scholarly journals Persistence of Human Immunodeficiency Virus (HIV) Type 1 DNA in Peripheral Blood Despite Prolonged Suppression of Plasma HIV‐1 RNA in Children

2002 ◽  
Vol 185 (10) ◽  
pp. 1409-1416 ◽  
Author(s):  
Akihiko Saitoh ◽  
Karen Hsia ◽  
Terence Fenton ◽  
Christine A. Powell ◽  
Cindy Christopherson ◽  
...  
Keyword(s):  
Human Immunodeficiency Virus ◽  
Peripheral Blood ◽  
Immunodeficiency Virus ◽  
Hiv Type 1 ◽  
Hiv 1

scholarly journals Membrane-Anchored Peptide Inhibits Human Immunodeficiency Virus Entry

2001 ◽  
Vol 75 (6) ◽  
pp. 3038-3042 ◽  
Author(s):  
Markus Hildinger ◽  
Matthias T. Dittmar ◽  
Patricia Schult-Dietrich ◽  
Boris Fehse ◽  
Barbara S. Schnierle ◽  
...  
Keyword(s):  
Human Immunodeficiency Virus ◽  
T Helper ◽  
Immunodeficiency Virus ◽  
Retrovirus Vector ◽  
Human Immunodeficiency Virus Entry ◽  
Hiv Type 1 ◽  
Heptad Repeats ◽  
Hiv 1 ◽  
Gp41 Envelope

ABSTRACT Peptides derived from the heptad repeats of human immunodeficiency virus (HIV) gp41 envelope glycoprotein, such as T20, can efficiently inhibit HIV type 1 (HIV-1) entry. In this study, replication of HIV-1 was inhibited more than 100-fold in a T-helper cell line transduced with a retrovirus vector expressing membrane-anchored T20 on the cell surface. Inhibition was independent of coreceptor usage.

scholarly journals Evolution of Envelope Sequences from the Genital Tract and Peripheral Blood of Women Infected with Clade A Human Immunodeficiency Virus Type 1

1998 ◽  
Vol 72 (10) ◽  
pp. 8240-8251 ◽  
Author(s):  
Mary Poss ◽  
Allen G. Rodrigo ◽  
John J. Gosink ◽  
Gerald H. Learn ◽  
Dana de Vange Panteleeff ◽  
...  
Keyword(s):  
Amino Acids ◽  
Human Immunodeficiency Virus ◽  
Human Immunodeficiency Virus Type ◽  
Virus Type ◽  
Peripheral Blood ◽  
Tissue Compartment ◽  
Immunodeficiency Virus ◽  
Hiv 1 ◽  
Over Time

ABSTRACT The development of viral diversity during the course of human immunodeficiency virus type 1 (HIV-1) infection may significantly influence viral pathogenesis. The paradigm for HIV-1 evolution is based primarily on studies of male cohorts in which individuals were presumably infected with a single virus variant of subtype B HIV-1. In this study, we evaluated virus evolution based on sequence information of the V1, V2, and V3 portions of HIV-1 clade A envelope genes obtained from peripheral blood and cervical secretions of three women with genetically heterogeneous viral populations near seroconversion. At the first sample following seroconversion, the number of nonsynonymous substitutions per potential nonsynonymous site (dn) significantly exceeded substitutions at potential synonymous sites (ds) in plasma viral sequences from all individuals. Generally, values of dn remained higher than values of ds as sequences from blood or mucosa evolved. Mutations affected each of the three variable regions of the envelope gene differently; insertions and deletions dominated changes in V1, substitutions involving charged amino acids occurred in V2, and sequential replacement of amino acids over time at a small subset of positions distinguished V3. The relationship among envelope nucleotide sequences obtained from peripheral blood mononuclear cells, plasma, and cervical secretions was evaluated for each individual by both phylogenetic and phenetic analyses. In all subjects, sequences from within each tissue compartment were more closely related to each other than to sequences from other tissues (phylogenetic tissue compartmentalization). At time points after seroconversion in two individuals, there was also greater genetic identity among sequences from the same tissue compartment than among sequences from different tissue compartments (phenetic tissue compartmentalization). Over time, temporal phylogenetic and phenetic structure was detectable in mucosal and plasma viral samples from all three women, suggesting a continual process of migration of one or a few infected cells into each compartment followed by localized expansion and evolution of that population.

scholarly journals Use of a Novel Chimeric Mouse Model with a Functionally Active Human Immune System To Study Human Immunodeficiency Virus Type 1 Infection

2007 ◽  
Vol 14 (4) ◽  
pp. 391-396 ◽  
Author(s):  
Dong Sung An ◽  
Betty Poon ◽  
Raphael Ho Tsong Fang ◽  
Kees Weijer ◽  
Bianca Blom ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Human Immunodeficiency Virus ◽  
Peripheral Blood ◽  
Small Animal ◽  
Small Animal Model ◽  
Human Immune System ◽  
Immunodeficiency Virus ◽  
Human Immune ◽  
Hiv 1

