Update: Influenza Activity --- United States, September 30, 2007--April 5, 2008, and Composition of the 2008--09 Influenza Vaccine
This report summarizes U.S. influenza activity* since September 30, 2007, the start of the 2007--08 influenza season, and updates the previous summary (1 (http://www.cdc.gov/mmwr/preview/mmwrhtml/mm5707a4.htm)). Low levels of influenza activity were reported from October through early December. Activity increased from mid-December and peaked in mid-February. Viral Surveillance
During September 30, 2007--April 5, 2008,† World Health Organization (WHO) and National Respiratory and Enteric Virus Surveillance System (NREVSS) collaborating laboratories in the United States reported testing 185,938 specimens for influenza viruses, and 34,380 (18.5%) tested positive (Figure 1 (http://www.cdc.gov/mmwr/preview/mmwrhtml/mm5715a4.htm#fig1)). Of these, 25,456 (74.0%) were influenza A viruses, and 8,924 (26.0%) were influenza B viruses. A total of 7,715 (30.3%) of the 25,456 influenza A viruses have been subtyped: 2,110 (27.3%) were influenza A (H1N1) viruses, and 5,605 (72.7%) were influenza A (H3N2) viruses. The percentage of specimens testing positive for influenza first exceeded 10% during the week ending January 12 and peaked at 32.0% during the week ending February 16. For the week ending April 5, 13.2% of specimens tested for influenza were positive. Although influenza A (H1N1) viruses predominated through mid-January, the proportion of reported influenza viruses that were A (H3N2) viruses increased rapidly during January, and during the week ending January 26, influenza A (H3N2) became the predominant virus for the season overall.
This season, more influenza A viruses than influenza B viruses have been identified in all surveillance regions. However, for weeks 13 and 14 (March 23--April 5), more influenza B than influenza A viruses were reported. Among influenza A viruses, influenza A (H3N2) has predominated in the East North Central, East South Central, Mid-Atlantic, New England, South Atlantic, West North Central, and West South Central regions, and influenza A (H1N1) has predominated in the Mountain and Pacific regions. Composition of the 2008--09 Influenza Vaccine
The Food and Drug Administration's Vaccines and Related Biological Products Advisory Committee recommended that the 2008--09 trivalent influenza vaccine for the United States contain A/Brisbane/59/2007-like (H1N1), A/Brisbane/10/2007-like (H3N2), and B/Florida/4/2006-like viruses. This represents a change in all three components from the 2007--08 influenza vaccine formulation used in the United States. These recommendations were based on antigenic analyses of recently isolated influenza viruses, epidemiologic data, post-vaccination serologic studies in humans, and the availability of candidate vaccine strains and reagents. Antigenic Characterization
States are requested to submit a subset of their influenza virus isolates to CDC for further antigenic characterization. Since September 30, 2007, CDC has antigenically characterized 608 influenza viruses submitted by WHO collaborating laboratories in the United States: 290 influenza A (H1N1), 161 influenza A (H3N2), and 157 influenza B viruses. A total of 200 (69%) of 290 influenza A (H1N1) viruses were characterized as A/Solomon Islands/3/2006-like, the influenza A (H1N1) component of the 2007--08 influenza vaccine for the Northern Hemisphere, and 70 (24%) were characterized as A/Brisbane/59/2007-like, the recommended H1N1 component of the 2008--09 Northern Hemisphere vaccine. Thirty-five (22%) of the 161 influenza A (H3N2) viruses were characterized as A/Wisconsin/67/2005-like, the influenza A (H3N2) component of the 2007--08 influenza vaccine for the Northern Hemisphere. One hundred fifteen (71%) of the 161 viruses were characterized as A/Brisbane/10/2007-like, the recommended influenza A (H3N2) component for the 2008 Southern Hemisphere and 2008--09 Northern Hemisphere vaccines. Influenza B viruses currently circulating can be divided into two antigenically distinct lineages represented by B/Victoria/02/87 and B/Yamagata/16/88. Eight (5%) of the 157 influenza B viruses characterized belong to the B/Victoria lineage of viruses. Six (75%) of these viruses from the B/Victoria lineage were characterized as B/Malaysia/2506/2004-like, the influenza B component of the 2007--08 influenza vaccine. One hundred forty-nine (95%) of the 157 influenza B viruses characterized belong to the B/Yamagata lineage. Outpatient Illness Surveillance
