Native CMV (Strain AD169) Antigen

Cytomegalovirus (CMV), one of the largest and most prevalent latent persistent viruses, is an opportunistic pathogen, most people infected with CMV do not develop significant disease, but people with compromised immune systems are at a higher risk of developing disease when infected with CMV, for example, transplant recipients, people with AIDS, and people with congenital immune deficiencies or immunosuppressive therapy. Currently, measures such as antiviral drugs are mainly taken to reduce the incidence of CMV, but these drugs themselves have significant side effects, and drug resistance has been observed in patients using them for a long period of time, therefore, there is a need to search for new antiviral targets to develop new therapeutic approaches for better treatment of CMV infections.

CMVs have a unique ability to evade host immune defenses while also altering the composition of the host immune system, and researchers have found that some of these changes are evident with age, raising the possibility that CMVs drive immune senescence. After acute CMV infection resolves, the virus establishes a lifelong infection in defined organ sites, and active genome replication and viral progeny production are undetectable in the latent state, but residual transcriptional activity can be detected at some viral loci, in which case the virus reactivates sporadically in response to external stimuli, and the viral progeny are shed from the asymptomatic host. CD34⁺ progenitor cells in the bone marrow are an important site for human CMV (HCMV) latency, and the HCMV-encoded G-protein-coupled receptor homolog US28 is a key factor in establishing and maintaining latency in CD34⁺ myeloid progenitor cells, with multifunctional signaling capabilities during lysis of infection. Normal CD34⁺ myeloid progenitor cells differentiate into CD14⁺ monocytes, which in turn differentiate into macrophages and dendritic cells, whereas secretions from CD34⁺ cells latently infected by CMV recruit suppressor CD4⁺ T cells, secretions from infected CD14⁺ monocytes attract activated immune cells via the chemokine CXCL10, and recruited cells upregulate CXCR3 expression and activate the ERK signaling pathway, thereby inducing HCMV reactivation from CD14⁺ monocytes. These observations suggest that viruses may influence immune system function by modulating host cell secretions. The researchers found a possible link between the inflammatory environment, activated T-cells, and the induction of CMV reactivation in older adults, leading to low levels of viremia.

Figure 1. Antiviral targets in replication cycle of CMV
(Source: Gourin C, et al. 2023)

Native cytomegalovirus (Strain AD169) Antigen