Human Immunodeficiency Virus (HIV) Type 1 Infection Status and In Vitro Susceptibility to HIV Infection among High-Risk HIV-I-Seronegative Hemophiliacs

1995 ◽  
Vol 172 (1) ◽  
pp. 228-231 ◽  
Author(s):  
M. M. Lederman ◽  
J. B. Jackson ◽  
B. L. Kroner ◽  
G. C. White ◽  
M. E. Eyster ◽  
...  
Keyword(s):  
Human Immunodeficiency Virus ◽  
High Risk ◽  
Hiv Infection ◽  
Infection Status ◽  
In Vitro Susceptibility ◽  
Immunodeficiency Virus ◽  
Hiv Type 1

scholarly journals Direct Phenotypical and Functional Dysregulation of Primary Human B Cells by Human Immunodeficiency Virus (HIV) Type 1 In Vitro

PLoS ONE ◽  
2012 ◽  
Vol 7 (7) ◽  
pp. e39472 ◽  
Author(s):  
Ana Judith Perisé-Barrios ◽  
María Ángeles Muñoz-Fernandez ◽  
Marjorie Pion
Keyword(s):  
Human Immunodeficiency Virus ◽  
B Cells ◽  
Human B Cells ◽  
Immunodeficiency Virus ◽  
Hiv Type 1

scholarly journals Manganese cations increase the mutation rate of human immunodeficiency virus type 1 ex vivo

1999 ◽  
Vol 80 (8) ◽  
pp. 1983-1986 ◽  
Author(s):  
Jean-Pierre Vartanian ◽  
Monica Sala ◽  
Michel Henry ◽  
Simon Wain-Hobson ◽  
Andreas Meyerhans
Keyword(s):  
Human Immunodeficiency Virus ◽  
Genetic Variation ◽  
Substrate Specificity ◽  
Hiv Infection ◽  
Mutation Rate ◽  
Reverse Transcription ◽  
Ex Vivo ◽  
Immunodeficiency Virus

Human immunodeficiency virus (HIV) reverse transcription is an error-prone process with an overall mutation rate of ∼3·4×10−5 per base per replication cycle. This rate can be modulated by changes in different components of the retrotranscription reaction. In particular, in vitro substitution of magnesium cations (Mg2+) by manganese cations (Mn2+) has been shown to increase misincorporation of deoxynucleotide triphosphates (dNTPs) and to alter substrate specificity. Here, it is shown that Mn2+ also increases the HIV mutation rate ex vivo. Treatment of permissive cells with Mn2+ and subsequent HIV infection resulted in at least 6-fold and 10-fold increases in the mutant and mutation frequencies respectively, thus illustrating a further example of how to influence HIV genetic variation.

scholarly journals Mutations That Confer Resistance to Template-Analog Inhibitors of Human Immunodeficiency Virus (HIV) Type 1 Reverse Transcriptase Lead to Severe Defects in HIV Replication

2002 ◽  
Vol 76 (8) ◽  
pp. 4068-4072 ◽  
Author(s):  
Timothy S. Fisher ◽  
Pheroze Joshi ◽  
Vinayaka R. Prasad
Keyword(s):  
Human Immunodeficiency Virus ◽  
Reverse Transcriptase ◽  
Dna Aptamer ◽  
Hiv Replication ◽  
Immunodeficiency Virus ◽  
Hiv Type 1 ◽  
High Level ◽  
Level Resistance

ABSTRACT We isolated two template analog reverse transcriptase (RT) inhibitor-resistant mutants of human immunodeficiency virus (HIV) type 1 RT by using the DNA aptamer, RT1t49. The mutations associated, N255D or N265D, displayed low-level resistance to RT1t49, while high-level resistance could be observed when both mutations were present (Dbl). Molecular clones of HIV that contained the mutations produced replication-defective virions. All three RT mutants displayed severe processivity defects. Thus, while biochemical resistance to the DNA aptamer RT1t49 can be generated in vitro via multiple mutations, the overlap between the aptamer- and template-primer-binding pockets favors mutations that also affect the RT-template-primer interaction. Therefore, viruses with such mutations are replication defective. Potent inhibition and a built-in mechanism to render aptamer-resistant viruses replication defective make this an attractive class of inhibitors.

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