By G. Gosztonyi
It has been famous that viruses can result in neuronal harm by means of a number of mechanisms. This quantity summarizes, for the 1st time, some of the ways in which neurons can degenerate less than the impact of viral an infection, starting from acute necrosis and virus-induced apoptosis to persistent harm in chronic infections. The mechanisms of neuronal latency are handled besides. the quantity additionally comprises chapters that evaluate the power harm as a result of viral proteins that intrude with differentiated features of the neuron, together with signaling by means of neurotransmitters and sign transduction by means of trophic components. different chapters take care of the arguable function of mobile immune reactions, that could be worthy in controlling an infection, yet can also be hazardous to the host apprehensive process. the explicit mechanisms of wear all in favour of retroviral infections and in prion ailments of the fearful approach are reviewed, and at last how autoimmune illnesses may end up in neuronal damage.
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Extra resources for The Mechanisms of Neuronal Damage in Virus Infections of the Nervous System
Virology 258:389-395 Kreutzberg GW (1996) Microglia: a sensor for pathological events in the CNS. Trends Neurosci 19: 312-318 Kristensson K, Dastur DK, Manghani DK, Tsiang H, Bentivoglio M (1996) Rabies: interactions between neurons and viruses. A review of the history of Negri inclusion bodies. Neuropathol Appl Neurobiol 22:179-187 Lannuzel A, Bamier JV, Hery C, Huynh VT, Guibert B, Gray F, Vincent JD, Tardieu M (1997) Human immunodeficiency virus type I and its coat protein gpl20 induce apoptosis and activate JNK and ERK mitogen-activated protein kinases in human neurons.
In contrast, studies that reveal low levels of HSV DNA in elderly human brains imply that cell death is not inevitable and strategies to repress reactivation may also operate. There are fundamental and unexplained differences between the eNS and peripheral nervous system, and unique mechanisms may protect the brain from a ubiquitous but potentially lethal virus. References Akaike T, Weihe E, Schaefer M, Fu ZF, Zheng YM, Vogel W, Schmidt H, Koprowski H, Dietzschold B (1995) Effect of neurotropic virus infection on neuronal and inducible nitric oxide synthase activity in rat brain.
E. cellular and immunological factors, interact simultaneously. In cases of acute lytic virus infections of the CNS, a rapid and efficient elimination of the pathogenic agent is necessary because nerve cells lack the capacity for regeneration, and loss of the highly specialised neurones may rapidly reach the threshold beyond which survival of the individual is endangered. On the other hand, the chances for viruses to persist and at least temporarily escape immune surveillance are facilitated. In the long run, however, persistent infections of the CNS lead to cell death, disturbed brain cell function, immunopathological disease and, if vital structures of the brain are involved, to the death of the individual.