Wild-Type Measles Viruses with Non-Standard Genome Lengths

Bankamp, Bettina; Liu, Chunyu; Rivailler, Pierre; Bera, Jayati; Shrivastava, Susmita; Kirkness, Ewen F.; Bellini, William J.; Rota, Paul A.

doi:10.1371/journal.pone.0095470

Cited by 28 publications

(26 citation statements)

References 47 publications

(43 reference statements)

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“…For example, distinct MeV strains isolated from clinical infections contained additions in the 3’ UTR of the M gene and deletions in the F 5’ UTR in the M/F intergenic region (Bankamp et al, 2014). Our study showed that this intergenic region contained the most abundant number of transposons in our screen, totaling ~34% of all reads with insertions.…”

Section: Discussionmentioning

confidence: 99%

Mutational Analysis of Measles Virus Suggests Constraints on Antigenic Variation of the Glycoproteins

et al. 2015

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Summary Measles virus undergoes error-prone replication like other RNA viruses, but over time it has remained antigenically monotypic. The constraints on the virus that prevent the emergence of antigenic variants are unclear. As a first step in understanding this question, we subjected the measles virus genome to unbiased insertional mutagenesis and viruses that could tolerate insertions were rescued. Only insertions in the nucleoprotein, phosphoprotein, matrix protein, as well as intergenic regions were easily recoverable. Insertions in the glycoproteins of measles virus were severely under-represented in our screen. Host immunity depends on developing neutralizing antibodies to the hemagglutinin and fusion glycoproteins; our analysis suggests that these proteins occupy very little evolutionary space and therefore have difficulty changing in the face of selective pressures. We propose that the inelasticity of these proteins prevents the sequence variation required to escape antibody neutralization in the host, allowing for long-lived immunity after infection with the virus.

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Section: Discussionmentioning

confidence: 99%

Mutational Analysis of Measles Virus Suggests Constraints on Antigenic Variation of the Glycoproteins

et al. 2015

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“…cDNA synthesis and nested PCR of the N, M, F, and H genes were performed as previously described (7). The P genes of one SSPE and two MIBE viruses were amplified using previously described primers (29). The L gene of the SSPE virus was amplified using primers from Bankamp et al (29).…”

Section: Methodsmentioning

confidence: 99%

“…The P genes of one SSPE and two MIBE viruses were amplified using previously described primers (29). The L gene of the SSPE virus was amplified using primers from Bankamp et al (29).…”

Section: Methodsmentioning

confidence: 99%

Analysis of a Subacute Sclerosing Panencephalitis Genotype B3 Virus from the 2009-2010 South African Measles Epidemic Shows That Hyperfusogenic F Proteins Contribute to Measles Virus Infection in the Brain

Angius

Smuts

Rybkina

et al. 2019

J Virol

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During a measles virus (MeV) epidemic in 2009 in South Africa, measles inclusion body encephalitis (MIBE) was identified in several HIV-infected patients. Years later, children are presenting with subacute sclerosing panencephalitis (SSPE). To investigate the features of established MeV neuronal infections, viral sequences were analyzed from brain tissue samples of a single SSPE case and compared with MIBE sequences previously obtained from patients infected during the same epidemic. Both the SSPE and the MIBE viruses had amino acid substitutions in the ectodomain of the F protein that confer enhanced fusion properties. Functional analysis of the fusion complexes confirmed that both MIBE and SSPE F protein mutations promoted fusion with less dependence on interaction by the viral receptor-binding protein with known MeV receptors. While the SSPE F required the presence of a homotypic attachment protein, MeV H, in order to fuse, MIBE F did not. Both F proteins had decreased thermal stability compared to that of the corresponding wild-type F protein. Finally, recombinant viruses expressing MIBE or SSPE fusion complexes spread in the absence of known MeV receptors, with MIBE F-bearing viruses causing large syncytia in these cells. Our results suggest that alterations to the MeV fusion complex that promote fusion and cell-to-cell spread in the absence of known MeV receptors is a key property for infection of the brain. IMPORTANCE Measles virus can invade the central nervous system (CNS) and cause severe neurological complications, such as MIBE and SSPE. However, mechanisms by which MeV enters the CNS and triggers the disease remain unclear. We analyzed viruses from brain tissue of individuals with MIBE or SSPE, infected during the same epidemic, after the onset of neurological disease. Our findings indicate that the emergence of hyperfusogenic MeV F proteins is associated with infection of the brain. We also demonstrate that hyperfusogenic F proteins permit MeV to enter cells and spread without the need to engage nectin-4 or CD150, known receptors for MeV that are not present on neural cells.

