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Size and Structure of Viral Genomes

Size and Structure of Viral Genomes

Viral genomes exhibit remarkable diversity in size, structure, and composition, influencing their replication strategies and interactions with host cells. These genomes consist of either DNA or RNA and may be linear or circular. Additionally, they can be single-stranded or double-stranded, with each configuration affecting how the virus propagates within a host. RNA viruses, for instance, generally have smaller genomes than DNA viruses, a factor that contributes to their high mutation rates and...

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CRISPR-Cas9-based Genome Engineering to Generate Jurkat Reporter Models for HIV-1 Infection with Selected Proviral Integration Sites

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HIV latency and integration site placement in five cell-based models.

Scott Sherrill-Mix¹, Mary K Lewinski, Marylinda Famiglietti

¹Department of Microbiology, University of Pennsylvania School of Medicine, Philadelphia, PA, USA. shescott@mail.med.upenn.edu

|August 20, 2013

Summary

Understanding human immunodeficiency virus (HIV) latency is key to eradication. This study found that while chromosomal position influences HIV latency, the exact molecular mechanisms may vary across different in vitro models.

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High Throughput In Vitro Assessment of Latency Reversing Agents on HIV Transcription and Splicing

High Throughput In Vitro Assessment of Latency Reversing Agents on HIV Transcription and Splicing

Published on: January 22, 2019

Area of Science:

Virology
Immunology
Genomics

Background:

Antiretroviral therapy effectively manages human immunodeficiency virus (HIV) infection.
Persistent latent reservoirs of integrated proviruses prevent HIV eradication.
The influence of chromosomal environment on HIV latency is known, but mechanisms remain unclear.

Purpose of the Study:

To investigate the determinants of HIV latency.
To compare latency mechanisms across different in vitro models.
To clarify the role of the chromosomal environment in HIV transcriptional repression.

Main Methods:

Comparison of five in vitro models of HIV latency using primary human T cells and a T cell line.
In vitro infection, separation of expressed and silent/inducible proviruses.
Sequencing of integration site populations and analysis of genomic annotations.

Main Results:

Analysis of 6,252 expressed and 6,184 silent/inducible proviruses revealed no consistent predictors of latency across models.
Genomic features showed significant associations with proviral expression in individual models.
Proviruses in the same chromosomal region shared status within a model but not across different models.

Conclusions:

The silent/inducible phenotype of HIV proviruses is linked to chromosomal position.
The precise molecular basis of this association is not fully elucidated.
Mechanisms driving HIV latency may differ across various in vitro models.