Nikhil Prasad Fact checked by:Thailand Medical News Team Jul 28, 2024 1 month, 3 weeks, 1 day, 13 hours, 30 minutes ago
HIV News: Canadian researchers from the Institut de Recherches Cliniques de Montréal, Université de Montréal, and the University of Manitoba have discovered a cunning new tactic employed by HIV-1 to evade the immune system. This
HIV News report delves into how HIV-1 downregulates a specific microRNA, miRNA-26a, to enhance the expression and packaging of the CD59 protein, thereby protecting the virus from being destroyed by the immune system.
HIV-1's new tactic to evade immune attack - hijacking human microRNA
The Role of MicroRNAs
MicroRNAs (miRNAs) are tiny molecules that play crucial roles in regulating gene expression. They work by binding to messenger RNA (mRNA) molecules, preventing them from being translated into proteins. This regulation is vital for numerous cellular processes, including the immune response to viral infections.
Study Details
The research involved RNA sequencing (RNA-seq) profiling of miRNAs and mRNAs in CD4+ T cells infected with HIV-1. The results showed significant alterations in both miRNA and mRNA expression profiles in infected cells compared to uninfected cells. The downregulation of miRNA-26a and the subsequent upregulation of CD59 were identified as key factors in the virus's ability to evade ADCML.
HIV-1's Strategy
The study found that HIV-1 infection significantly alters the expression profiles of both miRNAs and mRNAs in CD4+ T lymphocytes. Notably, one of the miRNAs, miRNA-26a, is markedly downregulated in HIV-1-infected cells. miRNA-26a typically targets the mRNA of the CD59 receptor, a protein that inhibits the formation of the membrane attack complex (MAC), which the immune system uses to destroy infected cells.
By downregulating miRNA-26a, HIV-1 causes an increase in CD59 expression on the surface of infected cells and in the viral envelope of new virions. This overexpression of CD59 protects both the infected cells and the virus itself from antibody-dependent complement-mediated lysis (ADCML), a mechanism the immune system uses to kill pathogens.
Validation of Findings
To validate these findings, researchers added miRNA-26a mimics to infected CD4+ T cells, which resulted in reduced CD59 levels at both the mRNA and protein levels. Consequently, the infected cells and the viruses they produced became more susceptible to ADCML. Conversely, knocking out CD59 in these cells made them and the viruses they produced more vulnerable to immune attack.
Implications for HIV-1 Treatment
These findings highlight a novel mechanism by which HIV-1 evades the immune system. By upregulating CD59 through the downmodulation of miRNA-26a, HIV-1 effectively shields itself from being destroyed by the body's defenses. This discovery opens up new avenues for therapeutic interventions that could potentially target this pathway to enhance the immune system's ability to fight HIV-1.
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Broader Impact on MicroRNA Research
This study not only provides insights into HIV-1's evasion strategies but also underscores the broader role of miRNAs in regulating immune responses. Understanding how viruses manipulate these regulatory molecules can lead to the development of new treatments for a variety of viral infections.
Future Directions
Future research will focus on further understanding the precise mechanisms by which HIV-1 downregulates miRNA-26a and exploring potential therapeutic strategies to counteract this evasion tactic. Additionally, the role of other miRNAs in HIV-1 infection and immune evasion will be investigated to develop a more comprehensive understanding of the virus's interactions with the host's immune system.
Conclusion
The study findings provide crucial insights into the complex interactions between HIV-1 and the human immune system.
The findings were published in the peer-reviewed journal Viruses.
https://www.mdpi.com/1999-4915/16/7/1076
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