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The pathogenesis of Rift Valley fever.

Ikegami T, Makino S - Viruses (2011)

Bottom Line: Rift Valley fever (RVF) is an emerging zoonotic disease distributed in sub-Saharan African countries and the Arabian Peninsula.RVFV infection in humans usually causes a self-limiting, acute and febrile illness; however, a small number of cases progress to neurological disorders, partial or complete blindness, hemorrhagic fever, or thrombosis.This review describes the pathology of RVF in human patients and several animal models, and summarizes the role of viral virulence factors and host factors that affect RVFV pathogenesis.

View Article: PubMed Central - PubMed

Affiliation: Department of Pathology, The University of Texas Medical Branch, 301 University Blvd., Galveston, TX 77555, USA. teikegam@utmb.edu

ABSTRACT
Rift Valley fever (RVF) is an emerging zoonotic disease distributed in sub-Saharan African countries and the Arabian Peninsula. The disease is caused by the Rift Valley fever virus (RVFV) of the family Bunyaviridae and the genus Phlebovirus. The virus is transmitted by mosquitoes, and virus replication in domestic ruminant results in high rates of mortality and abortion. RVFV infection in humans usually causes a self-limiting, acute and febrile illness; however, a small number of cases progress to neurological disorders, partial or complete blindness, hemorrhagic fever, or thrombosis. This review describes the pathology of RVF in human patients and several animal models, and summarizes the role of viral virulence factors and host factors that affect RVFV pathogenesis.

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Schematic representation of Rift Valley fever virus (RVFV) genome structure. S-encodes N and NSs proteins in an ambisense manner, the M-segment NSm, 78 kD protein Gn and Gc, and the L-segment L proteins. The 78 kD and NSm proteins are synthesized from 1st and 2nd AUG of M mRNA.
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f2-viruses-03-00493: Schematic representation of Rift Valley fever virus (RVFV) genome structure. S-encodes N and NSs proteins in an ambisense manner, the M-segment NSm, 78 kD protein Gn and Gc, and the L-segment L proteins. The 78 kD and NSm proteins are synthesized from 1st and 2nd AUG of M mRNA.

Mentions: The RVFV genome is comprised of three RNA segments named the S-, M- and L-segments (Figure 2) [1,2]. The S-segment encodes N and NSs genes in an ambisense manner, the M-segment. NSm (NSm2), 78 kD (NSm1), Gn and Gc genes, and the L-segment, the RNA-dependent RNA polymerase (L) gene [10]. RVFV virions bind to an unidentified cellular receptor, and enter the cells in a pH-dependent manner [94], probably through a clathrin-mediated endocytic pathway, as described for another phlebovirus [95]. After viral uncoating, viral ribonucleocapsid (RNP) composed of viral genomic RNA segments and N protein [96] is released into the cytoplasm, and the viral polymerase, which probably is attached to the RNP exerts primary transcription to synthesize viral mRNA [97]. Both N mRNA and NSs mRNA are transcribed during primary transcription as early as 40 min after infection from an efficiently packaged, viral-sense (negative-sense) S-segment and anti-viral-sense (positive-sense) S-segment, respectively; the packaging mechanism of RVFV RNP and the presence of specific cis-signals in the genomic RNA are not known [97]. Viral RNA replication starts around 1 to 2 h after infection [97] and an increase in the amount of viral genomic RNA results in increases in viral mRNAs and proteins. The RNP is packaged into viral virions probably by its interaction with the cytoplasmic domains of Gn/Gc at the Golgi apparatus, as reported for other bunyaviruses [98,99]. The three different RNA segments could be co-packaged in a coordinated manner, in which the co-packaging of M and S-segments could support the packaging of the L-segment [100]. The RVFV virion surface is highly symmetric T = 12 icosahedral lattice [101], which is formed by a shell of 122 glycoprotein capsomers most probably composed of 720 Gn-Gc heterodimers [102].


The pathogenesis of Rift Valley fever.

