Children with sickle cell disease experience more life-threatening complications from the H1N1 swine flu than from seasonal flu, a new study has found. The study authors analyzed the medical records of 123 children with sickle cell disease treated for any kind of flu between September 1993 and December 2009. Of those, 29 were infected with the 2009 H1N1 swine flu virus. However, those infected with H1N1 were nearly three times more likely to develop acute chest syndrome, a leading cause of death in children with sickle cell disease.

More via Sickle Cell Kids at Greater Risk of ‘Swine Flu’ Complications.

Further evolution was seen in the four sequences from Christchurch collected between July 5 and 12 from at least two locations (Rakai and Timaru). The most evolved sequence, A/Christchurch/16/2010 (from a 20M), had D225N as well as five additional non-synonymous changes, signaling rapid evolution. All four Christchurch sequences were closely related to each other and had evolved from the Australian sequences. This rapid evolution signals adaptation away from host defenses developed against last season’s vaccine or infections.

via H1N1 D225G/N In Recent Australia and New Zealand Cases.

Recently released 2010 sequence has demonstrated that these genetic changes are on the rise, raising concerns for the emergence of a more virulent H1N1 in the upcoming months or years. The acquisition of these new markers via recombination has similarities with the fixing of H274Y in seasonal H1N1 in the 2008/2009 season. H274Y confers Tamilfu resistance and began to appear in large numbers in seasonal H1N1 in selective countries in the 2007/2008 season.

More information via Hazardous WHO Pandemic Hopes and Dreams.

Two amino acids (lysine at position 627 or asparagine at position 701) in the polymerase subunit PB2 protein are considered critical for the adaptation of avian influenza A viruses to mammals. However, the recently emerged pandemic H1N1 viruses lack these amino acids. Here, we report that a basic amino acid at position 591 of PB2 can compensate for the lack of lysine at position 627 and confers efficient viral replication to pandemic H1N1 viruses in mammals. Moreover, a basic amino acid at position 591 of PB2 substantially increased the lethality of an avian H5N1 virus in mice. We also present the X-ray crystallographic structure of the C-terminus of a pandemic H1N1 virus PB2 protein. Arginine at position 591 fills the cleft found in H5N1 PB2 proteins in this area, resulting in differences in surface shape and charge for H1N1 PB2 proteins. These differences may affect the protein’s interaction with viral and/or cellular factors, and hence its ability to support virus replication in mammals.

via PLoS Pathogens: Biological and Structural Characterization of a Host-Adapting Amino Acid in Influenza Virus.

The current pandemic of a novel influenza A (H1N1) virus, commonly referred to as “swine flu”, began in Mexico in March 2009 and reached the UK in April 2009. By 21 July 2009, more than 850 suspected cases of influenza had been seen at Birmingham Heartlands Hospital (BHH), including 52 adults with laboratory-confirmed pandemic H1N1 influenza who were admitted. Of seven patients (13%) requiring intensive care, six needed mechanical ventilation, two needed extra-corporeal membrane oxygenation (ECMO) and one died. Of the 52 admitted adults, 42 (81%) had respiratory symptoms or signs and positive PCR tests for novel Influenza A (H1N1) virus. These patients also had chest radiographs (CXR) taken, which were abnormal for 12 patients (29%). Of these, six patients had bilateral consolidation, which was bibasal in three and widespread in three; all six had pleural effusions. A further six patients had unilateral consolidation with predominantly basal changes; one of these patients had a pleural effusion. The odds ratio for requiring intubation and ventilation with H1N1 influenza and an abnormal CXR was 29.0 (95% confidence interval 2.93-287.0). CXR changes were not common in swine flu, but a significant minority of those requiring admission had consolidation on their CXR. Those who required admission and had CXR changes are more likely to require intubation and ventilation than those without abnormalities on CXR.

via Chest radiography findings in adults with pandemic… [Br J Radiol. 2010] – PubMed result.

