scholarly journals Growth ability in various macaque cell lines of HIV-1 with simian cell-tropism

2010 ◽  
Vol 57 (3,4) ◽  
pp. 284-292 ◽  
Author(s):  
Naoya Doi ◽  
Sachi Fujiwara ◽  
Akio Adachi ◽  
Masako Nomaguchi
Keyword(s):  
Cell Lines ◽  
Cell Tropism ◽  
Hiv 1 ◽  
Simian Cell ◽  
Growth Ability

scholarly journals Identification of the Envelope V3 Loop as a Determinant of a CD4-Negative Neuronal Cell Tropism for HIV-1

Virology ◽  
1996 ◽  
Vol 217 (2) ◽  
pp. 613-617 ◽  
Author(s):  
J.ROBERTO TRUJILLO ◽  
WEI-KUNG WANG ◽  
TUN-HOU LEE ◽  
MAX ESSEX
Keyword(s):  
Neuronal Cell ◽  
V3 Loop ◽  
Cell Tropism ◽  
Hiv 1

scholarly journals Human Immunodeficiency Virus Type 1 Replication in the Absence of Integrase-Mediated DNA Recombination: Definition of Permissive and Nonpermissive T-Cell Lines

2001 ◽  
Vol 75 (17) ◽  
pp. 7944-7955 ◽  
Author(s):  
Noriko Nakajima ◽  
Richard Lu ◽  
Alan Engelman
Keyword(s):  
Human Immunodeficiency Virus ◽  
Cell Lines ◽  
Dna Recombination ◽  
Cell Types ◽  
Class Ii ◽  
Class I ◽  
Immunodeficiency Virus ◽  
T Cell Lines ◽  
Hiv 1

ABSTRACT Functional retroviral integrase protein is thought to be essential for productive viral replication. Yet, previous studies differed on the extent to which integrase mutant viruses expressed human immunodeficiency virus type 1 (HIV-1) genes from unintegrated DNA. Although one reason for this difference was that class II integrase mutations pleiotropically affected the viral life cycle, another reason apparently depended on the identity of the infected cell. Here, we analyzed integrase mutant viral infectivities in a variety of cell types. Single-round infectivity of class I integration-specific mutant HIV-1 ranged from <0.03 to 0.3% of that of the wild type (WT) across four different T-cell lines. Based on this approximately 10-fold influence of cell type on mutant gene expression, we examined class I and class II mutant replication kinetics in seven different cell lines and two primary cell types. Unexpectedly, some cell lines supported productive class I mutant viral replication under conditions that restricted class II mutant growth. Cells were defined as permissive, semipermissive, or nonpermissive based on their ability to support the continual passage of class I integration-defective HIV-1. Mutant infectivity in semipermissive and permissive cells as quantified by 50% tissue culture infectious doses, however, was only 0.0006 to 0.005% of that of WT. Since the frequencies of mutant DNA recombination in these lines ranged from 0.023 to <0.093% of the WT, we conclude that productive replication in the absence of integrase function most likely required the illegitimate integration of HIV-1 into host chromosomes by cellular DNA recombination enzymes.

scholarly journals Adenovirus encoding HIV-1 Vpr activates caspase 9 and induces apoptotic cell death in both p53 positive and negative human tumor cell lines

Oncogene ◽  
2002 ◽  
Vol 21 (30) ◽  
pp. 4613-4625 ◽  
Author(s):  
Karuppiah Muthumani ◽  
Donghui Zhang ◽  
Daniel S Hwang ◽  
Sagar Kudchodkar ◽  
Nathanael S Dayes ◽  
...  
Keyword(s):  
Cell Death ◽  
Tumor Cell ◽  
Cell Lines ◽  
Apoptotic Cell ◽  
Human Tumor ◽  
Tumor Cell Lines ◽  
Caspase 9 ◽  
Human Tumor Cell ◽  
Human Tumor Cell Lines ◽  
Hiv 1

scholarly journals Increased LAK activity against HIV-infected cell lines in HIV-1+ individuals

2008 ◽  
Vol 89 (3) ◽  
pp. 356-361 ◽  
Author(s):  
C. GRYLLIS ◽  
M. A. WAINBERG ◽  
Z. BENTWICH ◽  
M. GORNITSKY ◽  
B. G. BRENNER
Keyword(s):  
Infected Cell ◽  
Cell Lines ◽  
Hiv 1 ◽  
Lak Activity

