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

Multiple genetic subtypes of human immunodeficiency virus type 1 (HIV-1) have been identified among internationally collected isolates. The HIV-1 epidemic in Thailand is largely due to B and E subtypes of virus. Dual infection with distinct HIV-1 subtypes would suggest that antiviral immunity evoked by one subtype can be incompletely protective against a second. Polymerase chain reaction typing and serologic typing were used to screen a panel of specimens from HIV-1-infected subjects in Thailand. Two persons simultaneously harbored HIV-1 of env subtypes B and E, and this was confirmed by colony hybridization with subtype-specific probes and nucleotide sequence analysis of a 630-bp fragment of gp120 from multiple molecular clones. In addition, both subtypes were identified in cocultured peripheral blood mononuclear cells from 1 individual. These data provide the first evidence of dual HIV-1 infection in humans and reinforce the need for polyvalent vaccines.
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PMID:Dual infection with human immunodeficiency virus type 1 of distinct envelope subtypes in humans. 770 6

We detected by PCR (Polymerase Chain Reaction) HIV-1 proviral sequences in saliva cells of 89 HIV+ subjects at different stages of disease. Twenty negative individuals not at risk of HIV infection were considered as controls. The amplification of DNA was performed using the primers of genomic env region SK68 and SK69. The presence of HIV-1 in DNA was found in 16/89 (18.0%) saliva samples from HIV-1 subjects but in none of the 20 saliva samples from healthy subjects. No statistically significant difference in the presence of HIV-1 proviral sequences in saliva was observed when comparing patients receiving AZT or no treatment and patients at different stages of infection. Conversely, a statistically significant difference among subjects with CD4+ cell counts > 400/cmm and those with CD4+ cell counts from 200 to 400/cmm, was found stratifying the subjects according to their CD4+ cell counts.
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PMID:Presence of HIV-1 proviral sequences in saliva of infected individuals in relation with clinical stage and CD4+ lymphocyte count. 774 34

The explanation of marked global variation (between 12 and 65%) in the rate of mother-to-child transmission (MCT) of HIV-1 both in developed and developing countries is inadequate. The risk of MCT ranges from one in eight to one in 1.5 pregnancies. There are marked methodological differences in the case definitions, study designs and diagnostic criteria in the various MCT investigations. Although most HIV-1 MCT appears to occur in the peripartum period, it can also occur in the intrauterine phase or immediately postpartum requiring diagnostic techniques that are not often available. Polymerase chain reaction or in situ hybridization tests for early diagnosis of MCT have been found to lack specificity for both HIV-infected and uninfected infants who are born to HIV-infected mothers and who remain HIV-seropositive during their first year of life. A second explanation for the wide variability derives from the varying case mix of any given maternal cohort. HIV infection during pregnancy and pregnant women with advanced HIV-induced immunosuppression are particularly infectious to their children. A third source of MCT variation results from selection bias in many MCT studies. It is not known whether the only mechanism of transmission in the perinatal period is transplacental or transmission occurs during delivery. Data suggest that delivery via Caesarean section halves the risk of MCT. Antiretroviral treatment (zidovudine) for HIV-infected mothers in the immediate prepartum and intrapartum period, followed by postpartum administration to their infants has reduced these infants' chance of MCT by as much as 50%. A recent study from Malawi demonstrated that HIV-1-seropositive women with vitamin A deficiency had a twofold greater risk of transmitting HIV-1 infection to their infants. The many biologic reasons for the wide variation in MCT make it unlikely that prevention will be possible through a single biologic and/or pharmacologic approach.
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PMID:Reasons for the wide variation in reported rates of mother-to-child transmission of HIV-1. 781 16

Polymerase chain reaction was performed in 251 infants born to HIV-1-seropositive mothers to diagnose HIV-1 infection. Assay specificity was invariably > 95%, regardless of age at testing, while sensitivity ranged from 15% in neonates (within 48 h of birth) to > 95% in infants over 1 month of age. Evaluation of viral burden in 43 infected infants by means of quantitative DNA-PCR disclosed that the number of HIV-1 proviruses ranged from 5 to 947 per 100,000 peripheral blood mononuclear cells. Clinical follow-up demonstrated that a high viral burden was associated significantly with disease onset.
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PMID:Mother-to-child HIV-1 transmission: quantitative assessment of viral burden as a diagnostic tool and prognostic parameter in HIV-1-infected children. 783 55

