Abstract
History illustrates the remarkable public health impact of mass vaccination, by dramatically improving life expectancy and reducing the burden of infectious diseases and co-morbidities worldwide. It has been perceived that if an individual adhered to the MMR vaccine schedule that immunity to mumps virus (MuV) would be lifelong. Recent mumps outbreaks in individuals who had received two doses of the Measles Mumps Rubella (MMR) vaccine has challenged the efficacy of the MMR vaccine. However, clinical symptoms, complications, viral shedding and transmission associated with mumps infection has been shown to be reduced in vaccinated individuals, demonstrating a benefit of this vaccine. Therefore, the question of what constitutes a good mumps vaccine and how its impact is assessed in this modern era remains to be addressed. Epidemiology of the individuals most affected by the outbreaks (predominantly young adults) and variance in the circulating MuV genotype have been well-described alluding to a collection of influences such as vaccine hesitancy, heterogeneous vaccine uptake, primary, and/or secondary vaccine failures. This review aims to discuss in detail the interplay of factors thought to be contributing to the current mumps outbreaks seen in highly vaccinated populations. In addition, how mumps diagnoses has progressed and impacted the understanding of mumps infection since a mumps vaccine was first developed, the limitations of current laboratory tests in confirming protection in vaccinated individuals and how vaccine effectiveness is quantified are also considered. By highlighting knowledge gaps within this area, this state-of-the-art review proposes a change of perspective regarding the impact of a vaccine in a highly vaccinated population from a clinical, diagnostic and public perspective, highlighting a need for a paradigm shift on what is considered vaccine immunity.
Highlights
Mumps Virusmumps virus (MuV) is an enveloped, non-segmented, negative-sense, single stranded RNA virus that varies between a spherical and pleiomorphic shape of ∼200 nm (85–300 nm) [1, 2]
The MuV genome of seven genes consists of 15,384 nucleotides, and encodes six structural proteins and at least two non-structural proteins; the nucleocapsid protein (NP), V protein (V), phosphoprotein (P), matrix (M) protein, fusion (F) protein, small hydrophobic (SH) protein, hemagglutininneuraminidase (HN) protein, and large (L) protein
Genotypes C, D, E, G, and H are prevalent in Europe and the United States of America (USA) whereas genotypes B, F and I are more common in Asian countries (Table 1) [10, 18, 86, 87]
Summary
MuV is an enveloped, non-segmented, negative-sense, single stranded RNA virus that varies between a spherical and pleiomorphic shape of ∼200 nm (85–300 nm) [1, 2]. MuV is responsible for an acute viral infection, spread by respiratory droplets (via coughs, sneezes) and urine [3, 4]. With an incubation period of 14–25 days, MuV replicates in the nasopharynx and regional lymph nodes, with a secondary viremia occurring late in the incubation period [5, 6]. MuV can be detected from saliva up to 7 days prior, and as late as 9 days after clinical onset of parotitis [7]
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