Summary review of the 2011 southern hemisphere winter influenza season

This review summarizes the chronology, epidemiology, and virology of the southern hemisphere winter influenza season encompassing the time period from May 2011 through the end of September 2011. It is an expanded version of the WHO Weekly Epidemiological Record (WER) 28 October 2011, vol. 86 (pp 480-496). It contains additional graphics and a summary of transmission in tropical areas of the world during the time of the southern hemisphere winter.

The data presented are primarily derived from reports published by national ministries of health and reported through FluNet. Data sources and references are listed at the bottom of the page.

Southern cone of South America


Active influenza transmission in the southern cone of South America was first noted during mid-May to late May in both Argentina and Chile. Activity peaked during mid-July in Argentina and Uruguay, and 2 weeks later in Chile. Transmission had returned to baseline levels by the end of September 2011.
The predominant virus circulating in the southern cone differed among countries. Transmission in Chile and Uruguay was almost entirely associated with influenza A(H1N1)pdm09 virus. Influenza A(H1N1)pdm09 virus was initially the most common influenza virus circulating in Argentina, but by the peak of transmission in early August, influenza A(H3N2) virus accounted for nearly all subtyped viruses, and influenza A(H1N1)pdm09 virus became almost undetectable. Influenza type-B virus was detected only rarely in any of the 3 countries.

Illness and mortality

The overall severity of influenza during the season in the southern cone was relatively mild. The number of cases of influenza-like illness (ILI) and severe acute respiratory infection (SARI) generally remained within expected levels for both Argentina and Chile throughout the season. In Argentina, the cumulative number of cases of influenza-like illness and pneumonia reported by the end of August was lower than for the same period in 2010. In Chile, visits to emergency rooms for respiratory disease were markedly lower for all age groups throughout the season, and the number of laboratory confirmed cases of severe influenza and death were much lower than those reported in 2009 and 2010.
In Chile, 184/1495 (12%) of people admitted for SARI tested positive for influenza during the season; 140/152 (92%) of the subtyped viruses from SARI cases were influenza A(H1N1)pdm09 virus, 103 of 184 (56%) of SARI cases had a pre-existing medical condition, and of the 140 A(H1N1) SARI cases, 5 (4%) were pregnant.
The distribution of influenza A(H1N1)pdm09 virus and influenza A(H3N2) virus among the severe cases varied by age. Of the 12 SARI cases related to influenza A(H3N2) virus, 4 (33%) occurred in children aged <2 years and 3 (25%) in people aged >60 years; no severe cases associated with influenza A(H3N2) virus occurred among people aged 15–39 years. In contrast, only 21/140 (15%) cases associated with influenza A(H1N1)pdm09 virus were reported among people aged >60 years and 34/140 (24%) cases occurred among people aged 15–39 years. Of the 140 laboratory-confirmed SARI cases related to influenza A(H1N1)pdm09 virus, 31 (22%) occurred in children aged <2 years.
In Chile, between January and the end of September 2011, 13 deaths associated with influenza A(H1N1)pdm09 virus were reported with a median age of 56 years (range: 19–80 years); 6 out of 10 with gender information occurred among women, and 11 cases had a history of >=1 comorbidities. In Uruguay, the proportion of all hospitalizations caused by SARI peaked at 4% in late July, coinciding with the peak in influenza virus detections; the peak proportions of admissions requiring intensive care was 16% and the peak ratio of respiratory disease deaths, 8%. These figures are slightly higher in comparison to 2010 data: 4%, 10% and 5%, respectively.

South Africa


In South Africa, active transmission was first noted at the beginning of May. The occurrence of influenza-related respiratory illness including ILI, SARI and outpatient consultations for pneumonia peaked towards the beginning of June 2011, and there was a second distinct, though smaller, peak in late August 2011. Transmission returned to low levels by the end of September 2011. Influenza A(H1N1)pdm09 virus was the predominant influenza subtype until the beginning of August 2011 and was associated with the first peak of influenza-like illness and SARI; the secondary peak was primarily associated with influenza A(H3N2) virus and influenza type-B virus.

