Classification Rhabdoviridae
Group V RNA -
Characteristics of Rhabdoviridae
Structure & genomic organization of Rhabdoviridae
Rhabdoviral replication
(-)RNP serves as template for both transcription and genome replication
Level of N protein determines which step occurs
Viral fusion proteins
Rhabdoviridae Class III
Rhabdoviral fusion
Rhabdoviral release
Rhabdovirus host range and transmission
humans, other vertebrates, invertebrates, and plants.
Rhabdoviruses human infections
RABV
causative agent of rabies
Tollwut
Rabies is a viral disease that causes encephalitis in humans and other mammals
dog transmitted rabies
vaccine
rabies vaccination
Spread of rabies in the nervous system
Rabies as a monosynaptic tracer
Single network monitoring
Network activity monitoring
Manipulation of neuronal activity of a network
Recombinant rabies virus technology
VSV
causative agent of vesicular stomatitis
VSV as oncolytic virus
interferoon response
Differences between VSV and RABV
Innate sensing of Rhabdoviruses + Inhibition of IFN signaling by RABV
Autophagy
Autophagy is the natural, conserved degradation of the cell that removes unnecessary or dysfunctional components
Autophagy pathway hijacked by rhabdoviruses
Apoptosis
is a form of programmed cell death
Intrinsic pathway (trigger: growth factor deprivation & cellular stress)
- Extrinsic pathway (trigger: recognition of FAS ligand (FASL)
Pyroptosis
inflammatory form of cell death
pyroptosis acts as “whistle blowers”, resulting in the release of alarmins and other proinflammatory signals into the cellular surroundings,
apoptosis vs pyroptosis
ISGs
ISGs inhibiting rhabdoviral replication
interferon-stimulated gene
inhibit secondary transcription
VSV M
VSV – vesicular stomatitis virus
The matrix (M) protein of the virus causes many of the cytopathic effectsof VSV, including an inhibition of host gene expression and the induction of cell rounding.
Last changeda year ago