Abstract
Human cytomegalovirus (HCMV) is ubiquitously prevalent. HCMV infection is typically asymptomatic and controlled by the immune system in healthy individuals, yet HCMV can be severely pathogenic for the fetus during pregnancy and in immunocompromised persons, such as transplant recipients or HIV infected patients. HCMV has co-evolved with the hosts, developed strategies to hide from immune effector cells and to successfully survive in the human organism. One strategy for evading or delaying the immune response is maintenance of the viral genome to establish the phase of latency. Furthermore, HCMV immune evasion involves the downregulation of human leukocyte antigens (HLA)-Ia molecules to hide infected cells from T-cell recognition. HCMV expresses several proteins that are described for downregulation of the HLA class I pathway via various mechanisms. Here, we review the wide range of immune evasion mechanisms of HCMV. Understanding the mechanisms of HCMV immune evasion will contribute to the development of new customized therapeutic strategies against the virus.
Highlights
Human cytomegalovirus (HCMV) infection is typically asymptomatic in healthy individuals, ~10% develop HCMV mononucleosis [9]; HCMV can be severely pathogenic in a few groups: a fetus during pregnancy and immunocompromised persons, especially HIV infected patients and transplant recipients
HCMV is associated with several circumstances of mortality and morbidity; including as a common opportunist in solid organ and bone marrow transplant recipients, a significant contributor to mortality in HIV infected patients and HCMV might be a cause of immunosenescence in the elderly population [6]
An HCMV infection means that virus could be isolated or detected; a recurrent HCMV infection means that a new HCMV infection could be detected in a patient with previous evidence of HCMV infection, this recurrent infection could be a result of reactivation of latent virus or reinfection; an HCMV disease means the diagnosis of HCMV infection in a patient with manifested symptoms
Summary
HCMV virion consists of an outer membrane envelope, a phosphoprotein tegument layer and a capsid enclosing viral genome. The outer membrane includes several glycoproteins that serve the function of viral attachment. The genome comprises of two major regions, the unique long (UL) and unique short (US) segments. After the attachment of virus to the host cell the alpha helical coils, formed from heptad repeat regions in gB and gH, cause membrane fusion and release of viral capsids into the host cytosol [43,44]. The IE genes are first to be transcribed independently of any de novo host or viral protein synthesis and function as transcription factors of early proteins. Proteins from the late genes serve as structural components of virions and are necessary in virion assembly and egress (Figure 1). Beside the classical IE proteins, US3, US2 and US11 are produced in the IE phase [58,59]; and these proteins serve as potent immune evasions (Figure 2)
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