title: Viruses, apoptosis, and neuroinflammation--a double-edged sword.
abstract: Apoptosis, or programmed cell death, is a fundamental and widespread cell biological process that is distinct from cell necrosis and can be induced by a wide variety of stimuli including viral infections. Apoptosis may occur via either the intrinsic or extrinsic pathways and confers several advantages to the virally infected host including the prevention of further viral propagation and the potential inhibition and resolution of inflammatory processes. Several viruses have been shown to have the capacity to induce apoptosis in susceptible cells including herpes simplex virus, Varicella-zoster virus, rabies virus, human immunodeficiency virus, and reovirus. Apoptosis has also been observed in human African trypanosomiasis which is an infection caused by a protozoan parasite. The mechanisms leading to apoptosis may differ depending on the type of infection. Apoptosis has been reported in several neurodegenerative diseases and also psychiatric disorders but the true clinical significance of such observations is not certain, and, though interesting, it is very difficult to ascribe causation in these conditions. The presence of inflammation in the central nervous system in any neurological condition, including those associated with a viral infection, is not necessarily an absolute marker of serious disease and the notion of 'good' versus 'bad' inflammation is considered to be valid in some circumstances. The precise relationship between viruses, apoptosis, and inflammation is viewed as a complex one requiring further investigation to unravel and understand its nature.
authors.affiliation: Department of Neurology, Institute of Neurological Sciences, Southern General Hospital, Glasgow University, Glasgow, G51 4TF, Scotland, UK, Peter.Kennedy@glasgow.ac.uk.
authors.forename: Peter G E
authors.initials: PG
authors.lastname: Kennedy
mesh_terms: D017209:Apoptosis; D002490:Central Nervous System / Q000503:physiopathology / Q000821:virology*; D006678:HIV / Q000472:pathogenicity / Q000502:physiology; D015658:HIV Infections / Q000503:physiopathology / Q000821:virology; D006561:Herpes Simplex / Q000503:physiopathology / Q000821:virology; D006562:Herpes Zoster / Q000503:physiopathology / Q000821:virology; D018259:Herpesvirus 1, Human / Q000472:pathogenicity / Q000502:physiology; D014645:Herpesvirus 3, Human / Q000472:pathogenicity / Q000502:physiology; D006801:Humans; D007249:Inflammation / Q000503:physiopathology / Q000821:virology; D009474:Neurons / Q000473:pathology / Q000821:virology*; D030102:Orthoreovirus, Mammalian / Q000472:pathogenicity; D011818:Rabies / Q000503:physiopathology / Q000821:virology; D011820:Rabies virus / Q000472:pathogenicity / Q000502:physiology; D012088:Reoviridae Infections / Q000503:physiopathology / Q000821:virology; D014779:Virus Replication