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Summary Influenza virus is responsible for 18.2%–33.3% of community-dwelling older adult influenza-like illness (ILI) cases in 2 consecutive seasons. Although vaccination protects against influenza virus infection, it had no effect on the overall number of ILI cases in older adults., Background Data on the relative contribution of influenza virus and other respiratory pathogens to respiratory infections in community-dwelling older adults (≥60 years) are needed. Methods A prospective observational cohort study was performed in the Netherlands during 2 winters. Nasopharyngeal and oropharyngeal swabs were collected during influenza-like illness (ILI) episodes and from controls. Viruses and bacteria were identified by multiplex ligation–dependent probe amplification assay and conventional bacterial culture. Results The ILI incidence in the consecutive seasons was 7.2% and 11.6%, and influenza virus caused 18.9% and 34.2% of ILI episodes. Potential pathogen were detected in 80% of the ILI events with influenza virus, coronaviruses, rhinoviruses, human metapneumovirus, respiratory syncytial virus, parainfluenza viruses, and Haemophilus influenzae being the most common. Influenza vaccination reduced influenza virus infection by 73% (95% confidence interval [CI], 26%–90%) and 51% (95% CI, 7%–74%) in ILI patients. However, ILI incidence was similar between vaccinated (7.6% and 10.8%) and nonvaccinated (4.2% and 11.4%) participants in 2011–2012 and 2012–2013, respectively (P > .05). Conclusions Influenza virus is a frequent pathogen in older adults with ILI. Vaccination reduces the number of influenza virus infections but not the overall number of ILI episodes: other pathogens fill the gap. We suggest the existence of a pool of individuals with high susceptibility to respiratory infections. Clinical Trials Registration NTR3386.

A/H3N2 variant (H3N2v) swine influenza virus containing the matrix (M) gene from the 2009 A/H1N1 pandemic virus was first identified in pigs in 2010 and subsequently detected in 12 people in the United States in 2011 [1]. The following year, 309 confirmed cases of H3N2v infection were reported across 12 states, resulting in 1 death and 16 hospitalizations [2]. The majority of cases were in children and adolescents; most cases reported agricultural fair attendance and/or contact with swine prior to illness [3]. Consequently, the US Department of Health and Human Services requested a clinical evaluation of candidate H3N2v influenza vaccines as part of their pandemic preparedness program. There were only 19 confirmed cases in 2013, suggesting restricted transmission of H3N2v virus [2, 4]. However sporadic person-to-person transmission demonstrates the epidemic potential of this emerging virus [3]. In addition, animal models have shown that H3N2v viruses have the capacity for efficient replication and transmission in mammals [5]. The aim of this Phase 1 study was to assess the safety and immunogenicity of MF59-adjuvanted and nonadjuvanted cell-culture-derived, inactivated swine origin H3N2v influenza monovalent subunit (H3N2c) vaccines in children, adolescents, adults, and the elderly, and to help identify the optimal antigen and adjuvant dose to be used in further clinical development in case the H3N2v virus threat increases. Here we present results from a planned interim analysis at Day 43; safety and antibody data from a 12-month follow-up will be presented separately.

The 2009 pandemic influenza A(H1N1) (A[H1N1]pdm09) vaccine component has remained unchanged from 2009. We estimate the effectiveness of current and prior inactivated influenza A(H1N1)pdm09 vaccination from influenza seasons 2010-2011 to 2015-2016.Patients attended with influenza-like illness were tested for influenza. Four periods with continued A(H1N1)pdm09 circulation were included in a test-negative design.We enrolled 1278 cases and 2343 controls. As compared to individuals never vaccinated against influenza A(H1N1)pdm09, the highest effectiveness (66%; 95% confidence interval, 49%-78%) was observed in those vaccinated in the current season who had received 1-2 prior doses. The effectiveness was not statistically lower in individuals vaccinated in the current season only (52%) or in those without current vaccination and2 prior doses (47%). However, the protection was lower in individuals vaccinated in the current season after2 prior doses (38%; P = .009) or those currently unvaccinated with 1-2 prior doses (10%; P.001). Current-season vaccination improved the effect in individuals with 1-2 prior doses and did not modify significantly the risk of influenza in individuals with2 prior doses.Current vaccination or several prior doses were needed for high protection. Despite the decreasing effect of repeated vaccination, current-season vaccination was not inferior to no current-season vaccination.

Avian influenza A(H5N1) was identified as a cause of death in poultry in 1996, with the first human cases of infection recorded in 1997 [1]. From 2003 until January 2014, influenza A(H5N1) has caused 650 cases of influenza in humans [2]. Around 90% of cases have occurred in individuals

Our understanding of the global ecology of influenza viruses is impeded by historically low levels of viral surveillance in Africa. Increased genetic sequencing of African A/H1N1 pandemic influenza viruses during 2009–2013 revealed multiyear persistence of 2 viral lineages within West Africa, raising questions about the roles of reduced air traffic and the asynchrony of seasonal influenza epidemics among West African countries in the evolution of independent lineages. The potential for novel influenza virus lineages to evolve within Africa warrants intensified influenza surveillance in Africa and other understudied areas.