Efficiencies of insertion and extension at a single site-directed abasic lesion, X, were measured while varying 5'- and 3'-template bases adjacent to X. The preference for insertion was found to be A > G > T approximately C, with the "upstream" (3'-neighboring) template base perturbing insertion efficiencies by an order of magnitude or more. Efficiencies of synthesis past the abasic lesion depended strongly on the "downstream" (5'-neighboring) template base and on the properties of the polymerase. HIV-1 RT favored "direct" extension of X.A > X.G > X.T > X.C, by addition of the next correct nucleotide. However, it was found that X.C, least favored for direct extension, was most favored for "misalignment" extension, occurring when the DNA structure in the vicinity of the lesion collapsed to realign a primer 3'-C terminus opposite a downstream template G site. Polymerase properties have an important role in copying abasic lesions. Drosophila DNA polymerase alpha, HIV-1, and AMV reverse transcriptases had "little" difficulty inserting opposite abasic lesions, with efficiencies comparable to misinsertions opposite normal template bases. However, AMV RT did not extent past the lesion using direct or misalignment mechanisms. Wild-type and mutant T4 DNA polymerases were used to show that although exonucleolytic proofreading inhibits lesion bypass, the presence of a highly active proofreading exonuclease is not sufficient to prevent bypass.
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PMID:Nucleotide insertion and primer extension at abasic template sites in different sequence contexts. 809 71

The pigtail macaque (Macaca nemestrina) has a marked sensitivity to infection by simian immunodeficiency virus and human immunodeficiency virus type 2 (HIV-2). On this basis, we previously studied this species' susceptibility to HIV-1 and demonstrated infection in six macaques inoculated with either cell-associated HIV-1 or cell-free virus alone. This report expands upon our initial in vitro and in vivo findings. Five laboratory-adapted and one primary clinical strain of HIV-1 replicated in vitro in human and M. nemestrina peripheral blood mononuclear cells (PBMCs). Replication was enhanced when CD4+ purified PBMCs were infected and inhibited when PBMC cultures were treated with zidovudine. All six macaques demonstrated HIV-1 infection of PBMCs from 2 to 8 weeks after inoculation but nearly all PBMC cultures were negative from weeks 10 to 40. Polymerase chain reaction showed HIV-1 gag DNA in the PBMCs of all infected macaques, including times when the macaques were culture negative. All macaques developed and maintained antibodies to gag and envelope HIV-1 proteins from week 4 after inoculation through the period of observation. Five macaques showed neutralizing antibody. These findings suggest that M. nemestrina can be infected by cell-free and cell-associated HIV-1. This model of acute HIV-1 infection may help in evaluating the pathogenesis of HIV-1 replication and candidate vaccines and therapies.
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PMID:Acute infection of Macaca nemestrina by human immunodeficiency virus type 1. 810 73

Human immunodeficiency virus 1 (HIV-1) infection is associated with a vigorous cellular immune response that allows detection of cytotoxic T lymphocyte (CTL) activity using freshly isolated peripheral blood mononuclear cells (PBMC). Although restricting class I antigens and epitopes recognized by HIV-1-specific CTL have been defined, the effector cells mediating this vigorous response have been characterized less well. Specifically, no studies have addressed the breadth and duration of response to a defined epitope. In the present study, a longitudinal analysis of T cell receptor (TCR) gene usage by CTL clones was performed in a seropositive person using TCR gene sequences as a means of tracking responses to a well-defined epitope in the glycoprotein 41 transmembrane protein. 10 CTL clones specific for this human histocompatibility leukocyte antigen-B14-restricted epitope were isolated at multiple time points over a 31-mo period. All clones were derived from a single asymptomatic HIV-1-infected individual with a vigorous response to this epitope that was detectable using unstimulated PBMC. Polymerase chain reaction amplification using V alpha and V beta family-specific primers was performed on each clone, followed by DNA sequencing of the V-D-J regions. All 10 clones utilized V alpha 14 and V beta 4 genes. Sequence analysis of the TCR revealed the first nine clones isolated to also be identical at the nucleotide level. The TCR-alpha junctional region sequence of the tenth clone was identical to the junctional region sequences of the other nine, but this clone utilized distinct D beta and J beta gene segments. This study provides evidence that the observed high degree of HIV-1-specific CTL activity may be due to monoclonal or oligoclonal expansion of specific effector cells, and that progeny of a particular CTL clone may persist for prolonged periods in vivo in the presence of a chronic productive viral infection. The observed limited TCR diversity against an immunodominant epitope may limit recognition of virus variants with mutations in regions interacting with the TCR, thereby facilitating immune escape.
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PMID:Longitudinal analysis of T cell receptor (TCR) gene usage by human immunodeficiency virus 1 envelope-specific cytotoxic T lymphocyte clones reveals a limited TCR repertoire. 814 43