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“…A variant of peste des petits ruminants virus (PPRV) with an insertion of six bases in the F gene 5′ UTR was recently identified in China in 2013 28 . Similarly, several variants of measles virus (MV) have been found with a net insertion of six bases [29][30][31] . The mechanism of how these insertions and deletions occur is not yet clear, though it has been suggested from studies of MV genome variants that it is the result of errors of the viral polymerase when transcribing regions with extended homopolymers 30 .…”

Section: Sequence Features In the Completed Genomesmentioning

confidence: 99%

Full genome sequencing of archived wild type and vaccine rinderpest virus isolates prior to their destruction

King

Rajko-Nenow

Ropiak

et al. 2020

Sci Rep

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When rinderpest virus (RPV) was declared eradicated in 2011, the only remaining samples of this once much-feared livestock virus were those held in various laboratories. in order to allow the destruction of our institute's stocks of RpV while maintaining the ability to recover the various viruses if ever required, we have determined the full genome sequence of all our distinct samples of RPV, including 51 wild type viruses and examples of three different types of vaccine strain. Examination of the sequences of these virus isolates has shown that the African isolates form a single disparate clade, rather than two separate clades, which is more in accord with the known history of the virus in Africa. We have also identified two groups of goat-passaged viruses which have acquired an extra 6 bases in the long untranslated region between the M and f protein coding sequences, and shown that, for more than half the genomes sequenced, translation of the f protein requires translational frameshift or non-standard translation initiation. curiously, the clade containing the lapinised vaccine viruses that were developed originally in Korea appears to be more similar to the known African viruses than to any other Asian viruses.Rinderpest (RP) was one of the most severe diseases of cattle ever recorded, with high morbidity rates, and mortality rates of 80% to 90% in naïve populations. The disease was declared eradicated in 2011 1 , thus becoming the second viral disease, after smallpox, to be eradicated, with global benefits estimated to be in the billions of dollars 2 . The RP virus (RPV) itself has not been entirely eliminated, with a number of laboratories known to have samples of wild type RPV. Accidental release of RPV from such a laboratory is thought to be the most likely pathway by which the virus might re-enter the environment 3,4 , although it might also be deliberately released as an act of sabotage or bioterrorism. The member states of the World Organisation for Animal Health (OIE), and the Food and Agricultural Organisation of the United Nations (FAO) agreed to restrict all work with the virus and to allow the storage of the virus only in highly secure Rinderpest Holding Facilities (RHFs) that have been inspected and approved jointly by OIE and FAO.The FAO-OIE RHF in the UK is the Pirbright Institute which, as the Institute for Animal Health, and before that the Animal Virus Research Institute, was a centre for research on RPV since the 1960s. The institute developed the monoclonal antibody-based competition ELISA (cELISA) used extensively for surveillance 5 , as well as the most widely used RT-PCR assay for RPV 6 and the concept of different geographic lineages of the virus based on the sequence of the product from the RT-PCR 7 . The first RPV genome sequences were determined at Pirbright 8,9 and the system for recovering RPV from a cDNA copy of the genome was developed there 10 . Because of this history, and its links to many of the countries where RPV was still endemic in the latter half of the 20 th century, t...

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Wild-Type Measles Viruses with Non-Standard Genome Lengths

Cited by 28 publications

References 47 publications

Mutational Analysis of Measles Virus Suggests Constraints on Antigenic Variation of the Glycoproteins

Mutational Analysis of Measles Virus Suggests Constraints on Antigenic Variation of the Glycoproteins

Analysis of a Subacute Sclerosing Panencephalitis Genotype B3 Virus from the 2009-2010 South African Measles Epidemic Shows That Hyperfusogenic F Proteins Contribute to Measles Virus Infection in the Brain

Full genome sequencing of archived wild type and vaccine rinderpest virus isolates prior to their destruction

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