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The Next Chapter in HIV: Molecular Pathways and Novel Therapeutic Strategies

Special Issue Editor


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Guest Editor
IRCCS Istituto Nazionale Malattie Infettive Lazzaro Spallanzani, Rome, Italy
Interests: HIV/AIDS; sepsis; cytomegalovirus infection; hepatitis; bone marrow aspiration

Special Issue Information

Dear Colleagues,

Combination antiretroviral (ART) regimens are extraordinarily effective at blocking HIV-1 replication and preserving the host immune system, but they must be administered for life and do not fully ameliorate co-morbidities, such as HIV-associated neurocognitive diseases, cardiovascular diseases, or cancer. In addition, ART regimens minimally reduce the HIV cellular reservoir. This is because HIV-1 integrates into a broad but nonrandom range of sites of the host genome, preferentially in actively transcribing cellular genes. Additionally, while the vast majority of proviral HIV cannot be a source of viral rebound because it is genetically defective, it can still lead to the expression of viral transcripts and antigens. ART regimens can elicit cytolytic immune responses but also undesirably contribute to the HIV-1-associated chronic state of immune activation that is harmful to multiple organs.

It has been shown that knowledge of the basic molecular mechanisms of virus–host interactions, particularly HIV transcription and latency, can pave the way for new therapeutic strategies to obtain an HIV cure. Epigenetic silencing of proviral transcription is performed with the aim of permanently silencing HIV-1, with one technique being the “Block and Lock” strategy. Another scheme to eliminate the residual reservoir is to deliberately reactivate the latent HIV-1 proviruses to clear latently infected cells, known as the “Shock and Kill” strategy, but the currently used latency-reversing agents are not efficient enough and are rather toxic to humans. Crispr-based strategies to cut out HIV from the genomes of infected cells have shown promise in reducing viral reservoirs, but their main limitation is that the delivery system cannot efficiently reach all infected cells.

This Special Issue aims to increase knowledge of the molecular bases of HIV–host interactions and provide insights into their use for curing HIV infection and related comorbidities.

Dr. Isabella Abbate
Guest Editor

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Keywords

  • HIV
  • transcription
  • provirus
  • microRNA
  • epigenetic silencing
  • reservoir
  • integration site
  • latency
  • immune activation

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