Background Because pneumococcal pneumonia was prevalent during previous influenza pandemics, we evaluated invasive pneumococcal pneumonia (IPP) rates during the 2009 influenza A(H1N1) pandemic. Methods We identified laboratory-confirmed, influenza-associated hospitalizations and IPP cases (pneumococcus isolated from normally sterile sites with discharge diagnoses of pneumonia) using active, population-based surveillance in the United States. We compared IPP rates during peak pandemic months (April 2009-March 2010) to mean IPP rates in nonpandemic years (April 2004-March 2009) and, using Poisson models, to 2006-2008 influenza seasons. Results Higher IPP rates occurred during the peak pandemic month compared to nonpandemic periods in 5-24 (IPP rate per 10 million: 48 vs 9 (95% confidence interval [CI], 5-13), 25-49 (74 vs 53 [CI, 41-65]), 50-64 (188 vs 114 [CI, 85-143]), and ≥65-year-olds (229 vs 187 [CI, 159-216]). In the models with seasonal influenza rates included, observed IPP rates during the pandemic peak were within the predicted 95% CIs, suggesting this increase was not greater than observed with seasonal influenza. Conclusions The recent influenza pandemic likely resulted in an out-of-season IPP peak among persons ≥5 years. The IPP peak's magnitude was similar to that seen during seasonal influenza epidemics.

The 2009 pandemic influenza A virus subtype H1N1 (A[H1N1]pdm09) was first detected in June 2009 in South Africa and later resulted in extensive transmission throughout Africa. Established routine surveillance programs and collaboration between private and public sector laboratories allowed for comprehensive molecular epidemiological and antigenic investigation of the first and second waves of 2009-2010 pandemic influenza in South Africa.We used reverse-transcription polymerase chain reaction to screen for influenza virus in 9792 specimens recovered during 2009 and 6915 specimens recovered during 2010 from inpatients and outpatients with influenza-like illness or severe acute respiratory illness symptoms identified by surveillance programs. Influenza-positive specimens were subjected to genetic and antigenic characterization. Bayesian and maximum likelihood analyses of the hemagglutinin genes of 96 A(H1N1)pdm09 strains were used for molecular epidemiological investigations. Hemagglutination inhibition assays and sequencing of the PB2 and neuraminidase genes were used to investigate pathogenicity and resistance mutations.The A(H1N1)pdm09 epidemic occurred as a second epidemic peak following seasonal influenza A virus subtype H3N2 cases in 2009 and in 2010. Progressive drift away from the A/California/7/2009 vaccine strain was observed at both the nucleotide and amino acid level, with 2010 strains clustering separate to 2009 strains. A few unique clusters of amino acid changes in severe cases were identified, but most strains were antigenically similar to the vaccine strain, and no resistance or known pathogenicity mutations were detected.Despite limited drift observed over the 2 seasons in South Africa, circulating A(H1N1)pdm09 strains remained antigenically similar to strains identified in other northern and southern hemisphere countries from 2010 and 2011.

Background. Because little is known about attitudes toward influenza and influenza vaccine among pregnant women in West Africa, before local distribution of A(H1N1)pdm09 vaccine in Ivory Coast we assessed knowledge of the pandemic and acceptance of the A(H1N1)pdm09 vaccine in a diverse population of pregnant women. Methods. A cross-sectional intercept survey of 411 pregnant women in 4 prenatal care settings was conducted during 15–28 February 2010 in Abidjan, Ivory Coast. Results. The majority (64.5%) of pregnant women said they had heard of the influenza pandemic, and of these, the majority (61.3%) were aware of the A(H1N1)pdm09 vaccine. However, awareness varied significantly by clinical setting, education level, and access to media (P

To provide vaccination against infection due to 2009 pandemic influenza A virus subtype H1N1 (A[H1N1]pdm09) to resource-constrained countries with otherwise very little access to the A(H1N1)pdm09 vaccine, the World Health Organization (WHO) coordinated distribution of donated vaccine to selected countries worldwide, including those in Africa. From February through November 2010, 32.2 million doses were delivered to 34 countries in Africa. Of the 19.2 million doses delivered to countries that reported their vaccination activities to WHO, 12.2 million doses (64%) were administered. Population coverage in these countries varied from 0.4% to 11%, with a median coverage of 4%. All countries targeted pregnant women (median proportion of all vaccine doses administered [mpv], 21% [range, 4%-72%]) and healthcare workers (mpv, 9% [range, 1%-73%]). Fourteen of 19 countries targeted persons with chronic conditions (mpv, 26% [range, 5%-66%]) and 10 of 19 countries vaccinated children (mpv, 54% [range, 17%-75%]). Most vaccine was distributed after peak A(H1N1)pdm09 transmission in the region. The frequency and severity of adverse events were consistent with those recorded after other inactivated influenza vaccines. Pandemic preparedness plans will need to include strategies to ensure more-rapid procedures to identify vaccine supplies and distribute and import vaccines to countries that may bear the brunt of a future pandemic.

Little is known about influenza in central Africa. We conducted sentinel surveillance for influenza-like illness, severe acute respiratory illness, and laboratory-confirmed influenza at 5 sites in Kinshasa, Democratic Republic of Congo, from January 2009 through April 2011. We obtained samples from 4156 patients, of whom 605 (15%) had specimens containing laboratory-confirmed influenza virus. Apart from the period of pandemic influenza due to influenza A virus subtype H1N1, which occurred during August-December 2009, influenza activity peaked at least once each year from January through March, predominantly among children. These data can guide interventions to reduce the burden of influenza in the Democratic Republic of Congo and central Africa.

Background Influenza surveillance data from tropical, sub-Saharan African countries are limited. To better understand the epidemiology of influenza, Nigeria initiated influenza surveillance in 2008. Methods Outpatients with influenza-like illness (ILI) and inpatients with severe acute respiratory illness (SARI) were enrolled at 4 sentinel facilities. Epidemiologic data were obtained, and respiratory specimens were tested for influenza viruses, using real-time reverse-transcription polymerase chain reaction assays. Results During April 2009-August 2010, 2841 patients were enrolled. Of 2803 specimens tested, 217 (7.7%) were positive for influenza viruses (167 [8%] were from subjects with ILI, 17 [5%] were from subjects with SARI, and 33 were from subjects with an unclassified condition). During the prepandemic period, subtype H3N2 (A[H3N2]) was the dominant circulating influenza A virus subtype; 2009 pandemic influenza A virus subtype H1N1 (A[H1N1]pdm09) replaced A(H3N2) as the dominant circulating virus during November 2009. Among persons with ILI, A(H1N1)pdm09 was most frequently found in children aged 5-17 years, whereas among subjects with SARI, it was most frequently found in persons aged ≥ 65 years. The percentage of specimens that tested positive for influenza viruses peaked at 18.9% in February 2010, and the majority were A(H1N1)pdm09. Conclusions Influenza viruses cause ILI and SARI in Nigeria. Data from additional years are needed to better understand the epidemiology and seasonality of influenza viruses in Nigeria.

