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Everything You Need to Know About Rabies

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doi: 10.1146/annurev-virology-100114-055157. Epub 2015 Jun 24.

Everything You Always Wanted to Know About Rabies Virus (Only Were Agape to Inquire)

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  • PMID: 26958924
  • PMCID: PMC6842493
  • DOI: 10.1146/annurev-virology-100114-055157

Gratuitous PMC article

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Everything You lot Always Wanted to Know About Rabies Virus (But Were Afraid to Ask)

Benjamin M Davis  et al. Annu Rev Virol. 2015 Nov .

Free PMC article

Abstract

The cultural bear upon of rabies, the fatal neurological illness caused by infection with rabies virus, registers throughout recorded history. Although rabies has been the bailiwick of large-calibration public health interventions, chiefly through vaccination efforts, the illness continues to have the lives of about 40,000-70,000 people per year, roughly 40% of whom are children. About of these deaths occur in resource-poor countries, where lack of infrastructure prevents timely reporting and postexposure prophylaxis and the ubiquity of domestic and wild animal hosts makes eradication unlikely. Moreover, although the disease is rarer than other human infections such as influenza, the prognosis following a bite from a rabid animal is poor: There is currently no effective treatment that will save the life of a symptomatic rabies patient. This review focuses on the major unanswered research questions related to rabies virus pathogenesis, especially those connecting the disease progression of rabies with the circuitous dysfunction caused by the virus in infected cells. The recent applications of cut-edge enquiry strategies to this question are described in item.

Keywords: lyssaviruses; neuroinvasive virus; neurotropic virus; rabies virus; viral transport.

Figures

Figure 1:
Figure 1:

The RABV transcription and replication strategy. The negative-sense genomic RNA (in orangish) is the template for the L-P polymerase complex. A) During transcription, Five 5′-end capped (C) and polyadenylated (A) mRNAs (in green) encode the viral proteins. The polymerase complex disassociates from the template at each termination signal (End). The polymerase does not ever re-engage successfully, leading to a negative transcription gradient from three′ to 5′. B) During replication, the negative-sense genome is transcribed into a positive-sense antigenomic RNA intermediate (in green) past a more than processive class of the viral polymerase. The anti-genome is then transcribed back into a negative-sense RNA to consummate replication.

Figure 2:
Effigy ii:

The path of RABV infection through the host. Most natural RABV infections kickoff with exposure of musculus tissue to RABV particles by an animate being bite or scratch. The infection spreads to the peripheral nervous arrangement through neuromuscular junctions (lesser insert). Virus particles travel as an enveloped vesicle using dynein-mediate retrograde axonal transport pathways (top insert), spreading trans-synaptically from postal service-synaptic to pre-synaptic neurons until widespread infection of the central nervous system is achieved.

Figure 3:
Figure 3:

The RABV neuroinvasive strategy. Two possible mechanisms are depicted, both of which accept been observed experimentally. A) RABV-G interacts with the nicotinic acetylcholine receptor (nAcHR; in light-green), mediating entry into muscle cells. This leads to local replication of the virus earlier budding into the synaptic crevice of the neuromuscular junction. B) Alternatively, RABV-Thousand interacts with one of several cellular receptors on the neuron, such as NCAM or p75NTR (shown in majestic or blue). This leads to direct entry into the neuron without prior local replication in musculus.

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