Novel Measles Virus Genotype, East Timor and Australia

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In This Article
Abstract and Introduction

 

Novel Measles Virus Genotype, East Timor and Australia


 

from Emerging Infectious Diseases
Posted 08/23/2002

Doris Chibo, Michaela Riddell, Michael Catton, and Christopher Birch

 


 

Abstract and Introduction

Abstract

Measles outbreaks in 1999 in Queensland and Victoria, Australia, were caused by a novel strain of clade G virus (proposed name g3). Epidemiologic and molecular evidence supports independent circulation of this virus in Queensland, northern Australia, in addition to importation of the virus by East Timor refugees seeking safe haven in Australia.

Introduction

Strategies to reduce Measles virus (MeV) circulation in industrialized countries, such as aggressive vaccination campaigns targeting children, have proven successful.[1] Nevertheless, through introduction from other geographic locations, the virus continues to cause outbreaks in industrialized countries in unvaccinated persons.

In Victoria, measles is a reportable disease, and an enhanced surveillance strategy has been operational since 1997. A registered nurse visits the homes of patients with reported cases to collect specimens for laboratory confirmation, by polymerase chain reaction or detection of MeV-specific immunoglobulin (Ig) M, of the clinical diagnosis and subsequent identification of the measles genotype.[6] For other Australian states, specimens from laboratory-confirmed cases are sent to the WHO regional measles reference laboratory for the western Pacific Region.

Variable regions in the MeV genome include the hemagglutinin (H) and nucleoprotein (N) genes. The most variable region is the carboxyl-terminal end (450 nucleotides [nt]) of the N gene. A uniform nomenclature approved by World Health Organization (WHO) has existed since 1998 and is used in classifying and naming measles viruses. Currently, 20 genotypes and 1 proposed new genotype exist, encompassing eight clades designated A-H. Each clade contains MeV genotypes that are related by >/=2.5% nt divergence in the 450-bp carboxyl-terminal end of the N gene and 2% in the H gene.[2] Clades are distinguished by greater nucleotide differences, location of nucleotides, and specific nucleotides shared in genotypes of a particular clade.

Until recently, MeV strains belonging to clade G had not been detected for >15 years, and the lineage was considered to be either extinct or inactive.[3] However, retrospective sequence analysis of a measles strain isolated from an immunocompromised infant from the Netherlands, who had been infected in Indonesia in 1997, and of measles strains associated with outbreaks in Indonesia and Malaysia in 1999 have demonstrated that this genotype has circulated in the intervening period.[4-5] We describe the circulation of a novel genotype of MeV in Australia and investigate its likely origin.

 


 

Section 1 of 2 Continue

 
Doris Chibo, Michaela Riddell, Michael Catton, and Christopher Birch, World Health Organization Regional Measles Reference Laboratory for the Western Pacific Region, North Melbourne, Victoria, Australia

Ms. Chibo is a medical scientist at the Victorian Infectious Diseases Reference Laboratory in Victoria, Australia. Her main interests are the use of molecular techniques and phylogenetic analysis to study viruses of public health importance and mechanisms associated with development of resistance to antiviral drugs by herpesviruses.


 


Emerg Infect Dis 8(7), 2002. © 2002 Centers for Disease Control and Prevention (CDC)



 

 


 


 

 


 


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