Illness and mortality

The majority of influenza-associated hospitalizations in 2011 were associated with influenza A(H1N1)pdm09 virus; smaller numbers of cases were hospitalized for influenza associated with influenza A(H3N2) virus and influenza type-B virus. Influenza A(H1N1)pdm09 virus accounted for 73% (1138/1551) of all influenza-positive cases, but only 56% (169/304) of SARI cases. In contrast, influenza A(H3N2) and influenza type B were detected for 15% (232/1551) and 11%(174/1551) of positive influenza cases, but accounted for 19%(59/304) and 25%(75/304) of SARI cases respectively.
In a preliminary analysis of a subset of hospitalized influenza-positive laboratory confirmed cases in South Africa during 2011, 8 patients died (case fatality rate [CFR]: 3%): 5 of these were infected with influenza A(H1N1)pdm09 virus, 1 with influenza type-B virus, 1 with influenza A(H3N2) and 1 was co-infected with influenza A(H1N1)pdm09 virus and influenza A(H3N2) virus. This is a lower CFR than during 2010 when influenza type-B virus predominated among SARI patients, and the CFR was 9%. Of the laboratory-confirmed cases testing positive for influenza in 2011, (15%) reported an underlying risk factor, excluding HIV infection. Of these, asthma was the risk factor in (6%) of cases followed by diabetes in (3%) and chronic obstructive pulmonary disease in (2%).

Australia and New Zealand


In Australia, active transmission of influenza was first noted in July, and peaked in early August. Transmission activity remained slightly increased at the time of this report but seemed to be returning to baseline. Australia also reported unusually high influenza activity during the Australian summer prior to the onset of the 2011 influenza season; this had not been reported in previous years.
In New Zealand, the time-course of transmission was similar to that in Australia, although rates of influenza-like illness reported nationally surpassed the seasonal baseline only slightly, and at times dipped below it during the course of the season.

The most commonly detected influenza viruses in the 2 countries were different. In Australia up until 16 September 2011, 22 303 laboratory-confirmed influenza cases were notified for 2011, 71% (17 167/24 179) of confirmed influenza cases were reported to be influenza A, which included 36%) (8 704/24 179) of influenza A untyped, 29% (7012/24 179) of influenza A(H1N1)pdm09 virus and 6% (1 451/24 179) of influenza A(H3N2) virus; 28% (6676/24 179) were influenza type-B virus. In Australia, the predominant virus was influenza A(H1N1)pdm09 which co-circulated with relatively low levels of influenza type-B virus, although this co-circulation differed among jurisdictions. In contrast, influenza type-B virus was the predominant strain in New Zealand accounting for 489/893 (55%) cases. There were also relatively small numbers of cases of infection with influenza A(H3N2) virus (242/893, 27%) and influenza A(H1N1)pdm09 virus (82/893, 9%); <10% of viruses were not subtyped.

Illness and mortality

In 2011, the overall severity of the influenza season was moderate in Australia. The sentinel hospital system of the Influenza Complications Alert Network (known as FluCAN) reported 155 hospitalizations (including 20 admissions to intensive-care units) associated with influenza between 1 May and 16 September 2011: 53% (82/155) of the hospitalizations and 60% (12/20) admissions to intensive-care units were associated with influenza A(H1N1)pdm09 virus and the mean age of patients hospitalized was 49 years.6 Australia also reported that between 1 July and 20 September 2011, 36 children aged <=15 years were hospitalized with severe influenza complications; this number included 17 admissions to intensive-care units. Of the patients who were hospitalized and completed questionnaires, 10/28 (36%) were noted to have had underlying chronic medical conditions.
In 2011, 11 influenza-associated deaths were reported; the median age of patients who died was 45 years. Eight of these cases were reported to be infected with influenza A(H1N1)pdm09 virus, 2 with influenza type-B virus and the other case was reported as influenza type A (untyped).

The 2011 influenza season in New Zealand was mild, as reflected by the low levels of weekly consultation rates for influenza-like illness when compared with previous years. Data on consultations for influenza-like illness from sentinel sites in 2011 indicated that when compared with data for the period 1992–2010, the cumulative incidence rate for 2011 of 734.2 consultations/100 000 population was the fourth lowest rate recorded. In addition, the peak consultation rate in 2011 was 66.1 consultations/100 000 population was the second lowest rate; the rate of hospitalizations for influenza in 2011 (268 hospitalizations, for a rate of 6.1/100 000 population) was the sixth lowest recorded for the period 1992–2011.
In 2011, influenza activity was unevenly distributed, with children (aged 0-19 years) and young adults (aged 20-34 years) having a higher disease burden than other age groups.

Tropical transmission zones


Generally the most intense transmission in the tropics occurred earlier in the year during the southern hemisphere summer; however, transmission was seen in more localized areas in the tropics over a long period of time. Notably, many countries, including those that test only a relatively small number of samples, demonstrated year-round transmission of influenza virus which typically transitioned over time from one predominate type or sub-type to another.