For the week ending April 5, 2008, the percentage of outpatient visits for influenza-like illness (ILI)§ reported by approximately 1,400 U.S. sentinel providers in 50 states, Chicago, the District of Columbia, New York City, and the U.S. Virgin Islands was 1.7%, which was below the national baseline of 2.2%.¶ This season, the percentage of outpatient visits for ILI exceeded the national baseline for 13 consecutive weeks. The percentage of outpatient visits for ILI first exceeded baseline during the week ending December 29 and peaked at 5.9% during the week ending February 16. The percentage of outpatient visits for acute respiratory illness (ARI)** reported by approximately 350 U.S. Department of Defense (DoD) and 800 Department of Veterans Affairs (VA) BioSense†† outpatient treatment facilities for the week ending April 5 was 2.2%, which was below the national baseline of 3.2%§§ (Figure 2 (http://www.cdc.gov/mmwr/preview/mmwrhtml/mm5715a4.htm#fig2)). State-Specific Activity Levels
During the week ending April 5, 2008, influenza activity was reported as widespread¶¶ in six states (Connecticut, Maine, Maryland, New York, Pennsylvania, and Vermont) (Figure 3 (http://www.cdc.gov/mmwr/preview/mmwrhtml/mm5715a4.htm#fig3)). In addition, regional activity was reported by 11 states (Alaska, California, Colorado, Hawaii, Illinois, Iowa, Massachusetts, New Jersey, North Dakota, Oregon, and Washington); local influenza activity was reported by 23 states (Alabama, Arizona, Georgia, Idaho, Indiana, Kentucky, Louisiana, Michigan, Minnesota, Montana, Nebraska, Nevada, New Hampshire, New Mexico, North Carolina, Ohio, Rhode Island, South Carolina, South Dakota, Texas, Utah, Virginia, and Wyoming); and sporadic activity was reported by the District of Columbia and 10 states (Arkansas, Delaware, Florida, Kansas, Mississippi, Missouri, Oklahoma, Tennessee, West Virginia, and Wisconsin). Activity peaked during weeks 7 and 8 (February 10--23), when 49 states reported widespread influenza activity and one state reported regional activity. Influenza-Associated Pediatric Hospitalizations
Pediatric hospitalizations associated with laboratory-confirmed influenza infections are monitored by two population-based surveillance networks, the Emerging Infections Program (EIP) and the New Vaccine Surveillance Network (NVSN). During November 4, 2007--March 22, 2008, the preliminary laboratory-confirmed influenza-associated hospitalization rate reported by NVSN for children aged 0--4 years was 5.61 per 10,000. During September 30, 2007--March 29, 2008, EIP sites reported a preliminary laboratory-confirmed influenza-associated hospitalization rate of 1.32 per 10,000 for children aged 0--17 years. For children aged 0--4 years, the rate was 3.47 per 10,000, and for children aged 5--17 years, the rate was 0.45 per 10,000. Differences in the rate estimates between the NVSN and the EIP systems likely result from the different case-finding methods and the different populations monitored.*** Pneumonia and Influenza-Related Mortality
Pneumonia and influenza (P&I) was listed as an underlying or contributing cause of death for 8.9% of all deaths reported through the 122 Cities Mortality Reporting System for the week ending April 5, 2008. This percentage was above the epidemic threshold of 6.9% for the week††† and marked the thirteenth consecutive week that the proportion of all deaths attributed to P&I was above the epidemic threshold (Figure 4 (http://www.cdc.gov/mmwr/preview/mmwrhtml/mm5715a4.htm#fig4)). The proportion of deaths from P&I exceeded the epidemic threshold during week ending January 5 and peaked at 9.1% during the week ending March 15. Influenza-Related Pediatric Mortality
During September 30, 2007--April 5, 2008, a total of 65 pediatric deaths among children aged <18 years associated with laboratory-confirmed influenza were reported from 26 states, New York City, and Chicago through the National Notifiable Diseases Surveillance System. The median age of decedents was 4.5 years (range: 1 month to 17.8 years). During the preceding three influenza seasons, the total number of influenza-related pediatric deaths reported to CDC ranged from 46 to 74. Resistance to Antiviral Medications
During this influenza season, an increase in the number of influenza viruses resistant to the neuraminidase inhibitor, oseltamivir, has been observed. Among the 1,153 influenza A and B viruses tested during the 2007--08 influenza season, to date, 84 (8.3%) have been found to be resistant to oseltamivir. All the oseltamivir-resistant viruses have been influenza A (H1N1) viruses and have been determined to share the same genetic mutation that confers oseltamivir resistance. These 84 viruses represent 10.2% of the 824 influenza A (H1N1) viruses that have been tested, an increase from four (0.7%) of 588 influenza A (H1N1) viruses tested during the 2006--07 season. No resistance to oseltamivir has been identified among the 194 influenza A (H3N2) or the 135 influenza B viruses tested, and no antiviral resistance to zanamivir has been detected in any influenza A or B viruses. Resistance to adamantanes (amantadine and rimantadine) continues to be high among influenza A viruses. Of 261 influenza A (H3N2) viruses tested, 260 (99.6%) were resistant to adamantanes. Adamantane resistance among influenza A (H1N1) viruses also has been detected, but at a lower level. Of 729 influenza A (H1N1) viruses tested, 81 (11.1%) were resistant to adamantanes. The adamantanes have no activity against influenza B viruses.
