Giuseppe
Emeritus
[Source: Journal of Clinical Virology, full text: (LINK). Abstract, edited.]
Journal of Clinical Virology
In Press, Corrected Proof - Note to users
doi:10.1016/j.jcv.2011.09.004
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Emergent 2009 influenza A(H1N1) viruses containing HA D222N mutation associated with severe clinical outcomes in the Americas<SUP>☆</SUP>
Huo-Shu H. Houng<SUP>a</SUP>, Jason Garner<SUP>b</SUP><SUP>, </SUP><SUP>c</SUP>, Yanfei Zhou<SUP>a</SUP>, Arthur Lyons<SUP>a</SUP>, Robert Kuschner<SUP>a</SUP>, Gregory Deye<SUP>a</SUP>, Kristina St. Clair<SUP>d</SUP>, Richard W. Douce<SUP>e</SUP>, Wilson Chicaiza<SUP>e</SUP>, Patrick J. Blair<SUP>f</SUP>, Christopher A. Myers<SUP>f</SUP>, Ronald L. Burke<SUP>g</SUP>, Jose L. Sanchez<SUP>c, </SUP><SUP>g</SUP>, Maya Williams<SUP>h</SUP>, Eric S. Halsey<SUP>h</SUP>
<SUP>a) </SUP>Walter Reed Army Institute of Research, Silver Spring, MA 20910, USA ? <SUP>b) </SUP>United States Air Force School of Aerospace Medicine, Brooks City-Base, TX 78235, USA ? <SUP>c) </SUP>Henry M. Jackson Foundation for the Advancement of Military Medicine, Rockville, MA 20852, USA ? <SUP>d) </SUP>National Naval Medical Center, Bethesda, MA 20889, USA ? <SUP>e) </SUP>Hospital Vozandes Quito, Casilla 0691, Quito, Ecuador, USA ? <SUP>f) </SUP>Navy Health Research Center, San Diego, CA 92106, USA ? <SUP>g) </SUP>Armed Forces Health Surveillance Center, Global Emerging Infections Surveillance and Response System, Silver Spring, MA 20904, USA ? <SUP>h) </SUP>United States Naval Medical Research Unit Six, Lima, Peru 20521-3230, USA
Received 25 May 2011; revised 2 September 2011; Accepted 7 September 2011. Available online 28 October 2011.
Abstract
Background
During the 2010?2011 influenza season, a small sub-group of 2009 influenza A(H1N1) viruses (hereafter referred to as 2009 A(H1N1)) emerged that was associated with more severe clinical outcomes in Ecuador and North America. Genetically, the haemagglutinin (HA) of this sub-clade was distinct from HAs found in viruses associated with severe outbreaks in 2010 from the United Kingdom and from other global specimens isolated earlier in the season.
Objective
We report the emergence of a novel 2009 A(H1N1) variant possessing a re-emergent HA D222N mutation obtained from patients with severe respiratory illnesses and phylogenetically characterise these D222N mutants with other severe disease-causing variants clustering within a common emerging sub-clade.
Case reports
In early 2011, three cases of 2009 A(H1N1) infection, two from Quito, Ecuador, and one from Washington, DC, USA, were complicated by severe pneumonia requiring mechanical ventilation, resulting in one fatality. These cases were selected due to the reported nature of the acute respiratory distress (ARD) that were captured in Department of Defence (DoD)-sponsored global influenza surveillance nets.
Results
Genetically, the 2009 A(H1N1) strains isolated from two of the three severe cases carried a prominent amino acid change at position 222 (D222N) within the primary HA receptor binding site. Furthermore, these cases represent an emerging sub-clade of viruses defined by amino acid changes within HA: N31D, S162N, A186T and V272I. Phylogenetically, these viruses share a high degree of homology with strains associated with recent fatal cases in Chihuahua, Mexico.
Discussion
Previously, enhanced virulence associated with the change, D222G, has been clinically linked to severe morbidity and mortality. Initial observations of the prevalence of a novel sub-clade of strains in the Americas suggest that viruses with a re-emergent D222N mutation may too correlate with severe clinical manifestations. These findings warrant heightened vigilance for emerging sub-clades of 2009 A(H1N1) and presumptive clinical implications.
