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The molecular biology of the preinte...

Pierson, Ted C.

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The molecular biology of the preintegration state of HIV-1 latency.

紀錄類型:	書目-語言資料,印刷品 : Monograph/item
正題名/作者:	The molecular biology of the preintegration state of HIV-1 latency./
作者:	Pierson, Ted C.
面頁冊數:	123 p.
附註:	Adviser: Robert F. Siliciano.
Contained By:	Dissertation Abstracts International62-10B.
標題:	Health Sciences, Immunology. -
電子資源:	http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3028315
ISBN:	0493403663

The molecular biology of the preintegration state of HIV-1 latency.
Pierson, Ted C.

The molecular biology of the preintegration state of HIV-1 latency. - 123 p.

Adviser: Robert F. Siliciano.

Thesis (Ph.D.)--The Johns Hopkins University, 2002.

The infection of activated CD4+ T lymphocytes by HIV-1 is characterized by the reverse transcription of the viral genome, which gives rise to a functional preintegration complex (PIC) capable of integrating the viral cDNA into the host cell chromosome. In contrast, the infection of resting cells is blocked prior to integration of the viral genome due to a block at virus entry, an inability to reverse transcribe the viral RNA and/or a failure to import the PIC into the nucleus. To clarify the nature of the viral cDNA in the preintegration state, we examined the fate of the viral genome following the infection of highly purified resting T cells. We demonstrate that both X4 and R5 viruses have some capacity to bind to and enter resting T lymphocytes. This finding is interpreted with respect to the chemokine receptor utilization of virus resident in the resting T cell compartment.

ISBN: 0493403663Subjects--Topical Terms:

1017716
Health Sciences, Immunology.

The molecular biology of the preintegration state of HIV-1 latency.
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245 1 0 $a The molecular biology of the preintegration state of HIV-1 latency.
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520 $a The infection of activated CD4+ T lymphocytes by HIV-1 is characterized by the reverse transcription of the viral genome, which gives rise to a functional preintegration complex (PIC) capable of integrating the viral cDNA into the host cell chromosome. In contrast, the infection of resting cells is blocked prior to integration of the viral genome due to a block at virus entry, an inability to reverse transcribe the viral RNA and/or a failure to import the PIC into the nucleus. To clarify the nature of the viral cDNA in the preintegration state, we examined the fate of the viral genome following the infection of highly purified resting T cells. We demonstrate that both X4 and R5 viruses have some capacity to bind to and enter resting T lymphocytes. This finding is interpreted with respect to the chemokine receptor utilization of virus resident in the resting T cell compartment.
520 $a To characterize the progress of the reverse transcription reaction in resting T cells, a novel linker ligation assay capable of detecting and characterizing the full-length double stranded cDNA was developed. We demonstrate that reverse transcription proceeds to completion in highly purified resting T cells with kinetics far slower than that observed in activated T cells. Analysis of the termini of the HIV-1 genome in resting cells revealed that the integrase protein had processed some of these molecules. Interestingly, a large fraction of the reverse transcription products contain truncations at their termini, making it highly unlikely that they could serve as a substrate for integration. Taken together, these data support a model of preintegration latency in which reverse transcription may proceed to completion followed by degradation of the integration substrate prior to gaining access to the host cell chromosome.
520 $a The development of surrogate markers capable of detecting residual ongoing HIV-1 replication in patients on highly active antiretroviral therapy is an important step in understanding viral dynamics and in developing new treatment strategies. In this study, we evaluate the utility of circular forms of the viral genome for the detection of recent infection of cells by HIV-1. We measured the fate of both 1- and 2-LTR circles following in vitro infection of logarithmically growing CD4<super>+</super> T cells under conditions where cell death was not a significant contributing factor. Circular forms of the viral genome were found to be highly stable and to decrease in concentration only as a function of dilution resulting from cell division. We conclude that these DNA circles are not intrinsically unstable in all cell types and suggest that the reported lability of the circles in vivo needs to be reevaluated before this assay can be used to measure recent HIV-1 infection of susceptible cells in vivo.
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