Based on the level of oseltamivir resistance observed in only one influenza A subtype (H1N1), persisting high levels of resistance to adamantanes in A (H3N2) viruses, and the predominance of A (H3N2) viruses circulating in the United States during the 2007--08 season with co-circulation of influenza B viruses, CDC continues to recommend the use of oseltamivir and zanamivir for the treatment or chemoprophylaxis of influenza (2). Use of amantadine or rimantadine is not recommended.
Reported by: World Health Organization Collaborating Center for Surveillance, Epidemiology, and Control of Influenza; C Dao, MPH, L Blanton, MPH, S Epperson, MPH, L Brammer, MPH, L Finelli, DrPH, T Wallis, MS, T Uyeki, MD, J Bresee, MD, A Klimov, PhD, N Cox, PhD, Influenza Div, National Center for Immunization and Respiratory Diseases, CDC. Editorial Note:
By some indicators, this influenza season has been more severe than the previous three seasons. Influenza activity in the United States remained low until January, peaked in mid-February, and decreased thereafter. For the week ending April 5, 2008, widespread activity was reported in six states, and regional activity was reported in 11 states, a decrease from mid-February, when 49 states reported widespread activity and one state reported regional activity. During peak activity of the previous three influenza seasons, the number of states reporting widespread or regional activity ranged from 41 to 49 states. During the 2007--08 season, the percentage of outpatient visits for ILI peaked at 5.9%, exceeded the national baseline for 13 consecutive weeks, and declined to 1.7% during the week ending April 5. During the previous three influenza seasons, the peak percentage of visits for ILI ranged from 3.2% to 5.4% and exceeded baseline levels for 14 to 16 consecutive weeks. To date, the percentage of deaths attributable to P&I peaked at 9.1% and exceeded the epidemic threshold for 13 consecutive weeks this season. For the week ending April 5, the proportion of deaths attributable to P&I was 8.9%. During the previous three seasons, the peak percentage of deaths attributable to P&I ranged from 7.7% to 8.9%, and the total number of weeks above the epidemic threshold ranged from 1 to 11 consecutive weeks. P&I mortality is higher this season than the previous three seasons, which were mild. The 2007--08 season is similar to the 2003--04 season, when the percentage of deaths attributable to P&I peaked at 10.4% and the number of consecutive weeks above the epidemic threshold was 9 weeks.
Influenza A (H1N1) viruses predominated through mid-January, but influenza A (H3N2) viruses were more frequently identified than influenza A (H1N1) viruses since late January and have predominated overall. The majority of influenza A (H1N1) viruses were characterized as A/Solomon Islands/3/2006, the influenza A (H1N1) component of the 2007--08 influenza vaccine for the Northern Hemisphere. To date, the majority of influenza A (H3N2) and influenza B viruses were characterized as A/Brisbane/10/2007 and B/Florida/04/2006, respectively, the recommended influenza A (H3N2) and influenza B components of the 2008--09 influenza vaccine for the Northern Hemisphere.
Clinical vaccine effectiveness cannot be accurately predicted using these data. A case-control study to estimate the effectiveness of trivalent inactivated influenza vaccine was conducted this season in Marshfield, Wisconsin. Preliminary results from subjects enrolled during January 21--February 8 show an overall vaccine effectiveness of 44%, suggesting that vaccination provided substantial protection against influenza-associated, medically attended illness in the study population, despite the suboptimal vaccine match (3 (http://www.cdc.gov/mmwr/preview/mmwrhtml/mm5715a1.htm)). These preliminary results are similar to previous studies, which have shown that influenza vaccination provides measurable protection against influenza illness and influenza-related complications and death, even when vaccine strains are antigenically distinct from circulating strains (4--7).
