関連する実験動画

Updated: Mar 1, 2026

A Technique to Simultaneously Visualize Virus-Specific CD8+ T Cells and Virus-Infected Cells In situ

A Technique to Simultaneously Visualize Virus-Specific CD8+ T Cells and Virus-Infected Cells In situ

Published on: August 13, 2009

治療中断後のSIVコントロールは、治療前および治療中断後のウイルス持続感染の特定の特性と関連している

Caroline Charre^1,2, Adeline Melard³, Antoine Chaillon⁴

¹Université Paris Cité, INSERM, U1016; CNRS, Paris, France. caroline.charre@aphp.fr.

Nature communications

|February 27, 2026

Abstract:

Mechanisms underlying durable control of HIV after antiretroviral therapy interruption remain poorly understood. Here we provide a comprehensive longitudinal analysis in a non-human primate model of post-treatment control using SIVmac251-infected male cynomolgus macaques (pVISCONTI study). Controllers exhibit lower levels of SIV DNA, intact proviruses, transcriptional activity, and viral evolution compared to non-controllers in blood and tissues long after therapy interruption. Before interruption, controllers already have fewer intact proviruses in lymph nodes, and this difference persists in blood shortly after interruption, prior to viral rebound. Intact provirus levels in lymph nodes before interruption negatively correlate with CD8⁺ T-cell capacity to suppress SIV and reflect rebound magnitude. The study demonstrates that markers of post-treatment control are detectable in lymph nodes before therapy interruption and in blood shortly after, and suggests that host immune responses may shape intact provirus profiles during treatment.

キーワード:

Post-treatment control HIV SIV viral reservoirs intact provirus ART interruption immune response lymph nodes viral suppression viral rebound

さらに関連する動画

Arbovirus Infections As Screening Tools for the Identification of Viral Immunomodulators and Host Antiviral Factors

Arbovirus Infections As Screening Tools for the Identification of Viral Immunomodulators and Host Antiviral Factors

Published on: September 13, 2018

Amplification of Near Full-length HIV-1 Proviruses for Next-Generation Sequencing

Amplification of Near Full-length HIV-1 Proviruses for Next-Generation Sequencing

Published on: October 16, 2018

関連する概念動画

Immune Response Against Viral Pathogens

Immune Response Against Viral Pathogens

The immune system's response to viral infections is a complex and coordinated process involving natural killer (NK) cells, T cell-mediated responses, and antibody-mediated responses.
NK Cells
NK cells are a crucial part of our innate immune system, acting as the first line of defense against viral infections. These cells can recognize and kill infected cells without prior exposure to the virus, effectively slowing down the spread of infection. Additionally, NK cells produce proinflammatory...

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...

Retrovirus Life Cycles

Retrovirus Life Cycles

Retroviruses have a single-stranded RNA genome that undergoes a special form of replication. Once the retrovirus has entered the host cell, an enzyme called reverse transcriptase synthesizes double-stranded DNA from the retroviral RNA genome. This DNA copy of the genome is then integrated into the host’s genome inside the nucleus via an enzyme called integrase. Consequently, the retroviral genome is transcribed into RNA whenever the host’s genome is transcribed, allowing the...

Viral Mutations

Viral Mutations

A mutation is a change in the sequence of bases of DNA or RNA in a genome. Some mutations occur during replication of the genome due to errors made by the polymerase enzymes that replicate DNA or RNA. Unlike DNA polymerase, RNA polymerase is prone to errors because it is not capable of “proofreading” its work. Viruses with RNA-based genomes, like HIV, therefore accrue mutations faster than viruses with DNA-based genomes. Because mutation and recombination provide the raw material...