Background: Pregnant women were at increased risk for serious outcomes of 2009 pandemic influenza A virus subtype H1N1 (influenza A[H1N1]pdm09) infection, but little is known about the overall impact of the pandemic on neonatal and maternal outcomes. Methods: We identified live births that occurred from 1 July 2008 through 31 May 2010 in 5 Kaiser Permanente regions. Pregnant women were considered to have influenza if they had a positive result of a laboratory test for influenza virus or if they received a diagnosis of influenza during a period in which seasonal influenza virus or A(H1N1)pdm09 was the predominant circulating virus. Results: There were 111 158 births from 109 015 pregnancies involving 107 889 mothers; 368 pregnant women (0.3%) received a diagnosis of influenza due to seasonal virus, and 959 (0.9%) received a diagnosis of influenza due to A(H1N1)pdm09; 107 688 did not receive an influenza diagnosis. Pregnant women with influenza due to A(H1N1)pdm09 were more likely than women with seasonal influenza infection to be hospitalized within 30 days of the diagnosis (27% vs 12%; odds ratio [OR], 2.84 [95% confidence interval {CI}, 2.01–4.02]). Pregnant women with A(H1N1)pdm09 who started antiviral treatment ≥2 days after the diagnosis were significantly more likely to be hospitalized than those who started antiviral treatment

Background We examined the influenza vaccine effectiveness (VE) during the 2013-2014 influenza season, in which 2009 pandemic influenza A(H1N1) virus (influenza A[H1N1]pdm09) predominated. In 2 previous years when influenza A(H3N2) virus predominated, the VE was low and negatively affected by prior year vaccination. Methods We enrolled and followed 232 households with 1049 members, including 618 children; specimens were collected from subjects with acute respiratory illnesses. The VE in preventing laboratory-confirmed influenza A(H1N1)pdm09 infection was estimated in adjusted models. Preseason hemagglutination-inhibition and neuraminidase-inhibition antibody titers were determined to assess susceptibility. Results Influenza A(H1N1)pdm09 was identified in 25 households (10.8%) and 47 individuals (4.5%). Adjusted VE against infection with influenza A(H1N1)pdm09 was 66% (95% confidence interval [CI], 23%-85%), with similar point estimates in children and adults, and against both community-acquired and household-acquired infections. VE did not appear to be different for live-attenuated and inactivated vaccines among children aged 2-8 years, although numbers were small. VE was similar for subjects vaccinated in both current and prior seasons and for those vaccinated in the current season only; susceptibility titers were consistent with this observation. Conclusions Findings, including substantial significant VE and a lack of a negative effect of repeated vaccination on VE, were in contrast to those seen in prior seasons in which influenza A(H3N2) virus predominated.

We describe the first confirmed person-to-person transmission of oseltamivir-resistant pandemic influenza A(H1N1) 2009 virus that occurred in a hematology unit in the United Kingdom. Eleven cases of (H1N1) 2009 virus infection were identified, of which, ten were related as shown by sequence analysis of the hemagglutinin and neuraminidase genes. H275Y analysis demonstrated that 8 of 10 case patients had oseltamivir-resistant virus, with 4 of 8 case patients infected by direct transmission of resistant virus. Zanamivir should be considered as first-line therapy for influenza in patients with lymphopenic hematological conditions and uptake of influenza vaccination encouraged to further reduce the number of susceptible individuals.

Levels of preexisting antibodies to the hemagglutinin of pandemic influenza A(H1N1) 2009 (hereafter pandemic H1N1) virus positively correlate with age. The impact of contemporary seasonal influenza vaccines on establishing immunity to other pandemic H1N1 proteins is unknown. We measured serum antibodies to the neuraminidase (NA) of pandemic H1N1 in adults prior to and after vaccination with seasonal trivalent inactivated influenza vaccines. Serum antibodies to pandemic H1N1 NA were observed in all age groups; however, vaccination elevated levels of pandemic H1N1 NA antibodies predominately in elderly individuals (age, ⩾60 years). Therefore, contemporary seasonal vaccines likely contribute to reduction of pandemic H1N1-associated disease in older individuals.

Although the mortality burden of the devastating 1918 influenza pandemic has been carefully quantified in the United States, Japan, and European countries, little is known about the pandemic experience elsewhere. Here, we compiled extensive archival records to quantify the pandemic mortality patterns in 2 Mexican cities, Mexico City and Toluca.We applied seasonal excess mortality models to age-specific respiratory mortality rates for 1915-1920 and quantified the reproduction number from daily data.We identified 3 pandemic waves in Mexico City in spring 1918, autumn 1918, and winter 1920, which were characterized by unusual excess mortality among people 25-44 years old. Toluca experienced 2-fold higher excess mortality rates than Mexico City but did not experience a substantial third wave. All age groups, including that of people 65 years old, experienced excess mortality during 1918-1920. Reproduction number estimates were2.5, assuming a 3-d generation interval.Mexico experienced a herald pandemic wave with elevated young adult mortality in spring 1918, similar to the United States and Europe. In contrast to the United States and Europe, there was no mortality sparing among Mexican seniors 65 years old, highlighting potential geographical differences in preexisting immunity to the 1918 virus. We discuss the relevance of our findings to the 2009 pandemic mortality patterns.

