Genetic variability and mRNA editing frequencies of the phosphoprotein genes of wild-type measles viruses

Bankamp, Bettina; Lopareva, Elena N.; Kremer, Jacques R.; Tian, Yun; Clemens, Matthew; Patel, Ravi R; Fowlkes, Ashley; Kessler, Julia R.; Muller, Claire; Bellini, William J.; Rota, Paul A.

doi:10.1016/j.virusres.2008.04.008

Cited by 34 publications

(21 citation statements)

References 32 publications

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“…The V protein was also found exclusively in the cytoplasm, but the distribution was more uniform than . Data regarding MeV P gene transcripts were from previous studies by Bankamp et al (2008) and Vanchiere et al (1995).…”

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confidence: 99%

Determination of the henipavirus phosphoprotein gene mRNA editing frequencies and detection of the C, V and W proteins of Nipah virus in virus-infected cells

Harcourt²,

Mungall

et al. 2009

Journal of General Virology

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The henipaviruses, Nipah virus (NiV) and Hendra virus (HeV), are highly pathogenic zoonotic paramyxoviruses. Like many other paramyxoviruses, henipaviruses employ a process of cotranscriptional mRNA editing during transcription of the phosphoprotein (P) gene to generate additional mRNAs encoding the V and W proteins. The C protein is translated from the P mRNA, but in an alternate reading frame. Sequence analysis of multiple, cloned mRNAs showed that the mRNA editing frequencies of the P genes of the henipaviruses are higher than those reported for other paramyxoviruses. Antisera to synthetic peptides from the P, V, W and C proteins of NiV were generated to study their expression in infected cells. All proteins were detected in both infected cells and purified virions. In infected cells, the W protein was detected in the nucleus while P, V and C were found in the cytoplasm.Nipah virus (NiV) and Hendra virus (HeV) are paramyxoviruses in the genus Henipavirus, the subfamily Paramyxovirinae, within the family Paramyxoviridae. HeV causes febrile respiratory illness in humans and animals; of all the febrile illnesses caused by HeV in Australia from 1994 to 2007, there were 17 equine deaths and two human fatalities out of three cases (Hanna et al., 2006;Hooper & Williamson, 2000; Murray et al., 1995a, b). The first human NiV infections were detected during an outbreak of severe febrile encephalitis in peninsular Malaysia and Singapore from autumn 1998 to spring 1999 (Chua et al., 2000). NiV has subsequently been established as the cause of fatal human encephalitis in Bangladesh in 2001, 2003, 2007(Banerjee, 2007Hsu et al., 2004) as well as in India in (Chadha et al., 2006.Fruit-eating bats of the genus Pteropus are a natural reservoir for NiV and HeV (Chua et al., 2002;Halpin et al., 2000;Yob et al., 2001). Humans are infected by exposure to infected fruit bats or material contaminated by infected bats (Hsu et al., 2004), but are also infected via intermediate hosts such as pigs (Amal et al., 2000;Chew et al., 2000;Paton et al., 1999) or by direct human-tohuman contact (Gurley et al., 2007). No vaccines or specific antiviral drugs are currently available for NiV. Although patients from the Malaysian outbreak who received ribavirin showed a lower mortality rate (Chong et al., 2001), ribavirin was unable to protect NiV-infected hamsters from fatal disease (Georges-Courbot et al., 2006).The genomes of NiV and HeV are 18 246 and 18 234 nt, respectively, making them significantly larger than most other paramyxoviruses, with the exceptions of rodentborne Beilong and J viruses (Jack et al., 2005;Li et al., 2006). The N, P and L proteins are required and sufficient for mini-genome replication, similar to other members of the subfamily Paramyxovirinae (Halpin et al., 2004). The P genes of the subfamily Paramyxovirinae, which are 2 704 nt for NiV and 2 698 nt for HeV ( Supplementary Fig. S1, available in JGV Online), contain several open reading frames (ORFs) in addition to the P ORF. Like most other paramyxovirinae, henipavir...

