Genetic variation in the HN and SH genes of mumps viruses: a comparison of strains from mumps cases with and without neurological symptoms

PLoS One. 2013 Apr 24;8(4):e61791. doi: 10.1371/journal.pone.0061791. Print 2013.

Abstract

Background: It is known that mumps virus (MuV) strains may vary in their neurovirulent capacity, and certain MuV strains may be highly neurotropic. In animal models and epidemiological studies, mutations at specific amino acids (aa) have been proposed to be associated with neurovirulence. To assess whether these genetic variations can be observed in clinical samples from patients and if they correlate with neurovirulence as determined by clinical symptoms, 39 mumps patients with or without neurological symptoms were investigated.

Principal findings: Respiratory samples, oral fluids, throat swabs, and neurological and cerebrospinal fluid samples were tested by RT-PCR and products sequenced. Sequences of the entire small hydrophobic (SH) gene and the partial hemagglutinin-neuraminidase (HN) gene were compared.

Conclusions: The results showed there was no significant difference between the samples of the two groups of patients at the aa sites in either the HN protein or the SH protein, which have previously been hypothesized to be associated with neurovirulence or antigenicity. The occurrence of neurological symptoms of mumps does not appear to be due to a single point mutation in either the HN or SH gene.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Amino Acid Sequence
  • Amino Acid Substitution
  • Genotype
  • HN Protein / chemistry
  • HN Protein / genetics*
  • Humans
  • Molecular Sequence Data
  • Mumps / virology*
  • Mumps virus / classification
  • Mumps virus / genetics*
  • Mumps virus / pathogenicity
  • Protein Interaction Domains and Motifs
  • Sequence Alignment
  • Viral Proteins / chemistry
  • Viral Proteins / genetics*
  • Virulence / genetics

Substances

  • HN Protein
  • Viral Proteins
  • small hydrophobic protein, Mumps virus

Associated data

  • GENBANK/JQ034428
  • GENBANK/JQ034429
  • GENBANK/JQ034430
  • GENBANK/JQ034431
  • GENBANK/JQ034432
  • GENBANK/JQ034433
  • GENBANK/JQ034434
  • GENBANK/JQ034435
  • GENBANK/JQ034436
  • GENBANK/JQ034437
  • GENBANK/JQ034438
  • GENBANK/JQ034439
  • GENBANK/JQ034440
  • GENBANK/JQ034441
  • GENBANK/JQ034442
  • GENBANK/JQ034443
  • GENBANK/JQ034444
  • GENBANK/JQ034445
  • GENBANK/JQ034446
  • GENBANK/JQ034447
  • GENBANK/JQ034448
  • GENBANK/JQ034449
  • GENBANK/JQ034450
  • GENBANK/JQ034451
  • GENBANK/JQ034452
  • GENBANK/JQ034453
  • GENBANK/JQ034454
  • GENBANK/JQ034455
  • GENBANK/JQ034456
  • GENBANK/JQ034467
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  • GENBANK/JQ034469
  • GENBANK/JQ034470
  • GENBANK/JQ034471
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  • GENBANK/JQ034473
  • GENBANK/JQ034474
  • GENBANK/JQ034475
  • GENBANK/JQ034476
  • GENBANK/JQ034477
  • GENBANK/JQ034478
  • GENBANK/JQ034479
  • GENBANK/JQ034480
  • GENBANK/JQ034481
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  • GENBANK/JQ034483
  • GENBANK/JQ034484
  • GENBANK/JQ034485
  • GENBANK/JQ034486
  • GENBANK/JQ034487
  • GENBANK/JQ034488
  • GENBANK/JQ034489
  • GENBANK/JQ034490
  • GENBANK/JQ034491
  • GENBANK/JQ034492
  • GENBANK/JQ034493
  • GENBANK/JQ034499
  • GENBANK/JQ034500
  • GENBANK/JQ034501
  • GENBANK/JQ034503

Grants and funding

This work was partially supported by the National Natural Science Foundation of China (project no. 81102170), the National Infectious Disease Surveillance Program of the Ministry of Science and Technology of the People’s Republic of China (2012ZX10004201-003 and 2013ZX10004202). The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.