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Review
. 2012 Apr;25(2):223-63.
doi: 10.1128/CMR.05012-11.

Two years after pandemic influenza A/2009/H1N1: what have we learned?

Vincent C C Cheng  1 , Kelvin K W To, Herman Tse, Ivan F N Hung, Kwok-Yung Yuen
Affiliations
Review

Two years after pandemic influenza A/2009/H1N1: what have we learned?

Vincent C C Cheng et al. Clin Microbiol Rev. 2012 Apr.

Abstract

The world had been anticipating another influenza pandemic since the last one in 1968. The pandemic influenza A H1N1 2009 virus (A/2009/H1N1) finally arrived, causing the first pandemic influenza of the new millennium, which has affected over 214 countries and caused over 18,449 deaths. Because of the persistent threat from the A/H5N1 virus since 1997 and the outbreak of the severe acute respiratory syndrome (SARS) coronavirus in 2003, medical and scientific communities have been more prepared in mindset and infrastructure. This preparedness has allowed for rapid and effective research on the epidemiological, clinical, pathological, immunological, virological, and other basic scientific aspects of the disease, with impacts on its control. A PubMed search using the keywords "pandemic influenza virus H1N1 2009" yielded over 2,500 publications, which markedly exceeded the number published on previous pandemics. Only representative works with relevance to clinical microbiology and infectious diseases are reviewed in this article. A significant increase in the understanding of this virus and the disease within such a short amount of time has allowed for the timely development of diagnostic tests, treatments, and preventive measures. These findings could prove useful for future randomized controlled clinical trials and the epidemiological control of future pandemics.

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Figures

Fig 1
Fig 1
Maximum-likelihood phylogenetic tree of 3,764 full-length hemagglutinin nucleotide sequences of A/2009/H1N1 strains from the NCBI Influenza Virus Resource. Phylogenetic reconstruction was performed using RAxML version 7.2.6. Positions of 1918 pandemic, 1976 New Jersey swine influenza, seasonal, and 2009 pandemic human influenza A virus strains are highlighted.
Fig 2
Fig 2
Potential diagnostic and antiviral targets in the viral life cycle of influenza virus.
Fig 3
Fig 3
Emergence of A/2009/H1N1 virus from other human and animal influenza viruses. Influenza viruses are usually limited to infecting specific hosts, with tissue tropism and receptor specificity being important restriction factors. A change in tropism sometimes occurs, with pigs being an important “mixing vessel” due to their tracheae containing receptors with both α-2,3-linked and α-2,6-linked sialic acid moieties. In the case of A/2009/H1N1 virus, sequential reassortment of genes from human, avian, and swine influenza viruses culminates in a virus with replication competence comparable to those of other human influenza viruses.
Fig 4
Fig 4
Histopathological examination in fatal cases of A/2009/H1N1. Hematoxylin and eosin (H&E) staining was used for panels A to C and E to H; Gram staining was used for panel D. (A) Lung parenchyma showing the acute phase of viral pneumonia and ARDS, with numerous macrophages within alveolar space. The aveolar septa are congested. Magnification, ×200. (B) A pneumocyte displaying cytopathic change with an enlarged nucleus during the acute phase of ARDS due to viral pneumonia. Magnification, ×400. (C) Lung parenchyma showing the chronic fibroproliferative phase of diffuse alveolar damage. The alveolar septa are thickened, and the alveolar spaces are replaced by fibrogranulation tissue. Magnification, ×200. (D) The alveolar spaces contain many Gram-positive cocci, with some being ingested by macrophages in a patient with secondary bacterial pneumonia. Magnification, ×200. (E) A case with myocarditis, showing lymphoid infiltrate in the myocardium. Magnification, ×200. (F) Organized thrombus of a branch of pulmonary artery. Magnification, ×100. (G) A branch of pulmonary artery with recent thrombus formation. The surrounding lung parenchyma shows heavy acute inflammatory infiltration. Magnification, ×40. (H) Splenic infarct associated with a thrombosed arteriole. Magnification, ×40. (All photos courtesy of Chung-Ying Leung, reproduced with permission.)
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