Giuseppe
Emeritus
[Source: World Health Organization, Weekly Epidemiological Record, full PDF document (LINK). Extracts, edited.]
Weekly Epidemiological Record, 27 May 2011, vol. 86, 22 (pp 221?232)
Review of the 2010?2011 winter influenza season, northern hemisphere
This report summarizes the chronology, epidemiology and virology of the winter influenza season in the northern hemisphere?s temperate regions, from October 2010 through the end of April 2011. The data presented have been derived primarily from reports published by national ministries of health and reported through Flu-Net.(1)
North America
Transmission
Active influenza transmission in North America was first noted in Mexico, starting in mid-to-late July 2010. Active transmission in Mexico continued throughout the remainder of 2010, and overlapped with the start of the winter season in the temperate areas of the continent in late November.
In the United States of America (USA), influenza activity began in the southern states in November,(2) slightly later that same month in the south-west, and then in the north-western states by the end of the month.(3) In Canada, active community transmission began in the provinces of Ontario and Quebec in early November, and later that month in the more western provinces.(4)
Influenza virus transmission peaked in temperate North America during late January and early February, and returned to national baseline levels by the end of April 2011 (Figure 1). Transmission in Mexico was almost entirely associated with influenza A(H3N2), and started in July in the southern part of the country; relatively small numbers of cases of influenza type-B viruses began to appear in August but only became common in November.
Influenza A(H3N2) was also the most common virus circulating in Canada and the USA throughout the winter, although the USA had more transmission of influenza type-B and influenza A(H1N1) 2009 virus than either Canada or Mexico.
Illness and mortality
When compared with the 2009?2010 season, the peak proportion of outpatient visits caused by influenza-like illness was lower during the 2010?2011 season in both Canada and the USA; however, mortality from pneumonia and influenza was at the epidemic threshold or exceeded it in the USA for a period of 12 consecutive weeks in February, March and April.
In the USA, hospitalization rates for influenza were highest among those aged ≥65 years, followed by children aged 0?4 years. Similarly, in Canada, 68% of adult hospitalizations and 79% of adult fatalities occurred among eople aged ≥65 years. Altogether, 95 children aged <18 years died in the USA and 5 died in Canada.
Influenza type-B appeared to be disproportionately associated with severe disease in children, being found in 39% of laboratory-confirmed paediatric deaths reported in the USA compared with 26% of viruses from outpatients in the general population, and in 26% of paediatric hospital admissions in Canada compared with 12%of viruses from outpatients in the general population. Data from the USA indicate that among adults hospitalized with laboratory-confirmed influenza the most commonly identified risk factors were cardiovascular disease, asthma or chronic lung disease, and metabolic disorders. Among paediatric patients hospitalized with laboratory- confirmed influenza in the USA, the most common underlying medical condition reported was asthma; this was reported in about 20% of cases.
Europe and the Middle East
Transmission
The influenza season in Europe first became evident in December 2010, with the report of a large number of cases requiring management in intensive care units in England and Scotland.(5) Within 2 weeks, countries in western Europe and the Middle East also reported increased numbers of cases with influenza-like illness and confirmed influenza cases.
Transmission occurred slightly later in eastern Europe. In western Europe transmission peaked during late January and early February; it peaked 2?3 weeks later in eastern Europe. In contrast with North America, influenza A(H1N1) 2009 virus was the predominant virus causing illness; influenza type-B was less common, and influenza A(H3N2) was rare.(6)
Illness and mortality
The 2010?2011season was marked by an increase in the number of influenza-related fatalities in the United Kingdom compared with the 2009?2010 season.(7) This was also reflected in an excess in all-cause mortality that was higher than the previous season, as were deaths caused by pneumonia and influenza.
In Greece, Georgia, Ireland and the United Kingdom, intensive care units were put under pressure by the high number of admissions. While other countries in Europe also reported fatalities and severe cases requiring management in intensive care units, the magnitude in comparison with last season is uncertain.
The risk groups for severe influenza caused by influenza A(H1N1) 2009 virus were similar to those during the previous season. Cases requiring intensive care or dying were more often young adults and middle-aged adults aged 45?65 years. In the United Kingdom, for example, of the 539 fatal cases for which data on age are available, only 119 (22%) were aged >64 years. Across Europe, 60?70% of severe cases had ≥1 recognized risk factor for severe disease, the most common of which was chronic respiratory disease or asthma. Most patients with severe disease had not been vaccinated against influenza during the season.
