Abstract
BackgroundIt 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 FindingsRespiratory 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.ConclusionsThe 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.
Highlights
Mumps is caused by mumps virus (MuV) and is an acute, communicable disease transmitted via the respiratory route
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 small hydrophobic (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
Summary
Mumps is caused by mumps virus (MuV) and is an acute, communicable disease transmitted via the respiratory route. Urabe (genotype B) and Odate-1 (genotype I) strains were both associated with a high incidence of aseptic meningitis in Japan [5]. Some MuV strains within genotype C, which have two different patterns of genetic mutations, show less neurovirulence than others [8]. 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
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