Understanding the risk of mortality during the 1918-1919 influenza pandemic could inform preparations for a future pandemic.Prospectively collected demographic, hospitalization, and death data from all individuals who served in the Australian Imperial Force from 1914 through 1919 in Europe and the Middle East were abstracted from archived records. Analyses were conducted to determine mortality risk factors.Hospitalization with a respiratory illness during the spring-summer of 1918 protected soldiers from death (odds ratio, 0.37 [95% confidence interval, 0.25-0.53]; P.001) but not from hospitalization during the fall-winter of 1918-1919. During the fall-winter of 1918-1919, there was a strong inverse relationship between risk of dying of pneumonia-influenza and time in military service. The pneumonia-influenza death rate among men who enlisted in 1918 (6.33 deaths per 100 person-years) was 9 times higher than that among the 1917 enlistment cohort (0.72 deaths per 100 person-years) and14 times higher than that among the 1916 cohort (0.43 deaths per 100 person-years), 1915 cohort (0.29 deaths per 100 person-years), and 1914 cohort (0.28 deaths per 100 person-years).There was a strong inverse relationship between length of service in the Australian Imperial Force and mortality risk from pneumonia-influenza during the fall-winter of 1918-1919. The protective effect of increased service likely reflected increased acquired immunity to influenza viruses and endemic bacterial strains that caused secondary pneumonia and most of the deaths during the 1918-1919 influenza pandemic.

Animal model studies and human epidemiological studies have shown that some infectious diseases develop primarily in individuals with an inherited predisposition. A heritable contribution to the development of severe influenza virus infection (i.e., that which results in death) has not previously been hypothesized or tested. Evidence for a heritable contribution to death due to influenza was examined using a resource consisting of a genealogy of the Utah population linked to death certificates in Utah over a period of 100 years. The relative risks of death due to influenza were estimated for the relatives of 4,855 individuals who died of influenza. Both close and distant relatives of individuals who died of influenza were shown to have a significantly increased risk of dying of influenza, consistent with a combination of shared exposure and genetic effects. These data provide strong support for a heritable contribution to predisposition to death due to influenza.

The 1918-1919 H1N1 influenza pandemic was among the most deadly events in recorded human history, killing an estimated 50-100 million persons. Because recent H5N1 avian epizootics have been associated with sporadic human fatalities, concern has been raised that a new pandemic, as fatal as the pandemic of 1918, or more so, could be developing. Understanding the events and experiences of 1918 is thus of great importance. However, despite the genetic sequencing of the entire genome of the 1918 virus, many questions about the 1918 pandemic remain. In this review we address several of these questions, concerning pandemic-virus origin, unusual epidemiologic features, and the causes and demographic patterns of fatality. That none of these questions can yet be fully answered points to the need for continued pandemic vigilance, basic and applied research, and pandemic preparedness planning that emphasizes prevention, containment, and treatment with antiviral medications and hospital-based intensive care.

BACKGROUND The predominant strain during the 2013-2014 influenza season was 2009 pandemic influenza A(H1N1) virus (A[H1N1]pdm09). This vaccine-component has remained unchanged from 2009. METHODS The US Flu Vaccine Effectiveness Network enrolled subjects aged ≥6 months with medically attended acute respiratory illness (MAARI), including cough, with illness onset ≤7 days before enrollment. Influenza was confirmed by reverse-transcription polymerase chain reaction (RT-PCR). We determined the effectiveness of trivalent or quadrivalent inactivated influenza vaccine (IIV) among subjects ages ≥6 months and the effectiveness of quadrivalent live attenuated influenza vaccine (LAIV4) among children aged 2-17 years, using a test-negative design. The effect of prior receipt of any A(H1N1)pdm09-containing vaccine since 2009 on the effectiveness of current-season vaccine was assessed. RESULTS We enrolled 5999 subjects; 5637 (94%) were analyzed; 18% had RT-PCR-confirmed A(H1N1)pdm09-related MAARI. Overall, the effectiveness of vaccine against A(H1N1)pdm09-related MAARI was 54% (95% confidence interval [CI], 46%-61%). Among fully vaccinated children aged 2-17 years, the effectiveness of LAIV4 was 17% (95% CI, -39% to 51%) and the effectiveness of IIV was 60% (95% CI, 36%-74%). Subjects aged ≥9 years showed significant residual protection of any prior A(H1N1)pdm09-containing vaccine dose(s) received since 2009, as did children

The "Spanish influenza" pandemic of 1918 was the most devastating influenza epidemic reported in history and killed >30 million people worldwide. The factors contributing to the severe pathogenicity of this influenza virus are of great interest, because avian influenza viruses circulating today pose the threat of a new pandemic if they develop sustained human-to-human transmissibility. Recent characterization of the 1918 virus has illuminated which determinants may be the cause of virulence. Here, we wish to shed light on what has been learned to date about the 1918 virus with regard to pathogenicity and transmissibility, to supplement our understanding of the determinants of human virulence and transmission of pandemic influenza viruses. Monitoring the sequences of avian influenza viruses for genetic changes and diversity may help us to predict the risks that these viruses pose of causing a new pandemic.

During a pandemic, influenza vaccines that rely on neutralizing antibodies to protect against matched viruses might not be available early enough. Much broader (heterosubtypic) immune protection is seen in animals. Do humans also have cross-subtype immunity? To investigate this issue, archival records from the Cleveland Family Study, which was conducted before and during the 1957 pandemic (during which a shift from subtype H1N1 to H2N2 occurred), were analyzed. Only 5.6% of the adults who had had symptomatic influenza A in earlier study years developed influenza during the pandemic, despite living in households with participants who had influenza. In contrast, 55.2% of the children who had had symptomatic influenza A contracted it again. These findings suggest an impact of accumulated heterosubtypic immunity during a pandemic. Such immunity, as well as its implications for vaccination, should be further investigated.