As a supplement to influenza vaccination, antiviral drugs have aided in the control and prevention of influenza. Recent studies have identified a considerable protective effect of oseltamivir treatment against complications associated with influenza (8), including death among older adults hospitalized with laboratory-confirmed influenza (9). This season, resistance to the influenza antiviral drug oseltamivir among influenza A (H1N1) viruses (84 [10.2%] of 824 tested) has been detected. All 84 resistant influenza A (H1N1) viruses identified in the United States this season share the same genetic mutation; this mutation is the most common mutation in this subtype that confers resistance to oseltamivir. Increased resistance to oseltamivir among influenza A (H1N1) viruses has been reported from many countries this season (10). No oseltamivir resistance has been detected among influenza A (H3N2) or B viruses currently circulating in the United States. Given the low level of resistance to oseltamivir, the finding of resistance only in some influenza A (H1N1) viruses, and no resistance to zanamivir, these drugs continue to be recommended for the treatment and prophylaxis of influenza (2). Although recommendations for use of antiviral medications have not changed, enhanced surveillance for detection of oseltamivir-resistant influenza viruses is ongoing and will enable continued monitoring of changing trends over time. In addition to vaccination and antivirals, other means of decreasing the spread and impact of influenza include staying home from work or school when ill, avoiding others who are sick, covering the nose or mouth with a tissue when coughing or sneezing, and frequent hand washing. Additional information is available at http://www.cdc.gov/flu/protect/habits.htm (http://www.cdc.gov/flu/protect/habits.htm).
Influenza surveillance reports for the United States are posted online weekly during October--May and are available at http://www.cdc.gov/flu/weekly/fluactivity.htm (http://www.cdc.gov/flu/weekly/fluactivity.htm). Additional information regarding influenza viruses, influenza surveillance, the influenza vaccine, and avian influenza is available at http://www.cdc.gov/flu (http://www.cdc.gov/flu).
Acknowledgments
This report is based on data contributed by participating state and territorial health departments and state public health laboratories, World Health Organization collaborating laboratories, National Respiratory and Enteric Virus Surveillance System collaborating laboratories, the U.S. Influenza Sentinel Provider Surveillance System, the U.S. Department of Veterans Affairs/U.S. Department of Defense BioSense Outpatient Surveillance System, the New Vaccine Surveillance Network, the Emerging Infections Program, and the 122 Cities Mortality Reporting System. References
CDC. Update: influenza activity---United States, September 30--February 9, 2008. MMWR 2008;57:179--83. (http://www.cdc.gov/mmwr/preview/mmwrhtml/mm5707a4.htm)
CDC. Health Advisory: influenza antiviral use for persons at high risk for influenza complications or who have severe influenza illness. Atlanta, GA: US Department of Health and Human Services, CDC; 2008 Available at http://www2a.cdc.gov/han/archivesys/viewmsgv.asp?alertnum=00271 (http://www2a.cdc.gov/han/archivesys/viewmsgv.asp?alertnum=00271).
CDC. Interim within-season estimate of the effectiveness of trivalent inactivated influenza vaccine---Marshfield, Wisconsin, 2007--08 influenza season. MMWR 2008;57:393--8. (http://www.cdc.gov/mmwr/preview/mmwrhtml/mm5715a1.htm)
Edwards KM, Dupont WD, Westrich MK, Plummer WD Jr, Palmer PS, Wright PF. A randomized controlled trial of cold-adapted and inactivated vaccines for the prevention of influenza A disease. J Infect Dis 1994;169:68--76.
Nichol KL, Nordin JD, Nelson DB, Mullooly JP, Hak E. Effectiveness of influenza vaccine in the community-dwelling elderly. N Engl J Med 2007;357:1373--81.
Shuler CM, Iwamoto M, Bridges CB. Vaccine effectiveness against medically attended, laboratory-confirmed influenza among children aged 6 to 59 months, 2003--2004. Pediatrics 2007;119:e587--95.
Russell KL, Ryan MA, Hawksworth A, et al. Effectiveness of the 2003--2004 influenza vaccine among U.S. military basic trainees: a year of suboptimal match between vaccine and circulating strain. Vaccine 2005;23:1981--5.
Kaiser L, Wat C, Mills T, Mahoney P, Ward P, Hayden F. Impact of oseltamivir treatment on influenza-related lower respiratory tract complications and hospitalizations. Arch Intern Med 2003;163:1667--72.
McGeer A, Green KA, Plevneshi A, et al. Antiviral therapy and outcomes of influenza requiring hospitalization in Ontario, Canada. Clin Infect Dis 2007;45:1568--75.
World Health Organization. Influenza A (H1N1) virus resistance to oseltamivir---last quarter 2007 to 4 April 2008. Geneva, Switzerland: World Health Organization; 2008 Available at http://www.who.int/csr/disease/influenza/H1N1ResistanceWeb20080403.pdf (http://www.who.int/csr/disease/influenza/H1N1ResistanceWeb20080403.pdf).
* The CDC influenza surveillance system collects five categories of information from 10 data sources. Viral surveillance: U.S. World Health Organization collaborating laboratories, the National Respiratory and Enteric Virus Surveillance System, and novel influenza A virus case reporting. Outpatient illness surveillance: U.S. Influenza Sentinel Provider Surveillance Network and the U.S. Department of Veterans Affairs/U.S. Department of Defense BioSense Outpatient Surveillance System. Mortality: 122 Cities Mortality Reporting System and influenza-associated pediatric mortality reports. Hospitalizations: Emerging Infections Program and New Vaccine Surveillance Network. Summary of geographic spread of influenza: state and territorial epidemiologist reports.