Northern Asia
Transmission
The influenza season in the northern temperate areas of Asia began during late October and early November 2010, and peaked by the end of December 2010.(8) During the early weeks of the season in Mongolia and northern China nearly all influenza was caused by influenza A(H3N2) virus, which was a continuation of summertime influenza A(H3N2) transmission that occurred primarily in southern China. In both China and Mongolia, influenza A(H1N1) 2009 virus was detected by the first week of 2011 and became the most commonly detected subtype within a few weeks.
In the Republic of Korea, the timing of transmission was similar to that seen in China and Mongolia but influenza A(H1N1) 2009 virus was the most commonly detected virus from the beginning of the season; influenza A(H3N2) virus was detected much less often. In Japan, sustained community transmission began at around the same time as in countries on the mainland, but it peaked a few weeks later, in late January 2011.
While early transmission in Japan was due to a mix of influenza A(H3N2) virus and influenza A(H1N1) 2009 virus, by January 2011, influenza A(H1N1) 2009 virus was clearly the predominant virus, and it remained so throughout the rest of the season. Only small numbers of cases caused by influenza type-B viruses were detected in northern Asia during the 2010?2011 season.
Illness and mortality
Rates of influenza-like illness were lower in all countries during 2010?2011 than they had been during the previous season but they were similar in magnitude to previous years.
In Mongolia, the proportion of hospitalizations for pneumonia and the number of deaths reported to have been caused by pneumonia were lower than they had been during the 2009?2010 season. Similarly, a number of severe and fatal cases were reported in China, but in lower numbers than during the previous season.
Antigenic testing
Altogether, 99% of influenza A(H1N1) 2009 viruses and 96% of influenza A(H3N2) viruses characterized antigenically were related to the strains contained in the trivalent seasonal influenza vaccine during the 2010?
2011 season. Approximately 91% of influenza type-B viruses were of the Victoria lineage, a small percentage of which had low cross-reactive antibody titres to B/Brisbane/60/2008; the remainder were of the Yamagata lineage. These proportions did not vary substantially from region to region.
Antiviral sensitivity testing
More than 98% of the 9300 influenza A(H1N1) 2009 viruses tested for antiviral susceptibility by the WHO Global Influenza Surveillance Network(9) were sensitive to oseltamivir, although there was some regional variation. All resistance to oseltamivir was associated with a substitution of H275Y in the neuraminidase gene.
Europe detected more cases of resistance to oseltamivir than did the USA (3% and 0.7% respectively), but many European specimens had been selected for testing because of suspected resistance (for example, they came from patients who had undergone prolonged treatment or whose treatment had failed). Specimens collected from the community in Europe had rates of resistance closer to 1%.
Europe also reported oseltamivir resistance in cases without any known prior exposure to the medicine, indicating that low-level community transmission of resistant virus may have occurred.10 The frequency with which oseltamivir resistance was detected did not appear to increase during the season at any of the testing sites.
No resistance to zanamivir was evident in any of the viruses tested. All influenza A(H1N1) 2009 viruses tested by the Global Influenza Surveillance Network were resistant to the M2 inhibitors amantadine and rimantadine as a result of an S31N substitution in the M2 protein. Influenza A(H3N2) virus and influenza type-B virus were all sensitive to both oseltamivir and zanamivir with the exception of 1 isolate of influenza A(H3N2) with oseltamivir resistance detected in the USA in April 2011.
Conclusions
Influenza A(H1N1) 2009 virus continues to circulate widely. However, in contrast to the pattern observed during the pandemic, the virus is now cocirculating with other influenza viruses, and in many countries was not the predominant influenza type-A virus that caused illness. During the 2010?2011 season circulation occurred during the expected time frame, and no out-of-season community transmission was reported in temperate northern countries. The pattern of association between severe disease and age was similar to that observed previously.
Influenza A(H1N1) 2009 virus continues to be more pathogenic for young adults and middle-aged adults, while influenza A(H3N2) virus causes more severe disease in people aged >65 years. Influenza type-B virus appears to affect young children disproportionately.