Ultimate victory over influenza will rank among the great achievements of humankind because the defeats have been so bitter. The defense is growing stronger, and losses are less extreme. Incomplete successes against a lethal foe are great successes that fuel the determination for a shared and total victory. Studies reported in this issue of The Journal of Infectious Diseases invite consideration of the strengths and limitations of influenza vaccination, an especially important defense against life-threatening influenza disease and its transmission. Influenza vaccination has not yet fulfilled the hope of complete protection against disease. Influenza vaccine effectiveness against all forms of influenza disease is variable. However, the prevention of influenza morbidity in all forms is less grave a need than prevention of mortality, and influenza vaccine performance is generally better in this regard. Consequently, persons at high risk for severe influenza disease benefit most from influenza vaccination, a conclusion that underpins the strongest recommendations for vaccination of this population [1]. Children who are older than 6 months, thus eligible for influenza vaccination, suffer high attack rates of influenza, though lower hospitalization rates than children younger than 6 months [2]. Children play an important role in the epidemic spread of influenza virus [3– 6]. Childhood influenza deaths are devastating losses, and their ongoing prevention by vaccination would be a tremendous achievement; nowhere is the struggle with influenza more hard fought than in the red zone of our pediatric intensive care units (PICUs).

To the Editor— We thank Wilson et al [1] for their comments on our study of the 1918–1919 influenza pandemic in Kentucky [2]. Our key findings were to provide evidence of break points in the mortality profile of the fall 1918 pandemic wave among individuals aged 9–10 years (ie, cohorts born during 1908–1909) and those aged 24–26 years (ie, cohorts born during 1892–1894) [2]. These age break points do not strictly align with known dates of past pandemic events, and, hence, it is not intuitive that they support or refute the hypothesis proposed by Wilson et al, in which aberrant immune responses mediated by CD8+ T cells were more frequent among young adults whose first influenza virus exposures were to the 1889 pandemic virus [1]. In their letter, Wilson et al contribute interesting data on influenza mortality patterns in New Zealand [1]. They report a mortality peak at ages 29–30 years in males and females (ie, cohorts born during 1888–1889), which is more in line with hypotheses invoking the 1889 pandemic than our Kentucky data. These findings could reflect true differences in the pandemic experience of geographically distant populations. Alternatively, the mortality profile in New Zealand could be influenced by a preponderance of influenza risk factors in aboriginal Maori populations or by high variance in mortality estimates due to small population size (approximately 0.85 million). Methodological factors may also contribute to the observed differences between the 2 studies, as our Kentucky analysis relied on “above baseline” excess mortality in the lethal months of October–December 1918 [2]. Future studies could compare the risks profiles of different populations via the excess mortality approach to help tease out influenza-specific effects from unrelated background mortality [3]. Wilson et al note that US population size estimates from this period may be inaccurate, potentially resulting in imprecise death rate estimates—an issue emphasized by an earlier historical study from Canada and the United States [4]. We agree that estimates of male population sizes during wartime are prone to bias because of troop movements. Hence, like Wilson et al, we combined female mortality counts with population information collated from carefully conducted decennial censuses to present a relatively unbiased picture of mortality risk at the time. We have now repeated our analysis with death count data, which we show in parallel with our analysis of excess death rates in Figure ​Figure1.1. Both curves indicate mortality peaks at ages 25–26 years (ie, cohorts born during 1892–1893), consistent across various diagnostic outcomes and in female-specific data. These sensitivity analyses confirm that the Kentucky cohorts at highest risk of influenza-related death were those born a few years after the 1889 pandemic, irrespective of whether we use population denominators. Figure 1. Age-specific patterns of mortality due to respiratory disease during the October–December 1918 influenza pandemic wave in Kentucky. A, Data obtained using a regression model to estimate the influenza-related mortality rate (ie, the excess mortality ... Overall, our historical analysis provides unprecedented detail on the age and sex patterns of the pandemic in Kentucky [2]. Similar to Wilson et al [1], we found a substantially increased risk of death among military populations, perhaps due to crowding and/or increased circulation of coinfecting pathogenic bacteria. However, these factors alone cannot account for the mortality risk of the 1918 pandemic among young adult civilian females. While the reasons for the unusual age patterns of the 1918 pandemic are difficult to elucidate from epidemiological data alone, the steep rise in the risk of mortality among individuals aged 10–20 years during the influenza pandemic is worth noting, especially as it consistent in data from New Zealand, Canada, and the United States [1, 2, 4]. Historical morbidity surveys indicate that clinical attack rates were similar in these age cohorts [5], suggesting that the severity of influenza-related infection increased sharply between ages 10 and 20 years, likely because of a heightened risk of pneumonia caused by common bacterial respiratory pathogens (especially pneumococci, streptococci, and staphylococci) [5–7]. People aged 10–20 years had not lived through the 1889 pandemic, although they could have been infected by descendants of the 1889 influenza virus that persisted during 1892–1918. Although the reasons for the atypical mortality risk profile of the 1918–1919 pandemic may remain elusive, it is important to pursue efforts to analyze archival mortality records from a variety of locations, building upon the work by Wilson et al and others [1, 2, 4, 5, 8, 9]. A systematic epidemiological description of the pandemic in a variety of globally sampled populations may provide unique insights into the host and geographic factors responsible for the unusual severity of disease associated with the 1918 pandemic virus.

