Involvement of cellular death signals in the reactivation of herpes simplex virus type 1 and lambda bacteriophage from a latent state.
Herpes simplex virus (HSV) 1 has adapted to the human host through two modes of infection, the acute-transient infection that may cause diseases (such as encephalitis) and the latent state, which is a source for recurrent infection and disease. While much information has been gathered on the cellular and molecular concomitants of establishment and maintenance of HSV-1 latent state, the biological basis of viral reactivation is still unclear. Despite their obvious differences, HSV-1 and the bacterial temperate virus, the bacteriophage lambda, shares four distinct features that may help understand the viral latency phenomenon: (i) two modes of life cycle and a decision point to choose either latency (HSV-1) and lysogeny (bacteriophage lambda), or active replication, that results in cell destruction, (ii) establishment of lysogeny/latency of the respective virus is associated with protection from cell death, (iii) immunity/resistance to super-infection, (iv) agents that trigger mammalian and bacterial cell death also induce reactivation of both HSV-1 and lambda bacteriophage. Thus, despite their differences, these two viruses might display analogous mechanism(s) of reactivation. Based on clinical and experimental data, we propose in this hypothesis that while HSV-1 latency, like bacteriophage lambda lysogeny, is associated with protection from cell death and restriction to super-infection, viral reactivation from the latent state is triggered by exogenous stress signals that interfere with cellular viability and may eventually lead to cell death.
Panet
Amos
A
Department of Virology, Hadassah University Hospital, P.O. Box 12000, Jerusalem 91120, Israel.
Braun
Efrat
E
Honigman
Alik
A
Steiner
Israel
I
D001419:Bacteria / Q000821:virology; D010582:Bacteriophage lambda / Q000502:physiology*; D016923:Cell Death / Q000502:physiology; D005724:Ganglia / Q000473:pathology / Q000821:virology*; D015967:Gene Expression Regulation, Viral; D017781:Genes, Immediate-Early; D006561:Herpes Simplex / Q000276:immunology / Q000473:pathology / Q000821:virology*; D018259:Herpesvirus 1, Human / Q000502:physiology*; D006801:Humans; D008242:Lysogeny; D008954:Models, Biological; D015398:Signal Transduction / Q000502:physiology; D014775:Virus Activation; D017735:Virus Latency