A few countries had a higher number of severe cases during the 2010?2011 season than during the previous season; the reasons for this are unclear. This increase was most notable in the United Kingdom, although this observation may well be a surveillance artefact related to the active surveillance for severe disease that was carried out there. All 3 circulating viruses demonstrated little antigenic drift during the past year, and were closely related to the 3 strains contained in the seasonal influenza vaccine. In addition, all but a small percentage of the viruses that were tested remained sensitive to neuraminidase inhibitors. This re-emphasizes the need to continue to vaccinate patients considered to be at high risk for severe disease and to treat them at an early stage; those who should be targeted for vaccination and early treatment are people at the extremes of age, those with certain chronic illnesses and pregnant women.(11, 12)
(1) For additional information, see (LINK).
(2) Influenza: situation report. Washington, DC, Pan American Health Organization, 2011 (LINK), accessed May 2011.
(3) For additional information, see the United States Centers for Disease Control and Prevention?s FluView at (LINK).
(4) For additional information, see the Public Health Agency of Canada?s FluWatch at (LINK).
(5) The European Centre for Disease Prevention and Control?s Weekly influenza surveillance overview is available at (LINK).
(6) WHO/Europe influenza surveillance (EuroFlu.org) is available at (LINK).
(7) The United Kingdom Health Protection Agency?s National influenza report is available at (LINK).
(8) WHO Regional Office for the Western Pacific?s Influenza situation update is available at (LINK).
(9) Information from the WHO Global Alert and Response?s Global influenza surveillance network is available at (LINK).
(10) Lackenby A, et al. Continued emergence and changing epidemiology of oseltamivirresistant influenza A (H1N1)2009 virus, United Kingdom, winter 2010?2011. Eurosurveillance, 2011, 16(5)
ii=19784 ((LINK); accessed April 2011).
(11) WHO guidelines for pharmacological management of pandemic (H1N1) 2009 influenza and other influenza viruses Geneva, World Health Organization, 2011 ((LINK), accessed May 2011).
(12) Recommendations for influenza vaccines. Geneva, World Health Organization, 2011 ((LINK), accessed May 2011).
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Weekly Epidemiological Record, 27 May 2011, vol. 86, 22 (pp 221?232)
Review of the 2010?2011 winter influenza season, northern hemisphere
This report summarizes the chronology, epidemiology and virology of the winter influenza season in the northern hemisphere?s temperate regions, from October 2010 through the end of April 2011. The data presented have been derived primarily from reports published by national ministries of health and reported through Flu-Net.(1)
North America
Transmission
Active influenza transmission in North America was first noted in Mexico, starting in mid-to-late July 2010. Active transmission in Mexico continued throughout the remainder of 2010, and overlapped with the start of the winter season in the temperate areas of the continent in late November.
In the United States of America (USA), influenza activity began in the southern states in November,(2) slightly later that same month in the south-west, and then in the north-western states by the end of the month.(3) In Canada, active community transmission began in the provinces of Ontario and Quebec in early November, and later that month in the more western provinces.(4)
Influenza virus transmission peaked in temperate North America during late January and early February, and returned to national baseline levels by the end of April 2011 (Figure 1). Transmission in Mexico was almost entirely associated with influenza A(H3N2), and started in July in the southern part of the country; relatively small numbers of cases of influenza type-B viruses began to appear in August but only became common in November.
Influenza A(H3N2) was also the most common virus circulating in Canada and the USA throughout the winter, although the USA had more transmission of influenza type-B and influenza A(H1N1) 2009 virus than either Canada or Mexico.
Illness and mortality
When compared with the 2009?2010 season, the peak proportion of outpatient visits caused by influenza-like illness was lower during the 2010?2011 season in both Canada and the USA; however, mortality from pneumonia and influenza was at the epidemic threshold or exceeded it in the USA for a period of 12 consecutive weeks in February, March and April.
In the USA, hospitalization rates for influenza were highest among those aged ≥65 years, followed by children aged 0?4 years. Similarly, in Canada, 68% of adult hospitalizations and 79% of adult fatalities occurred among eople aged ≥65 years. Altogether, 95 children aged <18 years died in the USA and 5 died in Canada.