Pandemic (H1N1) 2009 virus causes severe illness, including pneumonia, which leads to hospitalization and even death. To characterize the kinetic changes in viral load and identify factors of influence, we analyzed variables that could potentially influence the viral shedding time in a hospital-based cohort of 1,052 patients. Viral load was inversely correlated with number of days after the onset of fever and was maintained at a high level over the first 3 days. Patients with pneumonia had higher viral loads than those with bronchitis or upper respiratory tract infection. Median viral shedding time after the onset of symptoms was 9 days. Patients <13 years of age had a longer median viral shedding time than those >13 years of age (11 days vs. 7 days). These results suggest that younger children may require a longer isolation period and that patients with pneumonia may require treatment that is more aggressive than standard therapy for pandemic (H1N1) 2009 virus.

via Pandemic (H1N1) 2009 Viral Load and Shedding | CDC EID.

Influenza viruses continue to cause yearly epidemics and occasional pandemics in humans. In recent years, the threat of a possible influenza pandemic arising from the avian influenza A(H5N1) virus has prompted the development of comprehensive pandemic preparedness programs in many countries. The recent emergence of the pandemic influenza A(H1N1) 2009 virus from the Americas in early 2009, although surprising in its geographic and zoonotic origins, has tested these preparedness programs and revealed areas in which further work is necessary. Nevertheless, the plethora of epidemiologic, diagnostic, mathematical and phylogenetic modeling, and investigative methodologies developed since the severe acute respiratory syndrome outbreak of 2003 and the subsequent sporadic human cases of avian influenza have been applied effectively and rapidly to the emergence of this novel pandemic virus. This article summarizes some of the findings from such investigations, including recommendations for the management of patients infected with this newly emerged pathogen.

via Emerging, Novel, and Known Influenza Virus Infections in Humans.

Because influenza virus A (H1N1) circulated continually after 1918 until 1957, most persons born before 1957 had been infected primarily with subtype H1N1. According to the theory of original antigenic sin, these persons may have partial protection from severe disease from infection with the new influenza virus A (H1N1), i.e., pandemic (H1N1) 2009. Supporting this hypothesis is the paucity of infections in Mexico from persons now in their 50s and 60s and few reports in the United States or Australia of cases in this age group.1 This fact should inform policy decisions and merits further immunologic consideration. Influenza surge planning is premised on a high incidence of illness among elderly persons, but if the current pattern of illness continues, healthcare facilities also should prepare to treat younger persons who may constitute the bulk of cases. Additionally, studies of persons born during 1957–1968 should be conducted to quantify antibody levels to pandemic (H1N1) 2009 virus, focusing on the degree of preexisting immunity that may have existed and was boosted by prior encounters with subtype H1N1 viruses.

Much more via Original Antigenic Sin and Pandemic (H1N1) 2009 — Center for Biosecurity of UPMC.

The co-circulation of a human adapted H1N1 with a swine H1N1 raises concerns sequences with extensive recombination will emerge in 2010, as happened in 1918.

More aggressive surveillance of H1N1 in swine worldwide is warranted, as is increased sequencing of human H1N1, since PCR testing may not distinguish between the two swine H1N1 strains.

via Emergence of Novel H1N1 Raises Pandemic Concerns.

In the online early edition of Proceedings of the National Academy of Sciences on June 7, 2010, the team reported creating a recombinant influenza A strain carrying a green fluorescent protein (GFP) reporter gene. The reporter gene was placed in the NS segment of the influenza genome.

The new NS1-GFP virus infected and replicated well in mouse lungs, although it was less pathogenic than the wild type virus, the form that typically occurs in nature. Using the fluorescence as a marker, the researchers traced the course of infection in mouse lungs and found that it started in areas close to the large airways (near the trachea) and later spread to deeper sections of the lungs. In addition to epithelial cells, a large proportion of immune cells were GFP positive, suggesting active infection of these cells.

via Tracing Flu Infections in Mice – NIH Research Matters – National Institutes of Health (NIH).