† Data as of April 5, 2008.
§ Defined as a temperature of >100.0°F (>37.8°C), oral or equivalent, and cough and/or sore throat, in the absence of a known cause other than influenza.
¶ The national and regional baselines are the mean percentage of visits for ILI during noninfluenza weeks for the previous three seasons plus two standard deviations. A noninfluenza week is a week during which <10% of specimens tested positive for influenza. National and regional percentages of patient visits for ILI are weighted on the basis of state population. Use of the national baseline for regional data is not appropriate.
** Based on International Classification of Diseases, Ninth Revision codes for ARI: 460-66 and 480-88.
†† BioSense is a national surveillance system that receives, analyzes, and evaluates health data from multiple sources, include 1) approximately 1,150 VA/DoD hospitals and ambulatory-care clinics; 2) multihospital systems, local hospitals, and state and regional syndromic surveillance systems in 37 states; and 3) Laboratory Corporation of America (LabCorp) test results.
§§ The national, regional, and age-specific baselines are the mean percentage of visits for ARI during noninfluenza weeks for the previous three seasons plus two standard deviations. A noninfluenza week is a week during which <10% of specimens tested positive for influenza. Use of a national baseline for regional data is not appropriate.
¶¶ Levels of activity are 1) no activity; 2) sporadic: isolated laboratory-confirmed influenza cases or a laboratory-confirmed outbreak in one institution, with no increase in activity; 3) local: increased ILI , or at least two institutional outbreaks (ILI or laboratory-confirmed influenza) in one region with recent laboratory evidence of influenza in that region (virus activity no greater than sporadic in other regions); 4) regional: increased ILI activity or institutional outbreaks (ILI or laboratory-confirmed influenza) in at least two but less than half of the regions in the state with recent laboratory evidence of influenza in those regions; and 5) widespread: increased ILI activity or institutional outbreaks (ILI or laboratory-confirmed influenza) in at least half the regions in the state with recent laboratory evidence of influenza in the state.
*** NVSN conducts surveillance in Monroe County, New York; Hamilton County, Ohio; and Davidson County, Tennessee. NVSN provides population-based estimates of laboratory-confirmed influenza hospitalization rates in children aged <5 years admitted to NVSN hospitals with fever or respiratory symptoms. Children are prospectively enrolled, and respiratory samples are collected and tested by viral culture and reverse transcription--polymerase chain reaction (RT-PCR). EIP conducts surveillance in 60 counties associated with 12 metropolitan areas: San Francisco, California; Denver, Colorado; New Haven, Connecticut; Atlanta, Georgia; Baltimore, Maryland; Minneapolis/St. Paul, Minnesota; Albuquerque, New Mexico; Las Cruces, New Mexico; Albany, New York; Rochester, New York; Portland, Oregon; and Nashville, Tennessee. EIP conducts surveillance for laboratory-confirmed, influenza-related hospitalizations in persons aged <18 years. Hospital laboratory and admission databases and infection-control logs are reviewed to identify children with a positive influenza test (i.e., viral culture, direct fluorescent antibody assays, RT-PCR, or a commercial rapid antigen test) from testing conducted as a part of their routine care.
††† The expected seasonal baseline proportion of P&I deaths reported by the 122 Cities Mortality Reporting System is projected using a robust regression procedure in which a periodic regression model is applied to the observed percentage of deaths from P&I that occurred during the preceding 5 years. The epidemic threshold is 1.645 standard deviations above the seasonal baseline.
Figure 1
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Figure 2
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Figure 3
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Figure 4
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http://www.cdc.gov/mmwr/preview/mmwrhtml/mm5715a4.htm
Dr Niman commentary cites European Union H1N1/Brisbane isolation frequency. Recently, A/H1N1 represent only 35% of Italian total isolates (according CIRI website), while at the season beginning was the majority.
In Italy only one of almost 109 isolates reported to be resistant to oseltamivir. http://www.flutrackers.com/forum/showpost.php?p=149785&postcount=11
Perhaps these data may be useful.
Phylogenetic tree:
http://img89.imageshack.us/img89/6164/alb081sb6.jpg (http://imageshack.us)
http://img89.imageshack.us/img89/8488/alb083do0.jpg (http://imageshack.us)
[SOURCE : CIRI, http://www.influciri.it/frsetcn.html]
Thanks for the data. The top tree is H1N1 and it looks like the isolates in Italy are not as closely related to Brisbane/59 as the H274Y positive isolates in the US, Turkey, England (and I suspect Norway and France). I have to do a tree with a few of the US sequences listed above to say for sure. The US, Turkey, and English isolates were EXACT matches with each other.
these phylogenetic trees, are they available from other countries ?