In the Caribbean and tropical South America active transmission was variable with no consistent trends and mixed transmission of influenza subtypes throughout the region at different times; influenza A(H1N1)pdm09 and influenza A(H3N2) co-circulated with one or the other predominant at different times across the region. In the Caribbean, Cuba, reported H3N2 most weeks of the past year with circulation peaking in late September. The Dominican Republic, in contrast, reported primarily H1N1pdm, which peaked in June and with no H3N2 detected in the entire 1 year period. Central American countries reported a mixture of primarily H3N2 and influenza type B, with the latter occurring somewhat earlier in the year most active circulation of the virus having diminished markedly by mid June. Peak transmission of H3N2 occurred in August in Honduras, September in El Salvador but many neighbouring countries in the area reported no detectable influenza virus transmission during those two months. In the tropical area of South America, Colombia and Brazil both experienced two peaks of transmission in the past one year, the first in December 2009 - January 2010 and the second in mid June. Both had persistent significant numbers of virus detections throughout the year, including the time between peaks. However, the virus types and subtypes detected occurred in somewhat different proportions with Brazil's first peak made up of at least 90% H3N2. A transition to a predominance of H1N1pdm was seen in the second peak but with persistence H3N2 and small numbers of influenza type B. Colombia reported roughly equal numbers of influenza A(H1N1)pdm09 and influenza A(H3N2) throughout the year, with lower numbers of influenza type B. The timing and distribution of virus types in Bolivia resembled that of Brazil, though the number of detections was much less.
South and South East Asia also experience two peaks of transmission during the year with persistence of virus circulation during the intervening period, though this was not reflected in the data of every country reporting in the region. A peak in transmission of influenza A(H1N1)pdm09 was seen early in the year occurring in the period from January to March primarily in Singapore, Indonesia, Malaysia, and Viet Nam (January peak); southern China and Hong Kong Special Administrative Region (February); and the Philippines (March). Countries in the region that did not experience coincident peaks include India, Bangladesh, Sri Lanka, and Thailand, each of which reported significant peaks of transmission of H1N1pdm in late 2009. The second 2010 peak of activity in the area was primarily associated with H3N2, with the exception of Viet Nam which continued to detect primarily H1N1pdm throughout the year. Following a pattern similar to that seen with the previous H1N1pdm peaks, the peak transmission of H3N2 occurred first in India, Bangladesh, and Singapore followed in July August in Thailand, and September in the Lao People's Democratic Republic. Notable exceptions to the overall pattern seen in Asia during the second peak include southern China, which had a minor peak in August of influenza type B and smaller amounts of H3N2; Viet Nam, Cambodia, and the Philippines, whose peaks occurred in September but were primarily associated with H1N1pdm; and Malaysia and Indonesia, which did not report increased transmission during the second regional peak.

Antigenic testing

Altogether, the vast majority of influenza A(H1N1)pdm09 viruses and influenza A(H3N2) viruses characterized antigenically by the WHO Global Influenza Surveillance and Response System were related to the viruses contained in the trivalent seasonal influenza vaccine for the 2011 season (A/California/7/2009 (H1N1)pdm09-like, A/Perth/16/2009 (H3N2)-like and B/Brisbane/60/2008-like viruses). Altogether, 72% of the influenza type-B viruses analysed between March 2011 and August 2011 by WHO collaborating centres were from the B/Victoria lineage, and only 28% were from the B/Yamagata lineage.
Antigenic characterization has shown that the influenza B/Victoria isolates are a close match with the composition of the 2011 influenza vaccine for the southern hemisphere, with some viruses showing reduced reactivity.

Antiviral sensitivity testing

A cluster of 29 cases infected with oseltamivir-resistant influenza A(H1N1)pdm09 virus -with onset between May and August 2011- was detected in the Hunter New England region of New South Wales, Australia. The viruses isolated from the cases carried the H275Y substitution (that is, the histidine-to-tyrosine substitution at amino acid 275, which confers high-level oseltamivir resistance. These viruses were shown to be sensitive to zanamivir, but resistant to amantadine and rimantadine. The resistant viruses were antigenically no different from other circulating influenza A(H1N1)pdm09 viruses that were sensitive to oseltamivir, and they were similar to A/California/7/2009, the virus contained in the 2011 seasonal influenza vaccine. A further 2 oseltamivir-resistant influenza A(H1N1)pdm09 viruses, collected from patients in July and August, have also been discovered. Both of these cases were detected outside the Hunter New England region, in people with no recent history of travel to the region. Only 1 of the cases reported having been treated with oseltamivir prior to having a positive test for influenza; however this case was not the earliest known case in the cluster. There is insufficient clinical information available to determine whether the viruses have altered virulence. Of the 29 cases with viruses resistant to oseltamivir, 3 were pregnant and 6 were hospitalized.
Sentinel community-based surveillance continued to find that approximately 99% of influenza A(H1N1)pdm09 viruses tested for antiviral susceptibility were sensitive to oseltamivir.11 Of the small number of oseltamivir-resistant influenza A(H1N1)pdm09 viruses detected, most were linked to the use of this medicine for prophylaxis or treatment. However, in some countries -such as Japan, the United Kingdom of Great Britain and Northern Ireland, and the United States of America, and notably in a cluster in Australia- increased proportions of resistant cases were found among people who had not been exposed to oseltamivir. In all instances, resistance was due to the H275Y substitution in the neuraminidase; the viruses remained sensitive to zanamivir. There were no reports of oseltamivir-resistant or zanamivir-resistant influenza A(H3N2) viruses.
The majority of influenza type-B viruses were sensitive to neuraminidase inhibitors; however a few viruses showed reduced sensitivity. M gene sequencing of influenza A(H1N1)pdm09 virus and influenza A(H3N2) virus revealed that those tested had the serine-to-asparagine substitution at amino acid 31 (S31N) of the M2 protein which is known to confer resistance to the M2 inhibitors, amantadine and rimantadine.


