. SCID-hu mice received intraperitoneal injections of human immunodeficiency virus type 1 (HIV1) at from 20 up to 20,000 median tissue culture infectious doses (TCID5). HIV1 infection was detected by means of cell culture and polymerase chain reaction both in blood and implants, up to 58 days after infection. The rate of infection was dependent upon the inoculated dose: the frequency of thymus infection ranged from 14% with 20-500 TCID50 up to 100% with 20,000 TCID50. HIV1 infection was detected less frequently in blood leukocytes than in thymus. Thymus virus load ranged from 40 to 50,000 HIV1 provirus copies per million cells and was not correlated with either infectious dose or viraemia. Thymus T-cell depletion was observed mainly in the CD1+4+8+ immature thymocyte compartment. The same rate of SCID-hu mouse infection was obtained using three different primary HIV1 isolates, suggesting that infection was not restricted to a few particular virus strains. The systemic infection of SCID-hu mice following intraperitoneal virus injection mimics some traits of human HIV infection and provides a promising, novel approach for future investigations in this field.
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PMID:Dose-dependent systemic human immunodeficiency virus infection of SCID-hu mice after intraperitoneal virus injection. 763 34

A nonselective ex vivo assay was used to directly detect and quantify zidovudine (AZT)-resistant human immunodeficiency virus type 1 (HIV-1) in the blood of treated and untreated patients. In contrast to previous reports, drug-resistant virus was detected in peripheral blood mononuclear cells of a few of the patients who had never received AZT. The AZT resistance of HIV-1 isolates from one untreated individual was confirmed by further susceptibility studies in vitro and by the finding of a characteristic mutation (Lys-->Arg at codon 70) in the reverse transcriptase. In patients who were clinically stable while on AZT, HIV-1 titers in plasma and mononuclear cells were generally low but resistant viruses already predominated. In those individuals who were deteriorating despite AZT administration, high levels of viremia were observed, and the resistance phenotype was nearly universal. These findings serve to emphasize the magnitude of the AZT-resistance problem in patients on drug treatment.
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PMID:Quantitation of zidovudine-resistant human immunodeficiency virus type 1 in the blood of treated and untreated patients. 767 40

The effect of zidovudine (500 mg/day) on 32 asymptomatic subjects seropositive for human immunodeficiency virus (HIV) was evaluated by monitoring the concentrations of infections HIV-carrying blood mononuclear cells and serum virus particles. After 3 months of treatment, a significant reduction in cellular virus load (P < .001) and a marginal decrease in serum viremia (P = .068) were noted. After 6 months, 14 patients (44%) maintained a > or = 50% reduction in virus load, 12 patients (37%) had a virus load that declined by > 50% at 3 months but returned to the initial level at 6 months, and 6 patients (19%) retained their initial virus load. Thus, virus load measurements permit reliable follow-up of antiviral therapy on an individual basis and may enable the identification of patients for whom zidovudine is efficacious.
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PMID:Early identification of human immunodeficiency virus-infected asymptomatic subjects susceptible to zidovudine by quantitative viral coculture and reverse transcription-linked polymerase chain reaction. 768 5

The prevalence and characteristics of hepatitis C virus (HCV) infection in 226 patients who were seropositive for human immunodeficiency virus (HIV) were determined. Antibody to HCV (anti-HCV) was detected by enzyme immunoassay (EIA), and positive results were confirmed by a neutralization EIA or recombinant immunoblot assay. The prevalence of anti-HCV was 8%. Intravenous drug use was the most common risk factor for HCV infection (61.1% of patients), and 52.4% of intravenous drug users were seropositive for anti-HCV (HCV+). Only 16.7% of HCV+ patients had AIDS, as compared with 37.4% of anti-HCV-seronegative (HCV-) patients (P = .04). The prevalence of hepatitis B virus markers in patients with and without anti-HCV was similar. The CD4+ lymphocyte counts were higher for HCV+ patients than for HCV- patients (P = .001), and the prevalence of anti-HCV decreased in parallel with CD4+ counts. Elevated liver function test values were more common for HCV+ patients than for HCV- patients (61.1% vs. 26.0%; P < .01), but abnormalities were usually slight (< 2-fold elevation in values). HCV viremia was detected by the polymerase chain reaction in 88.2% of HCV+ patients. Despite the coexistence of HIV and HCV infection, liver disease appeared to be mild, and HCV infection did not appear to increase the severity of HIV infection. Serological tests for HCV appear to underestimate the prevalence of HCV infection in patients with advanced HIV infection or AIDS.
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PMID:Hepatitis C virus infection in patients infected with the human immunodeficiency virus. 768 86

Methods for the absolute quantitation of nucleic acids present in small amounts in biological samples (competitive PCR and competitive reverse transcription PCR) were applied to the direct monitoring of specific anti-human immunodeficiency virus type 1 (HIV-1) therapy. With these techniques, different parameters of HIV-1 activity (including genomic RNA copy numbers in plasma, proviral and late transcript copy numbers in peripheral blood lymphocytes, and mean transcriptional activity per each HIV-1 provirus) were monitored during therapy with azidothymidine or ddI. In most of these treated patients, a direct response to the antiretroviral compounds employed was detected during the first few weeks of treatment, as documented by a fast decrease of all molecular indexes of HIV-1 activity. However, residual viral replication (albeit at minimal levels) was documented during therapy in all subjects monitored in this study. In a minority of the patients under study (3 of 12), the drug-dependent viral inhibition was maintained throughout the observation time (213 to 791 days), but in 9 patients a rebound in viremia level was detected during therapy with competitive reverse transcription PCR. Sequencing analysis of a portion of the HIV-1 gene pol from cell-free virions showed that circulating viral variants bearing at least two mutations compatible with azidothymidine or ddI resistance were detectable in the patients who exhibited a rebound in cell-free HIV-1 genomic RNA copy numbers in plasma but not in one patient who maintained (for 455 days) lowered levels of viral load during ddI treatment.
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PMID:Quantitative molecular monitoring of human immunodeficiency virus type 1 activity during therapy with specific antiretroviral compounds. 769 34

