title: [Herpesviruses survival strategies--latency and apoptosis].
abstract: Apoptosis is a process of programmed cell death in response to various stimuli, including virus infection. Herpesviruses have evolved the ability to interfere with apoptosis by its inhibition or activation in host cells. They can interfere with the extrinsic and intrinsic pathways of apoptosis. A special feature of herpesviruses is establishing a latent infection, during which expression of virus genes is strongly restricted and production of infectious virus particles is not observed. HSV-1 establishes latency in neurons, CMV in bone marrow progenitor cells and monocytes, EBV and HHV-8 in B cells. Studies show that latent infections also depend on prevention of the death of the infected cells. Control of apoptosis machinery by viruses may be critical for their reproduction and provision of the adequate yield of progeny virions. The present article summarizes the current knowledge about the latent viral infection and mechanisms of apoptosis modulation by selected viruses from the Herpesviridae family.
authors.affiliation: Interfaculty Studies of Biotechnology, Warsaw University of Life Sciences-SGGW, Warsaw, Poland.
authors.forename: Dariusz
authors.initials: D
authors.lastname: Miszczak
authors.forename: Anna
authors.initials: A
authors.lastname: Słońska
authors.forename: Anna
authors.initials: A
authors.lastname: Golke
authors.forename: Joanna
authors.initials: J
authors.lastname: Cymerys
mesh_terms: D017209:Apoptosis; D001402:B-Lymphocytes / Q000821:virology; D006564:Herpesviridae / Q000472:pathogenicity* / Q000502:physiology*; D006566:Herpesviridae Infections / Q000821:virology*; D018259:Herpesvirus 1, Human / Q000472:pathogenicity / Q000502:physiology; D019288:Herpesvirus 8, Human / Q000472:pathogenicity / Q000502:physiology; D006801:Humans; D017735:Virus Latency