Influenza type-B appeared to be disproportionately associated with severe disease in children, being found in 39% of laboratory-confirmed paediatric deaths reported in the USA compared with 26% of viruses from outpatients in the general population, and in 26% of paediatric hospital admissions in Canada compared with 12%of viruses from outpatients in the general population. Data from the USA indicate that among adults hospitalized with laboratory-confirmed influenza the most commonly identified risk factors were cardiovascular disease, asthma or chronic lung disease, and metabolic disorders. Among paediatric patients hospitalized with laboratory- confirmed influenza in the USA, the most common underlying medical condition reported was asthma; this was reported in about 20% of cases.
Europe and the Middle East
Transmission
The influenza season in Europe first became evident in December 2010, with the report of a large number of cases requiring management in intensive care units in England and Scotland.(5) Within 2 weeks, countries in western Europe and the Middle East also reported increased numbers of cases with influenza-like illness and confirmed influenza cases.
Transmission occurred slightly later in eastern Europe. In western Europe transmission peaked during late January and early February; it peaked 2?3 weeks later in eastern Europe. In contrast with North America, influenza A(H1N1) 2009 virus was the predominant virus causing illness; influenza type-B was less common, and influenza A(H3N2) was rare.(6)
Illness and mortality
The 2010?2011season was marked by an increase in the number of influenza-related fatalities in the United Kingdom compared with the 2009?2010 season.(7) This was also reflected in an excess in all-cause mortality that was higher than the previous season, as were deaths caused by pneumonia and influenza.
In Greece, Georgia, Ireland and the United Kingdom, intensive care units were put under pressure by the high number of admissions. While other countries in Europe also reported fatalities and severe cases requiring management in intensive care units, the magnitude in comparison with last season is uncertain.
The risk groups for severe influenza caused by influenza A(H1N1) 2009 virus were similar to those during the previous season. Cases requiring intensive care or dying were more often young adults and middle-aged adults aged 45?65 years. In the United Kingdom, for example, of the 539 fatal cases for which data on age are available, only 119 (22%) were aged >64 years. Across Europe, 60?70% of severe cases had ≥1 recognized risk factor for severe disease, the most common of which was chronic respiratory disease or asthma. Most patients with severe disease had not been vaccinated against influenza during the season.
Northern Asia
Transmission
The influenza season in the northern temperate areas of Asia began during late October and early November 2010, and peaked by the end of December 2010.(8) During the early weeks of the season in Mongolia and northern China nearly all influenza was caused by influenza A(H3N2) virus, which was a continuation of summertime influenza A(H3N2) transmission that occurred primarily in southern China. In both China and Mongolia, influenza A(H1N1) 2009 virus was detected by the first week of 2011 and became the most commonly detected subtype within a few weeks.
In the Republic of Korea, the timing of transmission was similar to that seen in China and Mongolia but influenza A(H1N1) 2009 virus was the most commonly detected virus from the beginning of the season; influenza A(H3N2) virus was detected much less often. In Japan, sustained community transmission began at around the same time as in countries on the mainland, but it peaked a few weeks later, in late January 2011.
While early transmission in Japan was due to a mix of influenza A(H3N2) virus and influenza A(H1N1) 2009 virus, by January 2011, influenza A(H1N1) 2009 virus was clearly the predominant virus, and it remained so throughout the rest of the season. Only small numbers of cases caused by influenza type-B viruses were detected in northern Asia during the 2010?2011 season.
Illness and mortality
Rates of influenza-like illness were lower in all countries during 2010?2011 than they had been during the previous season but they were similar in magnitude to previous years.
In Mongolia, the proportion of hospitalizations for pneumonia and the number of deaths reported to have been caused by pneumonia were lower than they had been during the 2009?2010 season. Similarly, a number of severe and fatal cases were reported in China, but in lower numbers than during the previous season.
Antigenic testing
Altogether, 99% of influenza A(H1N1) 2009 viruses and 96% of influenza A(H3N2) viruses characterized antigenically were related to the strains contained in the trivalent seasonal influenza vaccine during the 2010?
2011 season. Approximately 91% of influenza type-B viruses were of the Victoria lineage, a small percentage of which had low cross-reactive antibody titres to B/Brisbane/60/2008; the remainder were of the Yamagata lineage. These proportions did not vary substantially from region to region.