The 2011 influenza season in the southern hemisphere was mild: it began in May and was largely finished by the end of September, except in Australia and New Zealand where influenza activity was still being reported at the end of September. In most areas of the southern hemisphere the most commonly detected virus was influenza A(H1N1)pdm09; however, influenza virus types and subtypes varied considerably from country to country, and even between neighbouring countries and domestic jurisdictions. For example, Argentina and Chile had different virus profiles, and in Australia the relative frequency of infection with influenza A(H1N1)pdm09 virus and influenza type-B virus varied markedly among states.

Antiviral resistance in influenza A(H1N1)pdm09 virus remained low, although reports of cases with resistance in the absence of exposure to antiviral medications appear to be increasing. The appearance of a cluster of oseltamivir-resistant influenza A(H1N1)pdm09 cases detected in New South Wales, Australia, raises concerns about the eventual emergence of a circulating oseltamivir-resistant strain. All viruses of each type and subtype that have been tested have been shown to be resistant to amantadine and rimantadine. The majority of viruses detected around the world were similar antigenically to those found in the seasonal trivalent influenza vaccine. Therefore, people in high-risk population groups should be encouraged to be vaccinated in accordance with WHO policy to ensure early vaccination. The WHO consultation on the composition of influenza vaccines for the southern hemisphere for 2012 recommended that the following viruses be used for influenza vaccines during the 2012 influenza season in the southern hemisphere:
- an A/California/7/2009 (H1N1)pdm09-like virus;
- an A/Perth/16/2009 (H3N2)-like virus;
- a B/Brisbane/60/2008-like virus.

Data sources and references

1. WHO, FluNet
2. WHO Regional Office for the Americas, Influenza Situation Report (accessed in September 2011)
3. Ministerio de Salud, Buenos Aires, Argentina, 2011, Alerta epidemiologico [Status update of respiratory disease] (accessed in September 2011)
4. Ministerio de Salud de Chile, Santiago, Chile, 2011, Informe de influenza, semanas epidemiológicas 1 a 36 (2 enero al 10 de septiembre 2011). [Influenza report, epidemiological weeks 1 to 36 (2 January to 10 September 2011)] (accessed in October 2011)
5. National Health Laboratory Service, National Institute for Communicable Diseases, Johannesburg, South Africa, 2011, Influenza Surveillance Report - South Africa (accessed in September 2011)
6. Australian Government, Department of Health and Ageing, Woden, Australia, 2011, Australian influenza report 2011 (accessed in September 2011)
7. Institute of Environmental Science and Research, Public Health Surveillance, Wellington, New Zealand, 2011, Influenza weekly update (accessed in September 2011)
8. Huang S. The New Zealand 2011 influenza data. Canberra, Australia. WHO National Influenza Centre, Institute of Environmental Science and Research, New Zealand, 2011. Available upon request from WHO’s Global Influenza Programme ( )
9. WHO Collaborating Centres for influenza and Essential Regulatory Laboratories
10. The WHO Consultation on the Composition of Influenza Vaccines for the Southern Hemisphere 2012, Recommended composition of influenza virus vaccines for use in the 2012 southern hemisphere influenza season (WHO Weekly Epidemiologocal Record, Issue 14 October 2011, vol. 86, 42 [pp 457-468])
11. Eurosurveillance, Volume 16, Issue 5, 03 February 2011. Lackenby A, et al. Continued Emergence and Changing Epidemiology of Oseltamivir-Resistant Influenza A(H1N1)2009 Virus, United Kingdom, Winter 2010/11

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