Towards a sane and rational approach to management of Influenza H1N1 2009

Abstract

Beginning in March 2009, an outbreak of influenza in North America was found to be caused by a new strain of influenza virus, designated Influenza H1N1 2009, which is a reassortant of swine, avian and human influenza viruses. Over a thousand total cases were identified with the first month, chiefly in the United States and Mexico, but also involving several European countries. Actions concerning Influenza H1N1 2009 need to be based on fact and science, following recommendations of public health officials, and not fueled by political, legal or other interests. Every influenza outbreak or pandemic is unique, so the facts of each one must be studied before an appropriate response can be developed. While reports are preliminary, through the first 4 weeks of the outbreak it does not appear to be severe either in terms of the attack rate in communities or in the virulence of the virus itself. However, there are significant changes in both the hemagglutinin and neuraminidase proteins of the new virus, 27.2% and 18.2% of the amino acid sequence, from prior H1N1 isolates in 2008 and the current vaccine. Such a degree of change qualifies as an "antigenic shift", even while the virus remains in the H1N1 family of influenza viruses, and may give influenza H1N1 2009 significant pandemic potential. Perhaps balancing this shift, the novel virus retains more of the core influenza proteins from animal strains than successful human influenza viruses, and may be inhibited from its maximum potential until further reassortment or mutation better adapts it to multiplication in humans. While contact and respiratory precautions such as frequent handwashing will slow the virus through the human population, it is likely that development of a new influenza vaccine tailored to this novel Influenza H1N1 2009 strain will be essential to blunt its ultimate pandemic impact.

Figure 1

Amino acid sequence alignment of the mature hemagglutinin (H) proteins of Influenza H1N1 2009 and its predecessor H1N1 isolated in 2008. The amino acid sequence of the H protein shown for the Influenza H1N1 2009 virus is derived from the segment 4 sequence of the isolate A/California/08/2009(H1N1) submitted from the CDC by Shu et al. on April 29, 2009, as Genbank FJ971076. The sequence for Influenza H1N1 2008 is derived from the segment 4 sequence of the isolate A/District of Columbia/WRAMC-1154048/2008(H1N1) submitted from Walter Reed Army Institute of Research by Houng et al., collected from a patient on February 1, 2008, as Genbank CY038770. Only the sequences of the mature proteins, after cleavage of the signal sequence, are shown. Standard single-letter abbreviations for the amino acids are used. The collinear sequences were hand-aligned and also confirmed by online use of ClustalW. Amino acid positions showing differences between the two sequences are denoted with an “X”. There are 89 differences in 327 positions, or 27.2%. The canonical sites for N-linked glycosylation are underlined. Amino acid regions contributing to each of five antigenic sites are labeled Site A through Site E.