ABSTRACT The goal of this study was to develop a small-animal model to study human immunodeficiency virus type 1 (HIV-1) pathogenesis in blood and primary and secondary lymphoid organs. Rag2−/−γc −/− mice that are neonatally injected with human CD34+ cells develop a functional human immune system (HIS), with human hematopoietic cells being found in the thymuses, peripheral blood, spleens, and bone marrow of the animals (hereafter these animals are referred to as HIS-Rag2−/−γc −/− mice). HIS-Rag2−/−γc −/− mice were infected with small amounts of CCR5-tropic HIV-1. Viral replication and immunophenotypic changes in the human cells in peripheral blood and lymphoid organs were examined. The productive infection of human cells in peripheral blood, thymus and spleen tissue, and bone marrow was detected. Ratios of CD4+ T cells to CD8+ T cells in the infected animals declined. Although no specific anti-HIV-1 immune responses were detected, immunoglobulin M (IgM) and IgG antibodies to an unidentified fetal calf serum protein present in the virus preparation were found in the inoculated animals. Thus, we have shown that the HIS-Rag2−/−γc −/− mouse model can be used for infection with low doses of CCR5-tropic HIV-1, which is most commonly transmitted during primary infections. HIS-Rag2−/−γc −/− mice can serve as a small-animal model for investigating HIV-1 pathogenesis and testing potential HIV-1 therapies, and studies with this model may replace some long and costly studies with nonhuman primates.

scholarly journals Effect of Human Immunodeficiency Virus (HIV) Type 1 Viral Genotype on Mother‐to‐Child Transmission of HIV‐1

2000 ◽  
Vol 181 (2) ◽  
pp. 746-749 ◽  
Author(s):  
Melanie C. M. Murray ◽  
Joanne E. Embree ◽  
Sue G. Ramdahin ◽  
Aggrey O. Anzala ◽  
Simon Njenga ◽  
...  
Keyword(s):  
Human Immunodeficiency Virus ◽  
Mother To Child Transmission ◽  
Viral Genotype ◽  
Child Transmission ◽  
Immunodeficiency Virus ◽  
Hiv Type 1 ◽  
Mother To Child ◽  
Hiv 1

scholarly journals Inhibition of CD3/CD28-Mediated Activation of the MEK/ERK Signaling Pathway Represses Replication of X4 but Not R5 Human Immunodeficiency Virus Type 1 in Peripheral Blood CD4+T Lymphocytes

2000 ◽  
Vol 74 (6) ◽  
pp. 2558-2566 ◽  
Author(s):  
Waldemar Popik ◽  
Paula M. Pitha
Keyword(s):  
Human Immunodeficiency Virus ◽  
T Lymphocytes ◽  
Human Immunodeficiency Virus Type ◽  
Peripheral Blood ◽  
Erk Signaling ◽  
Erk Pathway ◽  
Immunodeficiency Virus ◽  
Hiv 1 ◽  
In Cells

ABSTRACT Binding of human immunodeficiency virus type 1 (HIV-1) to CD4 receptors induces multiple cellular signaling pathways, including the MEK/ERK cascade. While the interaction of X4 HIV-1 with CXCR4 does not seem to activate this pathway, viruses using CCR5 for entry efficiently activate MEK/ERK kinases (W. Popik, J. E. Hesselgesser, and P. M. Pitha, J. Virol. 72:6406–6413, 1998; W. Popik and P. M. Pitha, Virology 252:210–217, 1998). Since the importance of MEK/ERK in the initial steps of viral replication is poorly understood, we have examined the role of MEK/ERK signaling in the CD3- and CD28 (CD3/CD28)-mediated activation of HIV-1 replication in resting peripheral blood CD4+ T lymphocytes infected with X4 or R5 HIV-1. We have found that the MEK/ERK inhibitor U0126 selectively inhibited CD3/CD28-stimulated replication of X4 HIV-1, while it did not affect the replication of R5 HIV-1. Inhibition of the CD3/CD28-stimulated MEK/ERK pathway did not affect the formation of the early proviral transcripts in cells infected with either X4 or R5 HIV-1, indicating that virus reverse transcription is not affected in the absence of MEK/ERK signaling. In contrast, the levels of nuclear provirus in cells infected with X4 HIV-1, detected by the formation of circular proviral DNA, was significantly lower in cells stimulated in the presence of MEK/ERK inhibitor than in the absence of the inhibitor. However, in cells infected with R5 HIV-1, the inhibition of the MEK/ERK pathway did not affect nuclear localization of the proviral DNA. These data suggest that the nuclear import of X4, but not R5, HIV-1 is dependent on a CD3/CD28-stimulated MEK/ERK pathway.