Concerns that a new influenza strain may arise that would exhibit similar properties to the 1918-1919 pandemic virus prompted the decision in 1947 to establish a World Health Organization global program for influenza surveillance. This program has contributed greatly to understanding of the epidemiology of influenza and provides the basis for the timely updating of influenza vaccine formulations during interpandemic periods. The spread of pandemic influenza, however, is extremely rapid and, in 1957 and 1969, occurred before sufficient supplies of vaccine could be prepared and administered. Recent evidence regarding the origin of new influenza strains provides some opportunities for improving surveillance for pandemic influenza, but there is a danger that the benefits may be offset by even more rapid spread of a future pandemic due to changes in worldwide transportation and commerce.

Vaccination offers the best opportunity to prevent disease and death in a pandemic, but there will be limitations on the timeliness and availability of vaccine [1]. Optimistic projections are that it could take at least 6 months for the first pandemic vaccine doses to be prooduced after the identification of a pandemic strain. Global influenza-vaccine production capacity has nearly doubled over the preceding decade, and increased demand for annual influenza vaccine will continue to

Children are at increased risk of influenza infection compared with the general population, and influenza is associated with relatively high rates of serious illness in children of preschool age [1–5]. Among influenza virus types, influenza A is generally considered to represent the greatest public health concern, yet the burden of influenza B in children is substantial. Influenza-related hospitalizations and complications such as myositosis are more common in children infected with influenza B than with influenza A [6–8]. Annual influenza vaccination is the most effective method for preventing influenza and associated complications, and trivalent influenza vaccines include 2 influenza A strains (A/H1N1, A/H3N2) and 1 influenza B strain, selected using surveillance-based forecasts [9]. Two antigenically distinct influenza B lineages (B/Yamagata and B/Victoria) emerged globally in humans in the early 1980s and have co-circulated in the United States since 2001[10]. However, trivalent influenza vaccines provide limited or no cross-reactive protection between the 2 influenza B lineages [11]. Moreover, in the United States, the seasonal trivalent vaccine was mismatched for the circulating influenza B lineage in 5 of 10 influenza seasons between 2001 and 2010 and in Europe was mismatched in 4 of 8 seasons between 2003 and 2010 [12–14]. Given the burden of influenza B infection and the rate of B-lineage mismatch with trivalent vaccines, in February 2012, the World Health Organization (WHO) recommended B strains from both lineages for inclusion in quadrivalent vaccines for use in the 2012/2013 season in the Northern Hemisphere [15]. Here we report a Phase III, randomized, double-blind study of a candidate inactivated quadrivalent split viron influenza vaccine (QIV) containing both B lineages compared with 2 inactivated trivalent influenza vaccines (TIV) in children aged 3–17 years. The purpose of the study was to test the immunologic noninferiority of QIV vs TIV against shared influenza A and B strains, and superiority against influenza B of QIV vs TIVs containing an alternate-lineage B strain. QIV was also assessed in children aged 6–35 months as a separate open-label group.

Background. The 2009 influenza A virus subtype H1N1 (A[H1N1]pdm09) did not exhibit antigenic drift during the 2010–2011 influenza season, providing an opportunity to investigate the duration of protection after vaccination. We estimated the independent effects of 2010–2011 seasonal trivalent inactivated influenza vaccine (TIV) and A(H1N1)pdm09 vaccine for preventing medically attended influenza A virus infection during the 2010–2011 season. Methods. Individuals were tested for influenza A virus by real-time reverse transcription polymerase chain reaction (rRT-PCR) after a clinical encounter for acute respiratory illness. Case-control analyses compared participants with rRT-PCR–confirmed influenza A virus infection and test-negative controls. Vaccine effectiveness was estimated separately for monovalent pandemic vaccine and TIV and was calculated as 100 × [1 – adjusted odds ratio], where the odds ratio was adjusted for potential confounders. Results. The effectiveness of TIV against influenza A virus infection was 63% (95% confidence interval [CI], 37%–78%). The effectiveness of TIV against A(H1N1)pdm09 infection was 77% (95% CI, 44%–90%). Monovalent vaccine administered between October 2009 and April 2010 was not protective during the 2010–2011 season, with an effectiveness of −1% (95% CI, −146% to 59%) against A(H1N1)pdm09 infection. Conclusions. Monovalent vaccine provided no sustained protection against A(H1N1)pdm09 infection during the 2010–2011 season. This waning effectiveness supports the need for annual revaccination, even in the absence of antigenic drift in A(H1N1)pdm09.

Following the emergence of 2009 pandemic influenza A virus subtype H1N1 (A[H1N1]pdm09) in the United States and Mexico in April 2009, A(H1N1)pdm09 spread rapidly all over the world. There is a dearth of information about the epidemiology of A(H1N1)pdm09 in Africa, including Morocco. We describe the epidemiologic characteristics of the A(H1N1)pdm09 epidemic in Morocco during 2009-2010, including transmissibility and risk factors associated with fatal disease.We implemented influenza surveillance for patients presenting with influenza-like illness (ILI) at 136 private and public clinics for patients with severe acute respiratory illness (SARI) at 16 regional public hospitals from June 2009 through February 2010. Respiratory samples and structured questionnaires were collected from all enrolled patients, and samples were tested by real-time reverse-transcription polymerase chain reaction for influenza viruses. We estimated the risk factors associated with fatal disease as well as the basic reproduction number (R(0)) and the serial interval of the pandemic virus.From June 2009 through February 2010, we obtained 3937 specimens, of which 1452 tested positive for influenza virus. Of these, 1398 (96%) were A(H1N1)pdm09. Forty percent of specimens from ILI cases (1056 of 2646) and 27% from SARI cases (342 of 1291) were positive for A(H1N1)pdm09. Sixty-four deaths occurred among laboratory-confirmed A(H1N1)pdm09 SARI cases. Among these cases, those who had hypertension (age-adjusted odd ratio [aOR], 28.2; 95% confidence interval [CI], 2.0-398.7), had neurological disorders (aOR, 7.5; 95% CI, 1.5-36.4), or were obese (aOR, 7.1; 95% CI, 1.6-31.1), as well as women of gestational age who were pregnant (aOR, 2.5; 95% CI, 1.1-5.6), were at increased risk of death. Across the country, elevated numbers of locally acquired infections were detected 4 months after the detection of the first laboratory-confirmed case and coincided with the expected influenza season (October-January) in Morocco. We obtained an R(0) estimate of 1.44 (95% CI, 1.32-1.56) and a mean serial interval (±SD) of 2.3 ± 1.4 days (95% CI, 1.6-3.0).Widespread but delayed community transmission of A(H1N1)pdm09 occurred in Morocco in 2009, and A(H1N1)pdm09 became the dominant influenza virus subtype during the 2009-2010 influenza season. The transmissibility characteristics were similar to those observed in other countries.

