Abstract
The human immune system boasts a diverse array of strategies for recognizing and eradicating invading pathogens. Human betaherpesviruses, a highly prevalent subfamily of viruses, include human cytomegalovirus (HCMV), human herpesvirus (HHV) 6A, HHV-6B, and HHV-7. These viruses have evolved numerous mechanisms for evading the host response. In this review, we will highlight the complex interplay between betaherpesviruses and the human immune response, focusing on protein function. We will explore methods by which the immune system first responds to betaherpesvirus infection as well as mechanisms by which viruses subvert normal cellular functions to evade the immune system and facilitate viral latency, persistence, and reactivation. Lastly, we will briefly discuss recent advances in vaccine technology targeting betaherpesviruses. This review aims to further elucidate the dynamic interactions between betaherpesviruses and the human immune system.
Highlights
Betaherpesviruses, a widespread subfamily of viruses within the herpesviridae family, are nearly ubiquitous in the global population [1,2,3] and include human cytomegalovirus (HCMV), human herpesvirus (HHV) 6A, HHV-6B, and HHV-7 [4].Like other herpesviridae, betaherpesviruses are comprised of four primary sections: the double-stranded viral DNA, the capsid, the tegument, and the envelope
This review aims to illustrate the complex interplay between betaherpesviruses and the immune system, with a greater emphasis placed on HCMV due to the relative abundance of new research focusing on this virus
DNA. Cyclic GMP-AMP synthase (cGAS) stimulation leads to the creation of a cyclic GMP-AMP dinucleotide that activates stimulator of interferon genes (STING) [46], a dimeric transmembrane protein [47] primarily expressed in the endoplasmic reticulum [48]. cGAS binding stimulates the translocation of STING to post-golgi compartments [47,49], where it oligomerizes [47]
Summary
Betaherpesviruses, a widespread subfamily of viruses within the herpesviridae family, are nearly ubiquitous in the global population [1,2,3] and include human cytomegalovirus (HCMV), human herpesvirus (HHV) 6A, HHV-6B, and HHV-7 [4]. The cellular platelet-derived growth factor-α receptor (PDGFRα) interacts with the HCMV gH/gL/gO trimer complex (TC), which activates glycoprotein B (gB) to fuse the viral envelope with the cell membrane [13]. This review aims to illustrate the complex interplay between betaherpesviruses and the immune system, with a greater emphasis placed on HCMV due to the relative abundance of new research focusing on this virus. It will explore DNA sensors responsible for detecting the initial infection within a cell as well as interactions between betaherpesviruses and immune effector cells, natural killer cells and T cells. Betaherpesvirus immunoevasive strategies will be discussed throughout to better highlight the interactions between the human immune system and betaherpesviruses
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