Ikegami T, Makino S - Viruses (2011)

Schematic representation of Rift Valley fever virus (RVFV) genome structure. S-encodes N and NSs proteins in an ambisense manner, the M-segment NSm, 78 kD protein Gn and Gc, and the L-segment L proteins. The 78 kD and NSm proteins are synthesized from 1st and 2nd AUG of M mRNA.
© Copyright Policy
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC3111045&req=5

f2-viruses-03-00493: Schematic representation of Rift Valley fever virus (RVFV) genome structure. S-encodes N and NSs proteins in an ambisense manner, the M-segment NSm, 78 kD protein Gn and Gc, and the L-segment L proteins. The 78 kD and NSm proteins are synthesized from 1st and 2nd AUG of M mRNA.
Mentions: The RVFV genome is comprised of three RNA segments named the S-, M- and L-segments (Figure 2) [1,2]. The S-segment encodes N and NSs genes in an ambisense manner, the M-segment. NSm (NSm2), 78 kD (NSm1), Gn and Gc genes, and the L-segment, the RNA-dependent RNA polymerase (L) gene [10]. RVFV virions bind to an unidentified cellular receptor, and enter the cells in a pH-dependent manner [94], probably through a clathrin-mediated endocytic pathway, as described for another phlebovirus [95]. After viral uncoating, viral ribonucleocapsid (RNP) composed of viral genomic RNA segments and N protein [96] is released into the cytoplasm, and the viral polymerase, which probably is attached to the RNP exerts primary transcription to synthesize viral mRNA [97]. Both N mRNA and NSs mRNA are transcribed during primary transcription as early as 40 min after infection from an efficiently packaged, viral-sense (negative-sense) S-segment and anti-viral-sense (positive-sense) S-segment, respectively; the packaging mechanism of RVFV RNP and the presence of specific cis-signals in the genomic RNA are not known [97]. Viral RNA replication starts around 1 to 2 h after infection [97] and an increase in the amount of viral genomic RNA results in increases in viral mRNAs and proteins. The RNP is packaged into viral virions probably by its interaction with the cytoplasmic domains of Gn/Gc at the Golgi apparatus, as reported for other bunyaviruses [98,99]. The three different RNA segments could be co-packaged in a coordinated manner, in which the co-packaging of M and S-segments could support the packaging of the L-segment [100]. The RVFV virion surface is highly symmetric T = 12 icosahedral lattice [101], which is formed by a shell of 122 glycoprotein capsomers most probably composed of 720 Gn-Gc heterodimers [102].

Bottom Line: Rift Valley fever (RVF) is an emerging zoonotic disease distributed in sub-Saharan African countries and the Arabian Peninsula.RVFV infection in humans usually causes a self-limiting, acute and febrile illness; however, a small number of cases progress to neurological disorders, partial or complete blindness, hemorrhagic fever, or thrombosis.This review describes the pathology of RVF in human patients and several animal models, and summarizes the role of viral virulence factors and host factors that affect RVFV pathogenesis.

View Article: PubMed Central - PubMed

Affiliation: Department of Pathology, The University of Texas Medical Branch, 301 University Blvd., Galveston, TX 77555, USA. teikegam@utmb.edu

ABSTRACT
Rift Valley fever (RVF) is an emerging zoonotic disease distributed in sub-Saharan African countries and the Arabian Peninsula. The disease is caused by the Rift Valley fever virus (RVFV) of the family Bunyaviridae and the genus Phlebovirus. The virus is transmitted by mosquitoes, and virus replication in domestic ruminant results in high rates of mortality and abortion. RVFV infection in humans usually causes a self-limiting, acute and febrile illness; however, a small number of cases progress to neurological disorders, partial or complete blindness, hemorrhagic fever, or thrombosis. This review describes the pathology of RVF in human patients and several animal models, and summarizes the role of viral virulence factors and host factors that affect RVFV pathogenesis.

Show MeSH
Related in: MedlinePlus