Elucidating the mechanisms and dynamics of drug-mediated inhibition and latency reversal in HIV-1 (HIV-1)

2017 ◽  
Author(s):  
◽  
Obiaara Ukah
Keyword(s):  
Viral Load ◽  
Cell Lines ◽  
Histone Deacetylase Inhibitors ◽  
Limit Of Detection ◽  
Drug Efficacy ◽  
Highly Active ◽  
Template Sequence ◽  
Infected Cells ◽  
Dna Substrates ◽  
Hiv 1

[ACCESS RESTRICTED TO THE UNIVERSITY OF MISSOURI AT AUTHOR'S REQUEST.] The Human Immunodeficiency Virus Type-1 (HIV-1) is the etiological agent of Acquired Immunodeficiency Syndrome, a disease that causes the host to succumb to secondary infections. There is currently no cure for HIV-1 infection, but Highly Active Anti-Retroviral Therapy (HAART) can bring the viral load in patients down to undetectable levels in the blood (less than 50 copies/mL). Furthermore, when the minimal limit of detection has been reached and the patient stops HAART, the viral load in the blood increases at an exponential rate due to the reactivation of latent HIV-1 infected cells that evaded HAART. Ongoing efforts focus on the eradication of HIV-1 by the development of potent latency reversing agents (LRAs) that can successfully reactivate latently infected cells, and of antivirals that can effectively inhibit re-establishment of infection post reactivation. This dissertation focuses on the evaluations of 2 classes of HIV-1 drugs, Non-Nucleoside Reverse Transcriptase Inhibitors (NNRTIs), and LRAs, to better understand the mechanisms by which each drug class inhibits and reactivates HIV-1 replication respectively, to aid in the effort towards the development of antivirals that will lead to HIV-1 eradication. Chapter II describes the inhibitory mechanisms of NNRTIs using biochemical methods, which may further explain the differences in potency among drugs of this class. In addition, we explain how changes in the position of HIV-1 RT in the DNA substrate sequence, and the nucleotide terminating the primer 3'-end have a significant effect on the polymerase properties of the enzyme. We demonstrate that there are NNRTI- and site-dependent differences in the potency of NNRTIs, which is demonstrated by the repositioning, or lack there of, of the primer 3'-end of DNA/DNA substrates from the polymerase active site. This is further supported by the efficiency of dNTP or NRTI incorporation in the presence of NNRTI with multiple DNA/DNA substrates, which are representative of different sites in the template sequence. We also show that there are site-dependent differences in the polymerase properties of RT, which is demonstrated by rate of dNTP incorporation and incorporation efficiency at different sites in the template sequence. Chapter III describes the various effects of different types of LRAs, such as histone deacetylase inhibitors and histone methyltransferase inhibitors, on the dynamics of HIV-1 latency reversal in latent cell lines. Here, we demonstrate the use of branched DNA in situ hybridization in combination with immunocytochemistry to study the kinetics and dynamics of latency reversal in various latent cell lines. This technique is augmented with the use of automated screening using microscopy and flow cytometry to quickly detect different populations of latent and reactivated proviruses in thousands of cells in a short amount of time. Understanding the mechanisms by which a drug affects a biological process is important for establishing drug efficacy. Such information can influence what modifications are added to, or removed from drugs, which can cause a change in drug potency. This dissertation outlines assays used to evaluate the mechanisms of various drugs, and the influence of these drugs on the dynamics of HIV-1 replication. It is our hope that the work presented here will help progress efforts to eradicate HIV-1 infection.

Evidence for Differences in MT2 Cell Tropism According to Genetic Subtypes of HIV-1: Syncytium-Inducing Variants Seem Rare Among Subtype C HIV-1 Viruses

1999 ◽  
Vol 20 (2) ◽  
pp. 115-121 ◽  
Author(s):  
Martine Peeters ◽  
Rachel Vincent ◽  
Jean-Luc Perret ◽  
Mariama Lasky ◽  
Delphine Patrel ◽  
...  
Keyword(s):  
Cell Tropism ◽  
Subtype C ◽  
Genetic Subtypes ◽  
Hiv 1
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