ausblenden:
Schlagwörter:
HERPES-SIMPLEX-VIRUS; CD8(+) T-CELLS; VARICELLA-ZOSTER-VIRUS; GENOME
COPY NUMBER; LASER-CAPTURE MICRODISSECTION; PRIMARY SENSORY NEURONS;
IN-VIVO REACTIVATION; MHC CLASS-I; GAMMA-INTERFERON; INFECTED NEURONSNeurosciences; Virology; HSV-1; Latency; Human; CD8(+) T cells; Neurons;
Zusammenfassung:
Although recurrent Herpes simplex virus type 1 (HSV-1) infections are
quite common in humans, little is known about the exact molecular
mechanisms involved in latency and reactivation of the virus from its
stronghold, the trigeminal ganglion. After primary infection, HSV-1
establishes latency in sensory neurons, a state that lasts for the life
of the host. Reactivation of the virus leads to recurrent disease,
ranging from relatively harmless cold sores to ocular herpes. If herpes
encephalitis-often a devastating disease-is also caused by reactivation
or a new infection, is still a matter of debate. It is widely accepted
that CD8(+) T cells as well as host cellular factors play a crucial
role in maintaining latency. At least in the animal model, IFN gamma
and Granzyme B secretion of T cells were shown to be important for
control of viral latency. Furthermore, the virus itself expresses
factors that regulate its own latency-reactivation cycle. In this
regard, the latency associated transcript, immediate-early proteins,
and viral miRNAs seem to be the key players that control latency and
reactivation on the viral side. This review focuses on HSV-1 latency in
humans in the light of mechanisms learned from animal models.