Background The US Army Medical Research Unit-Kenya (USAMRU-K) conducts surveillance for influenza-like illness (ILI) in Kenya. We describe the temporal and geographic progression of A(H1N1)pdm09 as it emerged in Kenya and characterize the outpatient population with A(H1N1)pdm09 infection. Methods We included patients with ILI aged 2 months to 18 years enrolled during June 2009-August 2010. Respiratory specimens were tested by real-time reverse-transcription polymerase chain reaction for influenza virus. Patients with A(H1N1)pdm09 infection were compared to those with seasonal influenza A virus infection and those with ILI who had no virus or a virus other than influenza virus identified (hereafter, "noninfluenza ILI"). Results Of 4251 patients with ILI, 193 had laboratory-confirmed A(H1N1)pdm09 infection. The first pandemic influenza case detected by USAMRU-K surveillance was in August 2009; peak activity nationwide occurred during October-November 2009. Patients with A(H1N1)pdm09 infection were more likely to be school-aged, compared with patients with seasonal influenza A virus infection (prevalence ratio [PR], 2.0; 95% confidence interval [CI], 1.3-3.1) or noninfluenza ILI (PR, 3.2; 95% CI, 2.4-4.3). Conclusions USAMRU-K ILI surveillance detected the geographic and temporal distribution of pandemic influenza in Kenya. The age distribution of A(H1N1)pdm09 infections included more school-aged children, compared with seasonal influenza A virus infection and noninfluenza ILI.

Currently, the 2 main strategies for control of influenza are immunization and antiviral drugs. However, despite increasing uptake of influenza vaccine among the highest risk groups—namely, the elderly and persons with underlying cardiopulmonary diseases—morbidity and mortality from influenza continues to rise in the United States [ 1 ]. This paradox has stimulated a heated debate regarding the true efficacy of influenza vaccination in older persons [ 2 , 3 ]. Some investigators suggest efficacy may be negligible in this group, and even the most optimistic proponents of immunization concede that the current licensed standard dose of inactivated vaccine is less immunogenic and protective in older persons than in young healthy persons [ 4 , 5 , 6 ]. Antiviral therapy, principally with neuraminidase inhibitors, has been shown repeatedly in placebo-controlled trials to be effective when administered to both young and old outpatients early in the course of illness [ 7 , 8 ]. Although controlled studies in inpatients are strikingly absent, one observational analysis from Toronto noted a 79% reduction in mortality in patients treated with a neuraminidase inhibitor, even when administered after the 48-hour window following symptom onset [ 9 ]. Despite availability of vaccine and antivirals, additional therapeutic measures for influenza would be welcomed. In this issue of the Journal, Vandermeer and collaborators report that statin use is associated with reduced mortality during and after hospitalization with influenza infection [ 10 ]. The investigators analyzed 30-day mortality in 3043 patients hospitalized with influenza in 10 states as part of the Centers for Disease Control and Prevention’s Emerging Infections Program. After adjusting for other variables, such as age, underlying medical conditions, and influenza vaccination, they reported a striking 41% reduction in mortality (odds ratio, 0.59 [95% confidence interval, .38‐.92]) in persons on statins either prior to or during hospi

Background. The 2009 influenza pandemic led to guidelines emphasizing antiviral treatment for all persons hospitalized with influenza, including pregnant women. We compared antiviral use among adults hospitalized with influenza before and during the pandemic. Methods. The Emerging Infections Program conducts active population-based surveillance for persons hospitalized with community-acquired, laboratory-confirmed influenza in 10 states. We analyzed data collected via medical record review ofpatients aged $18 years admitted during prepandemic (1 October 2005through 14 April 2009) and pandemic (15 April 2009 through 31 December 2009) time frames. Results. Of 5943 adults hospitalized with influenza in prepandemic seasons, 3235 (54%) received antiviral treatment, compared with 4055 (82%) of 4966 during the pandemic. Forty-one (22%) of 187 pregnant women received antiviral treatment in prepandemic seasons, compared with 369 (86%) of 430 during the pandemic. Pregnancy was a negative predictor of antiviral treatment before the pandemic (adjusted odds ratio [aOR], 0.24; 95% confidence interval [CI], .16‐.35) but was independently associated with treatment during the pandemic (aOR, 1.97; 95% CI, 1.32‐2.96). Antiviral treatment among adults hospitalized .2 days after illness onset increased from 43% before the pandemic to 79% during the pandemic (P , .001). Conclusions. Antiviral treatment of hospitalized adults increased during the pandemic, especially among pregnant women. This suggests that many clinicians followed published guidance to treat hospitalized adults with antiviral agents. However, compliance with antiviral recommendations could be improved.