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confidence: 99%

Determination of the henipavirus phosphoprotein gene mRNA editing frequencies and detection of the C, V and W proteins of Nipah virus in virus-infected cells

Harcourt²,

Mungall

et al. 2009

Journal of General Virology

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“…Nevertheless, the P and H genes (and most other MV genes) also have considerable sequence diversity (5.5 and 6.1% [1]), which, as we showed here, can be exploited to monitor viruses with reduced genetic diversity. Thus, by extending the sequencing window for molecular epidemiology, a more refined picture of MV circulation was obtained with more clearly defined links between outbreaks and transmission chains.…”

Section: Discussionmentioning

confidence: 64%

“…PCR products for NP-HVR and P were generated by nested PCRs as described before (1,4). H genes were amplified using a seminested PCR strategy, generating two overlapping fragments in a first round using primers H1 and H6, as well as primers H5 and H2.…”

Section: Methodsmentioning

confidence: 99%

Revealing New Measles Virus Transmission Routes by Use of Sequence Analysis of Phosphoprotein and Hemagglutinin Genes

Kessler

Kremer

Shulga³

et al. 2011

J Clin Microbiol

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With improved measles virus (MV) control, the genetic variability of the MV-nucleoprotein hypervariable region (NP-HVR) decreases. Thus, it becomes increasingly difficult to determine the origin of a virus using only this part of the genome. During outbreaks in Europe and Africa, we found MV strains with identical NP-HVR sequences. However, these strains showed considerable diversity within a larger sequencing window based on concatenated MV phosphoprotein and hemagglutinin genes (P/H pseudogenes). In Belarus, Germany, Russia, and the Democratic Republic of Congo, the P/H pseudogenes provided insights into chains of transmission, whereas identical NP-HVR provided none. In Russia, for instance, the P/H pseudogene identified temporal clusters rather than geographical clusters, demonstrating the circulation and importation of independent variants rather than large local outbreaks lasting for several years, as suggested by NP-HVR. Thus, by extending the sequencing window for molecular epidemiology, a more refined picture of MV circulation was obtained with more clearly defined links between outbreaks and transmission chains. Our results also suggested that in contrast to the P gene, the H gene acquired fixed substitutions that continued to be found in subsequent outbreaks, possibly with consequences for its antigenicity. Thus, a longer sequencing window has true benefits both for the epidemiological surveillance of measles and for the better monitoring of viral evolution.

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“…Vero/hSLAM cells (generous gift of Dr. Yanagi) [22] were maintained and infected as described previously [23]. To produce viral lysates, infected cells were scraped into cell culture medium and stored at −70 °C.…”

Section: Viruses and Cellsmentioning

confidence: 99%

“…To measure the viability of measles viruses on FTA ® cards, a 6 mm punch was mixed with inoculation medium [23], incubated at RT for 10 min and mixed again. The medium (without the filter) was used to inoculate Vero/hSLAM cells which were monitored for cpe for five days.…”

Section: Preparation Of Fta ® Test Panelsmentioning

confidence: 99%

Improving molecular tools for global surveillance of measles virus

Bankamp

Byrd-Leotis

Lopareva

et al. 2013

Journal of Clinical Virology

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Genetic variability and mRNA editing frequencies of the phosphoprotein genes of wild-type measles viruses

Cited by 34 publications

References 32 publications

Determination of the henipavirus phosphoprotein gene mRNA editing frequencies and detection of the C, V and W proteins of Nipah virus in virus-infected cells

Determination of the henipavirus phosphoprotein gene mRNA editing frequencies and detection of the C, V and W proteins of Nipah virus in virus-infected cells

Revealing New Measles Virus Transmission Routes by Use of Sequence Analysis of Phosphoprotein and Hemagglutinin Genes

Improving molecular tools for global surveillance of measles virus

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