What keyword would have found this Italian tree from
search-engine ?
The Italian phylos' trees are available at CIRI (Centro Interuniversitario per lo studio dell'Influenza - http://www.influciri.it/frsetcn.html), and they can be directly accessed via home page.
German H1N1 from this season:
name,date,Caledonia-titers,Solomon-titers
A/Berlin/98/07,19.12.2007,10,160
A/Rheinland-Pfalz/63/07,19.12.2007,20,320
A/Brandenburg/29/07,19.12.2007,80,320
A/Niedersachsen/63/07,20.12.2007,80,640
A/Baden-Württemberg/1/08,02.01.2008,80,640
A/Thüringen/1/08,02.01.2008,80,640
A/Baden-Württemberg/5/08,09.01.2008,40,320
A/Berlin/2/08,14.01.2008,40,320
A/Sachsen/3/08,15.01.2008,40,320
A/Nordrhein-Westfahlen/1/08,15.01.2008,40,320
they also have full genomes ! But not public.
("genom analysis was done for a representative number of virus isolates")
http://influenza.rki.de/agi/GetBericht?id=180
phylo-tree H1 from last season: page 37
(this season not yet available)
last season they sent viruses to London for the first time
for the new WHO surveillance project.
Germany H1,2007: http://magictour.free.fr/panflu/phyde07.JPG
Italy H1,2007: http://www.influciri.it/ima/alb-081.jpg
Thanks Dr. Niman. I'll keep my eyes alert for more info on this "Florida" strain.
only if you speak Italian - I couldn't find it there
I found this site with WHO reports :
http://www.nimr.mrc.ac.uk/wic/report/
time for the March-2008 report to appear !
here is the last one:
http://www.nimr.mrc.ac.uk/wic/report/interim_report_sep_2007.pdf
page 10 is N1, 9 viruses Apr.-Jul.2007, no H274Y
I'm trying to gather information on:
B/Florida/04/2006. I understand it got it's name "Florida" because that was the area of the lab that first diagnosed it. I'm wondering about it's history? What it may have been called before the lab in Florida diagnosed it? Can't be Brisbane 10 or 59. Where did it come from? How much trouble did it cause?
these phylogenetic trees, are they available from other countries ?
What keyword would have found this Italian tree from
search-engine ?
The Italian phylos' trees are available at CIRI (Centro Interuniversitario per lo studio dell'Influenza - http://www.influciri.it/frsetcn.html), and they can be directly accessed via home page.
Thank you ironorehopper! We have other Italian members.
Dr Niman commentary cites European Union H1N1/Brisbane isolation frequency. Recently, A/H1N1 represent only 35% of total isolates (according CIRI website), while at the season beginning was the majority.
In Italy only one of almost 109 isolates reported to be resistant to oseltamivir.
Perhaps these data may be useful.
Phylogenetic tree:
http://img89.imageshack.us/img89/6164/alb081sb6.jpg (http://imageshack.us)
http://img89.imageshack.us/img89/8488/alb083do0.jpg (http://imageshack.us)
[SOURCE : CIRI, http://www.influciri.it/frsetcn.html]
H1N1 frequencies declined in the US also (H1N1 was common at begining of the season, but H3N2 dominated at the end).
Commentary
http://www.recombinomics.com/News/04210801/H274Y_Brisbane_Clades.html
Some clarifications please from Ironorehopper, "Ricombinazione genetica" is it the same as genetic reassortment or genetic Recombination ??
Graci, Snowy
Ricombinazione genetica fra virus umani e aviari — La possibilità che un virus influenzale umano e uno aviario infettino contemporaneamente un essere vivente e si scambino, durante la replicazione, materiale genetico, dando origine ad un nuovo virus che mantiene la proprietà di moltiplicarsi nell’uomo, ma presenta nuove proteine H ed N di superficie, è documentata dalla storia.
I think that the exact translation put the word ''ricombinazione'' as ''reassortment'' of viral sub-units.
The author highlights two of the main supposed way for an animal virus to breach the species barrier: one, progressive accumulation of adaptative mutations; two, reassortment of viral sub-units between an avian and human-derived virus, creating a new 'reassortant' strain.
I think that the 'elegant evolution' isn't in mind of dr Crovari.
Commentary
http://www.recombinomics.com/News/04200804/H274Y_Brisbane.html
I'm trying to gather information on:
B/Florida/04/2006. I understand it got it's name "Florida" because that was the area of the lab that first diagnosed it. I'm wondering about it's history? What it may have been called before the lab in Florida diagnosed it? Can't be Brisbane 10 or 59. Where did it come from? How much trouble did it cause?
