1918 influenza pandemic caused by highly conserved viruses with two receptor-binding variants

The Spanish influenza pandemic swept the globe in the autumn and winter of 1918-19, and resulted in the deaths of approximately 40 million people. Clinically, epidemiologically, and pathologically, the disease was remarkably uniform, which suggests that similar viruses were causing disease around th...

Full description

Saved in:
Bibliographic Details
Published in:Emerging infectious diseases Vol. 9; no. 10; pp. 1249 - 1253
Main Authors: Reid, Ann H, Janczewski, Thomas A, Lourens, Raina M, Elliot, Alex J, Daniels, Rod S, Berry, Colin L, Oxford, John S, Taubenberger, Jeffery K
Format: Journal Article
Language:English
Published: United States U.S. National Center for Infectious Diseases 01-10-2003
Subjects:
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
Description
Summary:The Spanish influenza pandemic swept the globe in the autumn and winter of 1918-19, and resulted in the deaths of approximately 40 million people. Clinically, epidemiologically, and pathologically, the disease was remarkably uniform, which suggests that similar viruses were causing disease around the world. To assess the homogeneity of the 1918 pandemic influenza virus, partial hemagglutinin gene sequences have been determined for five cases, including two newly identified samples from London, United Kingdom. The strains show 98.9% to 99.8% nucleotide sequence identity. One of the few differences between the strains maps to the receptor-binding site of hemagglutinin, suggesting that two receptor-binding configurations were co-circulating during the pandemic. The results suggest that in the early stages of an influenza A pandemic, mutations that occur during replication do not become fixed so that a uniform "consensus" strain circulates for some time.
Bibliography:ObjectType-Article-2
SourceType-Scholarly Journals-1
ObjectType-Feature-1
content type line 23
ObjectType-Article-1
ObjectType-Feature-2
ISSN:1080-6040
1080-6059
DOI:10.3201/eid0910.020789