*1.3. CMV Life Cycle*

CMV infection will start once a virion attaches a host cell with specific receptors on the cellular surface. For a lytic infection pathway, following linking of viral envelope glycoproteins to host cell membrane receptors, the virions enter the hosts by receptor-mediated endocytosis and membrane fusion. The viral capsid decomposes to release viral DNA genome to manipulates host enzyme systems to make new virions. During symptomatic infection, infected cells express lytic genes to demonstrate a lytic pathway [12]. Nevertheless, instead of this, some viral genes may transcribe latency associated transcripts to accumulate in host cells. In this pattern, viruses can persist in host cells indefinitely to have a latent infection pathway. The primary infection may be accompanied by limited illness and long-term latency is often asymptomatic. For the lysogenic pathway, the viruses are persistent in the host, not causing any adverse reactions, but can be transmitted to other hosts by direct contact. When CMV are stimulated by explanation or their host immune system is suppressed, the dormant viruses can reactivate to begin generating large number of viral progenies to cause symptoms and diseases, described as the lytic life cycle [12,13].

Viral latency can be divided into two models, namely proviral latency and episomal latency. CMV is defined as the episomal latency model which is essentially quiescent in myeloid progenitor cells. It can be reactivated by differentiation, inflammation, immunosuppression or critical diseases [14]. Latency is a specific phase in CMV life cycles in which virions stop producing posterior to infection, but the viral genome has not been entirely removed from host cells, that is, CMV latency is referred to as the absence of virions, despite the detection of viral DNA in hosts. In some clinical cases, the reactivation of latent infections is likely to lead to health risk. The molecular mechanisms by which

latency is established and maintained have been explored. However, our understanding of the biology of CMV latency and reactivation at the molecular level would be significantly strengthened through analyses of both experimental and natural latency using systematic approaches [14].