Antiviral sensitivity testing
More than 98% of the 9300 influenza A(H1N1) 2009 viruses tested for antiviral susceptibility by the WHO Global Influenza Surveillance Network(9) were sensitive to oseltamivir, although there was some regional variation. All resistance to oseltamivir was associated with a substitution of H275Y in the neuraminidase gene.
Europe detected more cases of resistance to oseltamivir than did the USA (3% and 0.7% respectively), but many European specimens had been selected for testing because of suspected resistance (for example, they came from patients who had undergone prolonged treatment or whose treatment had failed). Specimens collected from the community in Europe had rates of resistance closer to 1%.
Europe also reported oseltamivir resistance in cases without any known prior exposure to the medicine, indicating that low-level community transmission of resistant virus may have occurred.10 The frequency with which oseltamivir resistance was detected did not appear to increase during the season at any of the testing sites.
No resistance to zanamivir was evident in any of the viruses tested. All influenza A(H1N1) 2009 viruses tested by the Global Influenza Surveillance Network were resistant to the M2 inhibitors amantadine and rimantadine as a result of an S31N substitution in the M2 protein. Influenza A(H3N2) virus and influenza type-B virus were all sensitive to both oseltamivir and zanamivir with the exception of 1 isolate of influenza A(H3N2) with oseltamivir resistance detected in the USA in April 2011.
Conclusions
Influenza A(H1N1) 2009 virus continues to circulate widely. However, in contrast to the pattern observed during the pandemic, the virus is now cocirculating with other influenza viruses, and in many countries was not the predominant influenza type-A virus that caused illness. During the 2010?2011 season circulation occurred during the expected time frame, and no out-of-season community transmission was reported in temperate northern countries. The pattern of association between severe disease and age was similar to that observed previously.
Influenza A(H1N1) 2009 virus continues to be more pathogenic for young adults and middle-aged adults, while influenza A(H3N2) virus causes more severe disease in people aged >65 years. Influenza type-B virus appears to affect young children disproportionately.
A few countries had a higher number of severe cases during the 2010?2011 season than during the previous season; the reasons for this are unclear. This increase was most notable in the United Kingdom, although this observation may well be a surveillance artefact related to the active surveillance for severe disease that was carried out there. All 3 circulating viruses demonstrated little antigenic drift during the past year, and were closely related to the 3 strains contained in the seasonal influenza vaccine. In addition, all but a small percentage of the viruses that were tested remained sensitive to neuraminidase inhibitors. This re-emphasizes the need to continue to vaccinate patients considered to be at high risk for severe disease and to treat them at an early stage; those who should be targeted for vaccination and early treatment are people at the extremes of age, those with certain chronic illnesses and pregnant women.(11, 12)
(1) For additional information, see (LINK).
(2) Influenza: situation report. Washington, DC, Pan American Health Organization, 2011 (LINK), accessed May 2011.
(3) For additional information, see the United States Centers for Disease Control and Prevention?s FluView at (LINK).
(4) For additional information, see the Public Health Agency of Canada?s FluWatch at (LINK).
(5) The European Centre for Disease Prevention and Control?s Weekly influenza surveillance overview is available at (LINK).
(6) WHO/Europe influenza surveillance (EuroFlu.org) is available at (LINK).
(7) The United Kingdom Health Protection Agency?s National influenza report is available at (LINK).
(8) WHO Regional Office for the Western Pacific?s Influenza situation update is available at (LINK).
(9) Information from the WHO Global Alert and Response?s Global influenza surveillance network is available at (LINK).
(10) Lackenby A, et al. Continued emergence and changing epidemiology of oseltamivirresistant influenza A (H1N1)2009 virus, United Kingdom, winter 2010?2011. Eurosurveillance, 2011, 16(5)
ii=19784 ((LINK); accessed April 2011).(11) WHO guidelines for pharmacological management of pandemic (H1N1) 2009 influenza and other influenza viruses Geneva, World Health Organization, 2011 ((LINK), accessed May 2011).
(12) Recommendations for influenza vaccines. Geneva, World Health Organization, 2011 ((LINK), accessed May 2011).
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