Keywords: 2009 A(HINI); Influenza; Severe infections; D222N; HA receptor binding site
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Journal of Clinical Virology
In Press, Corrected Proof - Note to users
doi:10.1016/j.jcv.2011.09.004
Permissions & Reprints
Emergent 2009 influenza A(H1N1) viruses containing HA D222N mutation associated with severe clinical outcomes in the Americas<SUP>☆</SUP>
Huo-Shu H. Houng<SUP>a</SUP>, Jason Garner<SUP>b</SUP><SUP>, </SUP><SUP>c</SUP>, Yanfei Zhou<SUP>a</SUP>, Arthur Lyons<SUP>a</SUP>, Robert Kuschner<SUP>a</SUP>, Gregory Deye<SUP>a</SUP>, Kristina St. Clair<SUP>d</SUP>, Richard W. Douce<SUP>e</SUP>, Wilson Chicaiza<SUP>e</SUP>, Patrick J. Blair<SUP>f</SUP>, Christopher A. Myers<SUP>f</SUP>, Ronald L. Burke<SUP>g</SUP>, Jose L. Sanchez<SUP>c, </SUP><SUP>g</SUP>, Maya Williams<SUP>h</SUP>, Eric S. Halsey<SUP>h</SUP>
<SUP>a) </SUP>Walter Reed Army Institute of Research, Silver Spring, MA 20910, USA ? <SUP>b) </SUP>United States Air Force School of Aerospace Medicine, Brooks City-Base, TX 78235, USA ? <SUP>c) </SUP>Henry M. Jackson Foundation for the Advancement of Military Medicine, Rockville, MA 20852, USA ? <SUP>d) </SUP>National Naval Medical Center, Bethesda, MA 20889, USA ? <SUP>e) </SUP>Hospital Vozandes Quito, Casilla 0691, Quito, Ecuador, USA ? <SUP>f) </SUP>Navy Health Research Center, San Diego, CA 92106, USA ? <SUP>g) </SUP>Armed Forces Health Surveillance Center, Global Emerging Infections Surveillance and Response System, Silver Spring, MA 20904, USA ? <SUP>h) </SUP>United States Naval Medical Research Unit Six, Lima, Peru 20521-3230, USA
Received 25 May 2011; revised 2 September 2011; Accepted 7 September 2011. Available online 28 October 2011.
Abstract
Background
During the 2010?2011 influenza season, a small sub-group of 2009 influenza A(H1N1) viruses (hereafter referred to as 2009 A(H1N1)) emerged that was associated with more severe clinical outcomes in Ecuador and North America. Genetically, the haemagglutinin (HA) of this sub-clade was distinct from HAs found in viruses associated with severe outbreaks in 2010 from the United Kingdom and from other global specimens isolated earlier in the season.
Objective
We report the emergence of a novel 2009 A(H1N1) variant possessing a re-emergent HA D222N mutation obtained from patients with severe respiratory illnesses and phylogenetically characterise these D222N mutants with other severe disease-causing variants clustering within a common emerging sub-clade.
Case reports
In early 2011, three cases of 2009 A(H1N1) infection, two from Quito, Ecuador, and one from Washington, DC, USA, were complicated by severe pneumonia requiring mechanical ventilation, resulting in one fatality. These cases were selected due to the reported nature of the acute respiratory distress (ARD) that were captured in Department of Defence (DoD)-sponsored global influenza surveillance nets.
Results
Genetically, the 2009 A(H1N1) strains isolated from two of the three severe cases carried a prominent amino acid change at position 222 (D222N) within the primary HA receptor binding site. Furthermore, these cases represent an emerging sub-clade of viruses defined by amino acid changes within HA: N31D, S162N, A186T and V272I. Phylogenetically, these viruses share a high degree of homology with strains associated with recent fatal cases in Chihuahua, Mexico.
Discussion
Previously, enhanced virulence associated with the change, D222G, has been clinically linked to severe morbidity and mortality. Initial observations of the prevalence of a novel sub-clade of strains in the Americas suggest that viruses with a re-emergent D222N mutation may too correlate with severe clinical manifestations. These findings warrant heightened vigilance for emerging sub-clades of 2009 A(H1N1) and presumptive clinical implications.
Keywords: 2009 A(HINI); Influenza; Severe infections; D222N; HA receptor binding site