Influenza AH1N2 Viruses, United Kingdom, 2001-02 Influenza Season

Joanna S. Ellis, Adriana Alvarez-Aguero, Vicky Gregory, Yi Pu Lin, A. Hay, Maria C. Zambon


Emerging Infectious Diseases. 2003;9(3) 

In This Article

Abstract and Introduction

During the winter of 2001-02, influenza AH1N2 viruses were detected for the first time in humans in the U.K. The H1N2 viruses co-circulated with H3N2 viruses and a very small number of H1N1 viruses and were isolated in the community and hospitalized patients, predominantly from children <15 years of age. Characterization of H1N2 viruses indicated that they were antigenically and genetically homogeneous, deriving the hemagglutinin (HA) gene from recently circulating A/New Caledonia/20/99-like H1N1 viruses, whereas the other seven genes originated from recently circulating H3N2 viruses. Retrospective reverse transcription-polymerase chain reaction analysis of influenza A H1 viruses isolated in the U.K. during the previous winter identified a single H1N2 virus, isolated in March 2001, indicating that H1N2 viruses did not widely circulate in the U.K. before September 2001. The reassortment event is estimated to have occurred between 1999 and early 2001, and the emergence of H1N2 viruses in humans reinforces the need for frequent surveillance of circulating viruses.

The influenza A virus genome consists of eight single-stranded RNA segments of negative sense. The segmented nature of the genome allows reassortment of genes between different influenza A strains infecting one host, which may generate novel antigenic variants and give rise to pandemics of disease in humans. Although the influenza pandemic of 1918 appears to have followed the introduction of an avian-like H1N1 virus into the human population,[1] the H2N2 and H3N2 viruses responsible for the 1957 and 1968 human pandemics, respectively, were generated by reassortment between human and avian viruses.[2,3,4] Since the last influenza pandemic of 1977, which was caused by the reemergence of the H1N1 subtype, two subtypes of influenza A (H1N1 and H3N2) have been co-circulating in humans together with influenza B viruses.

The co-circulation of influenza A H1N1 and H3N2 viruses in humans has led to sporadic reports of the isolation of H1N1-H3N2 reassortant viruses in humans.[5,6,7,8,9,10] In contrast, after their isolation from pigs in 1994,[11,12] influenza A H1N2 reassortant viruses, derived from human and avian viruses, have become established in swine throughout the U.K. Influenza viruses of H1N2 subtype, derived from genetic reassortment of strains endemic in pigs, have also been established in pigs in Japan since 1978[13,14] and, more recently, in France[15] and North America.[16]

During 1988-89, several H1N2 viruses were isolated from humans in China.[9,10] Genetic analysis of these reassortant viruses indicated that only the hemagglutinin (HA) gene was derived from the prevailing human H1N1 virus, whereas all other genes, including the neuraminidase (NA) gene, were introduced from the prevailing human H3N2 strain. These reassortant viruses did not spread to other countries until 2001; further isolations of influenza A H1N2 viruses in humans have not been documented.

Influenza AH1N2 viruses were detected for the first time in humans in the U.K. during the winter of 2001-02. We examine the diversity of H1N2 viruses emerging in the U.K. over a 12-month period in 2001-02. The antigenic and genetic properties of these viruses are described, as well as the relationship of reassortant viruses to parental H1N1 and H3N2 strains. Furthermore, the impact of the circulation of H1N2 viruses on disease in the community is considered, as well as the implications for diagnostic testing of influenza strains.


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