Correct. Brisbane 10 and 59 are both influenza A (H3N2 and H1N1 respectively and isolated in Brisbane), while the isolate above, as its name implies, is influenza B and isolated in Florida.
The Italian phylogenetic tree can be found in:
Risultati > Sorvelianza Virologica (from Irororehopper's link)
Some clarifications please from Ironorehopper, "Ricombinazione genetica" is it the same as genetic reassortment or genetic Recombination ??
Graci, Snowy
Ricombinazione genetica fra virus umani e aviari — La possibilità che un virus influenzale umano e uno aviario infettino contemporaneamente un essere vivente e si scambino, durante la replicazione, materiale genetico, dando origine ad un nuovo virus che mantiene la proprietà di moltiplicarsi nell’uomo, ma presenta nuove proteine H ed N di superficie, è documentata dalla storia.
E’ oggi noto che la pandemia “Asiatica” del 1957 è stata causata da un virus A/H2N2, nuovo per l’uomo, derivante dal precedente virus umano A/H1N1 che si è rimescolato con un virus dell’anatra da cui ha ricevuto i geni che codificano l’H2 e l’N2. Lo stesso vale per la pandemia Hong Kong del 1968 con passaggio dal sottotipo A/H2N2 all’A/H3N2.
Se tale rimescolamento sia avvenuto nell’uomo o in un altro animale (maiale) che ha funzionato da “vaso di ricombinazione”, non è noto.
Si può concludere, pertanto, che il rischio per l’uomo delle epidemie influenzali dei polli, è di due tipi.
Uno è reale, riguarda, pressoché esclusivamente, chi ha contatto più o meno stretto con i polli ammalati e si esprime, comunque, su scala limitata.
L’altro è potenziale e deriva dalla possibilità che il virus dei polli si adatti all’uomo dando origine ad una pandemia.
L’esperienza fa ritenere che il meccanismo della “ricombinazione” sia quello da temere maggiormente.
La possibilità che tale evento si verifichi esiste da lungo tempo; tuttavia, in una situazione come la presente in cui vi è un’ampia circolazione di virus influenzali umani e una vasta epidemia di influenza aviaria, aumenta la probabilità che tale evento si realizzi.
E’ questo che la Sanità Pubblica Mondiale teme e per cui è allertata in tutto il mondo.
P. Crovari
(Prof. di Igiene, Direttore del Centro Interuniversitario di Ricerca sull’Influenza – CIRI)
Papers discussing H2N2 in 1957 and H3N2 in 1968 will be talking about reassortment.
H1N1 Tamiflu Resistance Linked to Brisbane Strain
Recombinomics Commentary 22:17
April 20, 2008
A total of 200 (69%) of 290 influenza A (H1N1) viruses were characterized as A/Solomon Islands/3/2006-like, the influenza A (H1N1) component of the 2007--08 influenza vaccine for the Northern Hemisphere, and 70 (24%) were characterized as A/Brisbane/59/2007-like, the recommended H1N1 component of the 2008--09 Northern Hemisphere vaccine.
All the oseltamivir-resistant viruses have been influenza A (H1N1) viruses and have been determined to share the same genetic mutation that confers oseltamivir resistance. These 84 viruses represent 10.2% of the 824 influenza A (H1N1) viruses that have been tested, an increase from four (0.7%) of 588 influenza A (H1N1) viruses tested during the 2006--07 season.
The above comments are from the recent (http://www.cdc.gov/mmwr/preview/mmwrhtml/mm5715a4.htm)MMWR on the influenza season in the United States. Recently released sequences from the current flu season have been released at Genbank, and sixteen had H274Y. However, all were A/Brisbane/59/2007-like suggesting that the frequency of H274Y in the Brisbane strain may be significantly higher than the 10.2% found in H1N1 in the US. Since Brisbane only represents 24% of the H1N1 isolates in the US, if H274Y is concentrated in Brisbane, the frequency of H274Y in the Brisbane strain could be closer to 40%. Indeed, there have been 59 Brisbane sequences released, so the 16 with H274Y represent 27% of the Brisbane/59 isolates in the US.
The frequency of Brisbane/59 in European countries may also explain the differences in H274Y frequencies. In the recent WHO report (http://www.who.int/csr/disease/influenza/recommended_compositionFeb08FullReport.pdf) on next year’s vaccine targets, two isolates with H274Y were mentioned, A/Paris/577/2007 and A/Norway/1735/2007, and both were the Brisbane strain. Norway and France have the highest levels of reported H274Y.