Cell-Mediated Immune Response to Human Immunodeficiency Virus (HIV) Type 1 in Seronegative Homosexual Men with Recent Sexual Exposure to HIV-1

1992 ◽  
Vol 165 (6) ◽  
pp. 1012-1019 ◽  
Author(s):  
Mario Clerici ◽  
Janis V. Giorgi ◽  
Chen-Cheng Chou ◽  
Vaheideh K. Gudeman ◽  
Jerome A. Zack ◽  
...  
Keyword(s):  
Immune Response ◽  
Human Immunodeficiency Virus ◽  
Homosexual Men ◽  
Cell Mediated Immune Response ◽  
Immunodeficiency Virus ◽  
Hiv Type 1 ◽  
Hiv 1

scholarly journals Human Immunodeficiency Virus Type 1 DNA Sequences Genetically Damaged by Hypermutation Are Often Abundant in Patient Peripheral Blood Mononuclear Cells and May Be Generated during Near-Simultaneous Infection and Activation of CD4+ T Cells

2001 ◽  
Vol 75 (17) ◽  
pp. 7973-7986 ◽  
Author(s):  
Mario Janini ◽  
Melissa Rogers ◽  
Deborah R. Birx ◽  
Francine E. McCutchan
Keyword(s):  
Human Immunodeficiency Virus ◽  
T Cells ◽  
Peripheral Blood Mononuclear Cells ◽  
Peripheral Blood ◽  
Mononuclear Cells ◽  
Peripheral Blood Mononuclear ◽  
Immunodeficiency Virus ◽  
Blood Mononuclear Cells ◽  
Hiv 1

ABSTRACT G-to-A hypermutation has been sporadically observed in human immunodeficiency virus type 1 (HIV-1) proviral sequences from patient peripheral blood mononuclear cells (PBMC) and virus cultures but has not been systematically evaluated. PCR primers matched to normal and hypermutated sequences were used in conjunction with an agarose gel electrophoresis system incorporating an AT-binding dye to visualize, separate, clone, and sequence hypermutated and normal sequences in the 297-bp HIV-1 protease gene amplified from patient PBMC. Among 53 patients, including individuals infected with subtypes A through D and at different clinical stages, at least 43% of patients harbored abundant hypermutated, along with normal, protease genes. In 70 hypermutated sequences, saturation of G residues in the GA or GG dinucleotide context ranged from 20 to 94%. Levels of other mutants were not elevated, and G-to-A replacement was entirely restricted to GA or GG, and not GC or GT, dinucleotides. Sixty-nine of 70 hypermutated and 3 of 149 normal sequences had in-frame stop codons. To investigate the conditions under which hypermutation occurs in cell cultures, purified CD4+ T cells from normal donors were infected with cloned NL4-3 virus stocks at various times before and after phytohemagglutinin (PHA) activation. Hypermutation was pronounced when HIV-1 infection occurred simultaneously with, or a few hours after, PHA activation, but after 12 h or more after PHA activation, most HIV-1 sequences were normal. Hypermutated sequences generated in culture corresponded exactly in all parameters to those obtained from patient PBMC. Near-simultaneous activation and infection of CD4+ T cells may represent a window of susceptibility where the informational content of HIV-1 sequences is lost due to hypermutation.

scholarly journals Human Immunodeficiency Virus Type 1 (HIV-1)-Induced GRO-α Production Stimulates HIV-1 Replication in Macrophages and T Lymphocytes

2001 ◽  
Vol 75 (13) ◽  
pp. 5812-5822 ◽  
Author(s):  
Brian R. Lane ◽  
Robert M. Strieter ◽  
Michael J. Coffey ◽  
David M. Markovitz
Keyword(s):  
Human Immunodeficiency Virus ◽  
Mononuclear Cells ◽  
Human Monocyte ◽  
Peripheral Blood Mononuclear ◽  
Chemokine Production ◽  
Immunodeficiency Virus ◽  
Hiv Type 1 ◽  
Early Effects ◽  
Hiv 1

ABSTRACT We examined the early effects of infection by CCR5-using (R5 human immunodeficiency virus [HIV]) and CXCR4-using (X4 HIV) strains of HIV type 1 (HIV-1) on chemokine production by primary human monocyte-derived macrophages (MDM). While R5 HIV, but not X4 HIV, replicated in MDM, we found that the production of the C-X-C chemokine growth-regulated oncogene alpha (GRO-α) was markedly stimulated by X4 HIV and, to a much lesser extent, by R5 HIV. HIV-1 gp120 engagement of CXCR4 initiated the stimulation of GRO-α production, an effect blocked by antibodies to CXCR4. GRO-α then fed back and stimulated HIV-1 replication in both MDM and lymphocytes, and antibodies that neutralize GRO-α or CXCR2 (the receptor for GRO-α) markedly reduced viral replication in MDM and peripheral blood mononuclear cells. Therefore, activation of MDM by HIV-1 gp120 engagement of CXCR4 initiates an autocrine-paracrine loop that may be important in disease progression after the emergence of X4 HIV.

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