Molecular biology, pathogenesis and

pathology of mumps virus

Intruduction
 Before routine mumps vaccination programmes were
introduced, 95% of adults had serological markers of
exposure, with peak acquisition during childhood
 Caused by Paramyxovirus family usually Called Mumps Virus
(Muv)
 Have many clinical features like parotitis, Orchitis, Mastitits,
Oophorithis
 Lead Cases of Enchepalithis in America
Method
 Depend on Hipocrates Theories
 With Prostulach Koch, tested with monkey
 By RT-PCR Test
 Clinical found in child, that had MuV without symtopm in
their upper respiratory tract
Discuss : The Virus

 ParamyxoVirus
 Enveloped
 size range 100–600 nm
 RNA
 Proteins :nucleo- (N), V/P/I (V/phospho-/I proteins),
matrix (M), fusion (F), small hydrophobic (SH),
haemagglutinin-neuraminidase (HN) and large (L) proteins.
Discuss : The Disease
Clinical features – pre vaccine era
 Targetting Upper Respiratory Tract Epithelium
 Systemic spread: from epitheliotropic to lymphotropic
After affect by it fuctional protein its spread by lymph node,
An blood, as outcomes :
- Parotithis : as submandibular, sub maxilar, and sublingual gland.
Virus replicated in Parotid too, as a result the virus found in the
saliva.
- Orchitis : Affect the Testes
- Mastitis and oophoritis : Affect Mammary duct and Ovarium
 Lymphotropic to neutropenic
In 5 – 10% cases as results : enchepalitis and meningitis
Conclusion
A number of important questions remain unresolved regarding MuV
pathogenesis. This is of particular relevance to renewed efforts
towards development of a more effiacious MuV vaccine, in light of the
resurgence of mumps in vaccinated populations. The classic method
of virus attenuation is extensive blind passage in vitro. While this often
leads to the desired effect of a loss of virulence and reactogenicity,
it can also lead to loss of immunogenicity and effiacy. Clearly, a more
rational approach to virus attenuation is needed, and understanding
the natural pathogenesis of the infectious agent is a prerequisite to any
such endeavour
Acknowledgements
This work was supported by the NIH R01 AI105063 to
WPD and by the Oak Ridge Institute for Science and
Education through an interagency agreement between
the US Department of Energy and the US Food and Drug
Administration. We wish to thank Christian Sauder and
Laurie Ngo (FDA, Silver Spring, MD) for critical reading of the
manuscript, and Jan Johannessen (FDA, Silver
Spring, MD) for providing the MRI rat brain images.
We dedicate this work to the memory of the late Dr
Philip Snoy, DVM, Director, CBER Veterinary Services,
respected scientist, admired leader and treasured friend,
who laid much of the groundwork towards development
of improved preclinical MuV neurotoxicity tests.
THANK YOU