Infections with the human cytomegalovirus (CMV), one of eight human herpesviruses, constitute a 'silent pandemic'. Millions of years of coevolution have resulted in a virus that infects most people at some point in their lives and stays with us indefinitely without usually causing overt disease. The lifelong relationship with CMV is based on our intrinsic, innate and adaptive immune responses as well as manifold viral countermeasures which collectively enable a dynamic balance between host and pathogen that largely precludes disease without eliminating the virus from our bodies. However, in situations where the immune system is suppressed or still immature, CMV can cause major disease or even death. In the absence of an effective vaccine and with a limited choice of antiviral drugs, CMV remains a major pathogen in transplant recipients and other critically ill patients and a leading cause of birth defects.
Although little is known about the details of viral pathogenesis, both direct cytolytic as well as indirect immunological effects including inflammation appear to contribute to CMV disease. Viral pathogenesis is most commonly initiated when environmental cues trigger molecular signaling pathways that reactivate CMV from a state referred to as latency, a hallmark of all herpesviruses. Hundreds of viral proteins and non-coding RNAs are produced in a temporal cascade during a productive CMV replication cycle that involves myriad virus-host interactions and culminates in the release of progeny virions. In contrast, viral gene expression was long thought to be silenced during latency when no virus particles are produced. However, recent findings have challenged this view and suggest that the viral genome is more actively expressed during latency than had been anticipated.
Our renewed understanding of viral latency and other recent discoveries, often driven by advances in technology, point to novel strategies for detecting, preventing and treating CMV infection and disease. The new developments may even provide opportunities for curing CMV infection to ultimately eliminate the individual and societal burdens linked to this highly sophisticated pathogen.
For this Research Topic, we invite topical submissions in all areas of virus-host interaction and pathogenesis relevant to CMV including related animal viruses. Although all manuscript types will be considered, Original Research articles, Brief Research Reports, and review articles are particularly welcome.
Infections with the human cytomegalovirus (CMV), one of eight human herpesviruses, constitute a 'silent pandemic'. Millions of years of coevolution have resulted in a virus that infects most people at some point in their lives and stays with us indefinitely without usually causing overt disease. The lifelong relationship with CMV is based on our intrinsic, innate and adaptive immune responses as well as manifold viral countermeasures which collectively enable a dynamic balance between host and pathogen that largely precludes disease without eliminating the virus from our bodies. However, in situations where the immune system is suppressed or still immature, CMV can cause major disease or even death. In the absence of an effective vaccine and with a limited choice of antiviral drugs, CMV remains a major pathogen in transplant recipients and other critically ill patients and a leading cause of birth defects.
Although little is known about the details of viral pathogenesis, both direct cytolytic as well as indirect immunological effects including inflammation appear to contribute to CMV disease. Viral pathogenesis is most commonly initiated when environmental cues trigger molecular signaling pathways that reactivate CMV from a state referred to as latency, a hallmark of all herpesviruses. Hundreds of viral proteins and non-coding RNAs are produced in a temporal cascade during a productive CMV replication cycle that involves myriad virus-host interactions and culminates in the release of progeny virions. In contrast, viral gene expression was long thought to be silenced during latency when no virus particles are produced. However, recent findings have challenged this view and suggest that the viral genome is more actively expressed during latency than had been anticipated.
Our renewed understanding of viral latency and other recent discoveries, often driven by advances in technology, point to novel strategies for detecting, preventing and treating CMV infection and disease. The new developments may even provide opportunities for curing CMV infection to ultimately eliminate the individual and societal burdens linked to this highly sophisticated pathogen.
For this Research Topic, we invite topical submissions in all areas of virus-host interaction and pathogenesis relevant to CMV including related animal viruses. Although all manuscript types will be considered, Original Research articles, Brief Research Reports, and review articles are particularly welcome.
