Human cytomegalovirus persistence

Abstract

Summary Viral persistence is the rule following infection with all herpesviruses. The β-herpesvirus, human cytomegalovirus (HCMV), persists through chronic and latent states of infection. Both the chronic and latent states of infection contribute to HCMV persistence and to the high HCMV seroprevalence worldwide. The chronic infection is poorly defined molecularly, but clinically manifests as low-level virus shedding over extended periods of time and often in the absence of symptoms. Latency requires long-term maintenance of viral genomes in a reversibly quiescent state in the immunocompetent host. In this review, we focus on recent advances in the biology of HCMV persistence, particularly with respect to the latent mode of persistence. Latently infected individuals harbor HCMV genomes in hematopoietic cells and maintain large subsets of HCMV-specific T-cells. In the last few years, impressive advances have been made in understanding virus-host interactions important to HCMV infection, many of which will profoundly impact latency and persistence. We discuss these advances and their known or potential impact on viral latency. As herpesviruses are met with similar challenges in achieving latency and often employ conserved strategies to persist, we discuss current and future directions of HCMV persistence in the context of the greater body of knowledge regarding α-and γ-herpesviruses persistence.

Sweet Is the Memory of Past Troubles: NK Cells Remember

“…Cytomegalovirus (CMV) is a member of the beta-herpes family of viruses and is known to establish lifelong persistent infections in humans and mice (Goodrum et al 2012). Although T cells are critical in controlling CMV latency and preventing reactivation (Hanley and Bollard 2014), a role for host NK cells has been established in the acute stages of this infection (López-Botet et al 2014;Tyznik et al 2014).…”

Transmission of human cytomegalovirus via breastmilk and potential risks to very preterm infants

“…HCMV, a b-herpesvirus, persists following primary infection for lifetime in hematopoetic CD34+ precursor cells and may be reactivated by stress, transient loss of CD4+ and CD8+ T-cell immunity, IL-6 signalling, cell cycle arrest, and DNA damage 3 . Interestingly, HCMV is also reactivated in healthy immunocompetent seropositive women during lactation 4 .…”

CMV and transfusions, an old story that's not quite over yet

“…A brief outline of the salient features will be provided; the interested reader is referred to three recent reviews of the subject. [31][32][33] Certain terms need to be defined. Latency is described as a situation where there is evidence of "viral DNA in tissues without transcription or translation of lytic or 'late' gene RNAs to protein and thereby absence of lytic virus.…”