In asymptomatic human immunodeficiency virus (HIV) infection in humans, disturbed T cell functions such as anergy and programmed cell death, thought to result from inappropriate signaling by antigen-presenting cells due to HIV infection, precede increase in virus load, decline in CD4+ T cell numbers, and subsequent disease progression. Here, in 3 long-term HIV-1-infected asymptomatic chimpanzees, antigen-presenting cell function was intact and T cells had normal proliferative capacity with no evidence of HIV-1-associated programmed cell death. Polymerase chain reaction analysis demonstrated low frequencies of cells harboring proviral DNA. Primary virus isolation from the infected animals demonstrated the absence of monocytotropic HIV-1 variants, in concordance with complete insusceptibility of chimpanzee monocytes for HIV-1 infection. Possibly, because of the incapacity of HIV-1 to infect monocytes, systemic immune dysfunction will not occur, contributing to controlled viral replication and maintenance of the asymptomatic state in HIV-infected chimpanzees.
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PMID:Lack of T cell dysfunction and programmed cell death in human immunodeficiency virus type 1-infected chimpanzees correlates with absence of monocytotropic variants. 819 28

Prophylactic zidovudine (ZDV) therapy was evaluated in the feline immunodeficiency virus (FIV)-inoculated cat model for HIV-1 infection in humans. ZDV treatment (30 mg/kg/day via continuous subcutaneous infusion) was initiated 48 h prior to virus inoculation and continued for 28 days. Transient plasma antigenemia evident in six of six untreated cats at week 2 post-inoculation (pi) was absent in the ZDV-treated cats although at 10 and 14 weeks pi (6 and 10 weeks after drug treatment), one of the ZDV-treated cats had low-level antigenemia. Both CD4 and CD8 lymphocyte numbers were consistently higher in the ZDV-treated cats when compared to both the FIV-inoculated untreated cats and the virus-naive, age-matched controls. CD4:CD8 ratios were lower for the ZDV-treated cats than either the FIV-inoculated untreated or virus-naive, control cats. The decreased CD4:CD8 ratios were the result of an increase in CD8 lymphocytes in the ZDV-treated cats while decreased ratios in the FIV-inoculated untreated cats were due to cell loss. Both ZDV-treated and untreated cats showed nearly identical FIV-specific antibody responses beginning 2 weeks pi. Polymerase chain reaction (PCR) results from blood lymphocytes showed that six of six ZDV-treated and six of six untreated cats were positive for FIV-specific gag sequences. Although primary infection was not prevented, these results suggest that prophylactic ZDV therapy deterred early systemic spread of infection mediated by viremia and delayed absolute CD4 and CD8 lymphocyte decline.
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PMID:Prophylactic ZDV therapy prevents early viremia and lymphocyte decline but not primary infection in feline immunodeficiency virus-inoculated cats. 838 67

Polymerase chain reaction (PCR) involves alternate denaturing and re-annealing of DNA in test samples in the presence of appropriate oligonucleotide primers complementary to opposite strands of the target DNA together with a heat-stable DNA polymerase, Mg2+ and the four nucleotide triphosphates. DNA target segments can be 'amplified' ten-millionfold by 25-35 such cycles. Even greater amplification (approximately 10(12)-fold) with enhanced specificity can be obtained by a second set of amplification cycles using a further pair of 'nested' primers sited within the DNA sequence defined by the original primers. PCR can be applied to the study of the whole range of transfusion-transmitted infections, both plasma and cell associated; RNA viruses can be analyzed if a DNA copy is made from the viral RNA by treatment with reverse transcriptase. In a transfusion context, the retroviruses (HIV-1, HIV-2, HTLV-I, HTLV-II), HCV and HBV have been the viruses most intensively subjected to PCR analysis. The advantages of PCR in this context include its ability to detect virus during the 'window period' or seronegative stages of infections and its value as a marker for viraemia and for the detection of viruses in products made from large pools of plasma. True immunity may also be differentiated from persistent infection in the presence of antibody. Similarly, PCR can overcome problems of diagnosis of acute infection caused by the presence of passively transferred antibody. Detailed strain differentiation is also possible by PCR, in conjunction with sequencing or with the aid of restriction endonucleases.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Polymerase chain reaction and transfusion microbiology. 838 93


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