Regulation of HIV-1 Transcription and Latency, 2nd Edition

A special issue of Viruses (ISSN 1999-4915). This special issue belongs to the section "Human Virology and Viral Diseases".

Deadline for manuscript submissions: 31 October 2025 | Viewed by 373

Special Issue Editor

Department of Molecular Biology and Microbiology, Case Western Reserve University School of Medicine, Cleveland, OH 44106, USA
Interests: HIV

Special Issue Information

Dear Colleagues,

The Special Issue “Regulation of HIV-1 Transcription and Latency”, which was launched in 2023, successfully garnered a number of informative articles on this important topic. We would like to introduce a second edition of this Special Issue, intended to update our understanding of the transcriptional control of HIV-1 latency via viral and host factors.

Residual cellular subsets of transcriptionally latent, but potentially inducible, HIV-1 reservoirs in infected people on antiretroviral therapy are considered to be the ultimate barrier to finding a cure for HIV-1 infection. Dissecting the host and viral mechanisms that are utilized by HIV-1 to emerge from latency is therefore crucial for the development of strategies to either eliminate or permanently silence persistent HIV-1 reservoirs. In the second edition of this Special Issue, we will maintain the theme of publishing review and research articles focused on host and viral mechanisms of HIV-1 transcriptional regulation as well as their applications for HIV-1 eradication or permanent silencing. In light of the fact that virtually all mechanistic studies of HIV-1 reservoirs conducted thus far have rarely utilized non-B subtypes, which are collectively responsible for 88% of the global HIV-1 infection burden, we also welcome review and original research articles that aim to incorporate an examination of the transcriptional regulation of non-B subtypes.

Dr. Uri Mbonye
Guest Editor

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Keywords

  • HIV provirus
  • HIV latency
  • latency reversal
  • HIV transcription initiation
  • HIV transcription elongation
  • transcription factors
  • epigenetic silencing
  • posttranscriptional control of HIV gene expression
  • transcriptomic analysis of HIV infection
  • HIV reservoir

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Published Papers (1 paper)

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18 pages, 2869 KiB  
Hypothesis
A Model of Non-Homologous Recombination Mediated by HIV-1 Reverse Transcriptase Explaining Sequence Motif Duplications That Confer a Replication Fitness Advantage
by Arun Panchapakesan and Udaykumar Ranga
Viruses 2025, 17(5), 680; https://doi.org/10.3390/v17050680 - 7 May 2025
Viewed by 177
Abstract
The Reverse Transcriptase of the Human Immunodeficiency Virus (HIV) is distinguished by its high rate of homologous recombination. A less-studied consequence of this phenomenon is the increased occurrence of non-homologous recombination, which results in length polymorphism. While most of these genome-wide variations are [...] Read more.
The Reverse Transcriptase of the Human Immunodeficiency Virus (HIV) is distinguished by its high rate of homologous recombination. A less-studied consequence of this phenomenon is the increased occurrence of non-homologous recombination, which results in length polymorphism. While most of these genome-wide variations are sporadic, some provide a replication advantage to variant strains, such as those in the Long Terminal Repeat (LTR) and p6-Gag regions. By analyzing sequences from these two regions in the HIV-1 databases, we categorize all types of non-homologous recombination into four groups based on the presence or absence of two molecular features. Additionally, drawing on established models of homologous recombination, we propose a model that describes the process of sequence duplication. This model can also be applied to explain non-homologous recombination in different types of HIV and other viruses. Full article
(This article belongs to the Special Issue Regulation of HIV-1 Transcription and Latency, 2nd Edition)
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