Similarly, two H274Y sequences were released at Genbank this week from Turkey (http://www.recombinomics.com/News/04190803/H274Y_Turkey_UK_US.html) and England (http://www.recombinomics.com/News/04190802/H274Y_England.html), and both were identical to Brisbane-like sequences in the US.
Thus, all public H1N1 sequences from the current season with H274Y have been the Brisbane strain, suggesting that the differences in H274Y frequencies in Europe are largely linked to the frequency of of the Brisbane strain in those countries.
The WHO recommendation, as well as the CDC recommendation, includes Brisbane/59 as the H1N1 target for the fall trivalent vaccine, indicating that Brisbane is becoming dominant and the frequencies of H274Y in H1N1 will increase. Moreover, the current vaccine, which is directed against Solomon Island-like H1N1 may have contributed to the increase in the H274Y frequency by limiting Solomon Island infections.
More information on the association of H274Y with the Brisbane strain would be useful.
I'm trying to gather information on:
B/Florida/04/2006. I understand it got it's name "Florida" because that was the area of the lab that first diagnosed it. I'm wondering about it's history? What it may have been called before the lab in Florida diagnosed it? Can't be Brisbane 10 or 59. Where did it come from? How much trouble did it cause?
Dr Niman commentary cites European Union H1N1/Brisbane isolation frequency. Recently, A/H1N1 represent only 35% of Italian total isolates (according CIRI website), while at the season beginning was the majority.
In Italy only one of almost 109 isolates reported to be resistant to oseltamivir. http://www.flutrackers.com/forum/showpost.php?p=149785&postcount=11
Perhaps these data may be useful.
Phylogenetic tree:
http://img89.imageshack.us/img89/6164/alb081sb6.jpg (http://imageshack.us)
http://img89.imageshack.us/img89/8488/alb083do0.jpg (http://imageshack.us)
[SOURCE : CIRI, http://www.influciri.it/frsetcn.html]
thanks, that comment is clearer about the possible resistance in
other H1N1.
Now, what's the reason that Brisbane starts to replace
Solomon ? Is it Tamiflu-resistance ?
Are Solomon-viruses with H274Y not viable, don't they spread ?
So can we expect resistance in Solomon too in the next years
or will resistant and nonresistant strains coexist ?
This "competition" between the different strains about the hosts
ist still mysterious, not understood/examined (but important !)
We might influence it by spreading some flu deliberate
thus increasing the chance to reduce some other targeted
flu-strains. Would it be ethical ?
Imagine some fight between several antiviral producers,
each one trying to "grow" "its" flu-strain thus reducing
other competing strains which require more expensive
antivirals from other companies ...
Some clarifications please from Ironorehopper, "Ricombinazione genetica" is it the same as genetic reassortment or genetic Recombination ??
Graci, Snowy
Ricombinazione genetica fra virus umani e aviari — La possibilità che un virus influenzale umano e uno aviario infettino contemporaneamente un essere vivente e si scambino, durante la replicazione, materiale genetico, dando origine ad un nuovo virus che mantiene la proprietà di moltiplicarsi nell’uomo, ma presenta nuove proteine H ed N di superficie, è documentata dalla storia.
E’ oggi noto che la pandemia “Asiatica” del 1957 è stata causata da un virus A/H2N2, nuovo per l’uomo, derivante dal precedente virus umano A/H1N1 che si è rimescolato con un virus dell’anatra da cui ha ricevuto i geni che codificano l’H2 e l’N2. Lo stesso vale per la pandemia Hong Kong del 1968 con passaggio dal sottotipo A/H2N2 all’A/H3N2.
Se tale rimescolamento sia avvenuto nell’uomo o in un altro animale (maiale) che ha funzionato da “vaso di ricombinazione”, non è noto.
Si può concludere, pertanto, che il rischio per l’uomo delle epidemie influenzali dei polli, è di due tipi.
Uno è reale, riguarda, pressoché esclusivamente, chi ha contatto più o meno stretto con i polli ammalati e si esprime, comunque, su scala limitata.
L’altro è potenziale e deriva dalla possibilità che il virus dei polli si adatti all’uomo dando origine ad una pandemia.
L’esperienza fa ritenere che il meccanismo della “ricombinazione” sia quello da temere maggiormente.
La possibilità che tale evento si verifichi esiste da lungo tempo; tuttavia, in una situazione come la presente in cui vi è un’ampia circolazione di virus influenzali umani e una vasta epidemia di influenza aviaria, aumenta la probabilità che tale evento si realizzi.
E’ questo che la Sanità Pubblica Mondiale teme e per cui è allertata in tutto il mondo.
P. Crovari
(Prof. di Igiene, Direttore del Centro Interuniversitario di Ricerca sull’Influenza – CIRI)
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