Parvovirus B19 has been described as a cause of chronic anemia in immunosuppressed patients, including those infected with human immunodeficiency virus (HIV). In this study serological assays and the polymerase chain reaction (PCR) were used to establish the prevalence of both prior and active infection due to parvovirus B19 among a general population of 105 HIV-infected individuals (cohort I) and among 22 HIV-infected patients with anemia (cohort II). Eight individuals in cohort I (7.6%) had IgG antibodies to parvovirus B19, while none had B19-specific IgM antibodies. In cohort II, four patients (18.2%) had B19-specific IgG antibodies and none had IgM antibodies. Only one person in cohort I (0.95%) and one person in cohort II (4.5%) had evidence on PCR of persistent infection with parvovirus B19; both of these patients lacked IgG and IgM antibodies to parvovirus. Both individuals with B19 viremia were anemic and had CD4 lymphocyte counts suggesting advanced immunosuppression (< 50/mm3). The observed low prevalences of B19 seropositivity and active B19 infection differ from the rates documented in previous studies and indicate that infection with parvovirus B19 is uncommon in some groups of HIV-infected patients.
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PMID:Infection due to parvovirus B19 in patients infected with human immunodeficiency virus. 772 46

In vitro, recombinant soluble CD4 (rsCD4) attaches to and inactivates human immunodeficiency virus (HIV). To determine if prolonged therapy with high-dose intravenous rsCD4 provides an in vivo benefit, we gave three HIV-1-infected patients with AIDS, whose isolates were susceptible in vitro to rsCD4, 10 mg/kg of rsCD4 for 4 weeks, 5 mg/kg for 4 weeks, and 1 mg/kg for 2 weeks. Single-dose pharmacokinetic studies performed prior to this showed transient in vivo decreases of HIV-1 plasma viremia in all three subjects. Surrogate markers of HIV activity, clinical status, HIV-1 p24 antigen, plasma HIV-1 titers, and peripheral blood mononuclear cell (PBMC) intracellular titers of virus were measured at entry, and every other week after onset of therapy. All subjects demonstrated rsCD4 concentration-dependent reduction in plasma viremia, with two subjects having complete neutralization of cell-free virus. The third subject's isolate was relatively resistant to the in vivo effects of rsCD4 and only partial reduction in plasma virus titers was obtained, even at the highest dose of 10 mg/kg. There was no change in the PBMC intracellular viral titer or surrogate markers of HIV-1 activity (including CD4 cell count and beta 2-microglobulin). There was subjective improvement in clinical symptoms, and all subjects gained weight with the highest doses of rsCD4. rsCD4 exhibited linear pharmacokinetics over the dose range studied. We conclude that high-dose intravenous rsCD4 can be safely given for up to 10 weeks and that it has a stable pharmacokinetic profile.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Phase I study of high-dose, intravenous rsCD4 in subjects with advanced HIV-1 infection. 774 91

The changes in viremia levels and the development of drug-related mutations were examined in 26 patients with symptomatic human immunodeficiency virus type 1 (HIV-1) infection participating in a randomized trial comparing alternating (A) and simultaneous (S) regimens of zidovudine and didanosine therapy. Patients on both arms had significant reduction in serum RNA copies from baseline throughout the 2 years of study. Significant differences between the two arms were demonstrated over the first 2-3 months of therapy. Analyses with nested polymerase chain reaction revealed that the emergence of the didanosine-related position 74 Leu-->Val mutation was significantly blocked in both regimens, while the zidovudine-related mutation at codon 215 was not affected. Determination of the overall durability of the antiviremic effect of the A and S regimens of zidovudine and didanosine and clinical implications of the results require further research.
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PMID:Human immunodeficiency virus type 1 (HIV-1) viremia changes and development of drug-related mutations in patients with symptomatic HIV-1 infection receiving alternating or simultaneous zidovudine and didanosine therapy. 775 11

We studied the perinatal transmission of hepatitis C virus (HCV) in 70 high risk mother/infant pairs. Seventy-six percent of the mothers (53 of 70) were coinfected with human immunodeficiency virus (HIV) and 79% (55 of 70) had a history of drug addiction. During the follow-up HCV RNA was detected in 14 of 70 (20%) infants: 12% (2 of 17) in infants born to HIV-negative mothers; and 23% (12 of 53) in infants to HIV-positive mothers. The rate of vertical transmission was significantly higher in vaginally delivered infants than in those delivered by cesarean section (32% vs. 6%; P < 0.05). All 56 uninfected infants lost passively acquired anti-HCV by age 9 +/- 4 months and only 2 of 56 infants (4%) had evidence of HIV infection. Four of 14 HCV RNA-positive infants (29%) had evidence of HIV coinfection. We observed 3 clinical patterns of HCV infection: a transient viremia in 2 infants; an acute pattern in 2 infants; and a chronic pattern in 10 infants. All 4 HIV-coinfected infants had chronic HCV infection. All infants with a chronic pattern, had increased alanine aminotransferase values for more than 6 months and 5 had a liver biopsy that showed signs of chronic persistent hepatitis. HCV perinatal transmission was more frequent in infants born to HIV-coinfected mothers than in infants born to HIV-noninfected women, particularly when delivered vaginally.
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PMID:Perinatal transmission and manifestation of hepatitis C virus infection in a high risk population. 776 Nov 84


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