Pregnancy has been identified as a risk factor for severe illness and death during all the influenza pandemics of the 20th century and in the 2009–2010 influenza A(H1N1) pandemic. In the 1957 influenza pandemic, ∼50% of the deaths in women of childbearing age occurred in pregnant women and resulted from primary viral pneumonia following influenza infection [1–3]. Similarly, although pregnant women comprise ∼1% of the US population today, they accounted for 5% of influenza-related deaths during the 2009 pandemic; furthermore, pregnant women were at elevated risk for admission to intensive care units and preterm delivery [4–6]. In contrast to the risk of maternal illness during pregnancy, the impact of influenza on the fetus and likelihood of miscarriage has been less studied [7]. Although studies have shown that maternal influenza vaccination improves fetal and infant outcomes [8, 9], little is known about whether maternal influenza infection has the potential to terminate pregnancies, and comprehensive data are lacking on the association between influenza and birth outcomes. This issue could have important implications for public health strategies and clinical care for pandemics as well as seasonal epidemics. Investigating the impact of influenza on pregnancy is a challenge, because miscarriages may not be directly linked to influenza when patients are referred to clinics, especially if miscarriage occurs several weeks after primary viral infection. In addition, early pregnancy loss may occur unbeknownst to women who have not yet discovered that they are pregnant. Clinical reports from the 1918 pandemic period support a link between influenza and elevated maternal morbidity, mortality, pregnancy loss, and preterm labor [10–12]. In a 1919 report of 1350 pregnant women with influenza, 26% of case subjects miscarried (the largest proportion in the first trimester), whereas 52% of pneumonia-complicated case subjects miscarried [13]. This phenomenon associated with the 1918 pandemic appears to have been geographically widespread; a preponderance of miscarriages following pandemic peak activity was described in the Philippines [14], and an increase in miscarriages in women 5–9 months pregnant followed by a baby boom was reported in Norway [15]. In more recent literature, a possible association was noted between seasonal influenza A(H3N2) and a cluster of miscarriages [16]. Small observational studies of pregnant women infected with the 2009 pandemic influenza A(H1N1) virus reported preterm deliveries and fetal deaths [17, 18]. Despite these geographically limited reports and case series, the association between maternal influenza and pregnancy loss has not been quantified. In this study, we utilized historical epidemiological records from the 1918 influenza pandemic in 3 Scandinavian countries and the United States to examine the relationship between influenza and pregnancy outcomes at the population level. We hypothesized that if influenza infection in pregnant women can cause miscarriages on a large scale, then a decline in births would occur within 9 months of the peak pandemic activity. Data from contemporaneous national surveillance systems were acquired from library archives to elucidate the potential temporal associations between influenza activity and birth patterns, and to quantify the risk of miscarriage associated with influenza infection.

Background. An age bias toward children and young adults has been reported for infection and hospitalizations with pandemic H1N1 influenza (A[H1N1]pdm) in the 2009 and 2010 influenza seasons in the Southern and Northern Hemispheres. Serological analysis of prepandemic samples has shown a higher incidence of cross-reactive antibodies to A(H1N1)pdm virus in older populations; conserved T cell epitopes between viruses have been identified. The contribution of preexisting immunity to seasonal influenza to protection against A(H1N1)pdm infection was analyzed in a ferret model. Methods. Ferrets were pre-infected with influenza A viruses and/or vaccinated with inactivated influenza viruses with adjuvant. Infection after challenge was assessed by measuring shedding virus, transmission to naive animals, and seroconversion. Results. Homologous vaccination reduced the incidence of infection and delayed transmission. Pre-infection with virus induced sterilizing immunity to homologous challenge. One prior infection with seasonal influenza A virus improved clearance of A(H1N1)pdm virus. Prior infection with A(H1N1)pdm virus reduced shedding after seasonal influenza A challenge. Two infections with seasonal influenza A viruses reduced the incidence of infection, the amount and duration of virus shedding, and the frequency of transmission following A(H1N1)pdm challenge. Conclusion. These data suggest the reduced incidence and severity of infection with A(H1N1)pdm virus in the adult population during the 2009-2010 influenza season may be a result of previous exposure to seasonal influenza A viruses.

In April 2009, an outbreak due to infection with the 2009 pandemic influenza A (H1N1) virus (pH1N1) was investigated in a New York City high school. We surveyed household contacts of ill students to characterize the extent of transmission within households, identify contact groups at highest risk for illness, and assess the potential for preventing household transmission. Influenza-like illness (ILI) was reported by 79 of 702 household contacts (11.3% attack rate). Multivariate analysis showed that older age was protective: for each increasing year of age, the risk of ILI was reduced 5%. Additional protective factors included antiviral prophylaxis and having had a household discussion about influenza. Providing care for the index case patient and watching television with the index case patient were risk factors among parents and siblings, respectively. Fifty percent of cases occurred within 3 days of onset of illness in the student. These factors have implications for mitigating the impact of pH1N1 transmission.

Recent outbreaks of infection with highly pathogenic H5N1 strains of avian influenza virus in poultry in Asia, Africa, Europe, and the Middle East have raised concern over the potential emergence of a pandemic strain that can easily infect humans and cause serious morbidity and mortality. To prevent and control a national outbreak, the US Department of Agriculture (USDA) conducts measures based on the ecology of avian influenza viruses. To prevent an outbreak in the United States, the USDA conducts surveillance of bird populations, restrictions on bird importation, educational outreach, and regulation of agricultural practices, in collaboration with local, state, and federal organizations. To manage an outbreak, the USDA has in place a well-established emergency management system for optimizing efforts. The USDA also collaborates with international organizations for disease prevention and control in other countries.

Background The first pandemic season of A/H3N2 influenza virus (1968/1969) resulted in significant mortality in the United States, but it was the second pandemic season of A/H3N2 influenza virus (1969/1970) that caused the majority of deaths in England. We further explored the global pattern of mortality caused by the pandemic during this period. Methods We estimated the influenza-related excess mortality in 6 countries (United States, Canada, England and Wales, France, Japan, and Australia) using national vital statistics by age for 1967-1978. Geographical and temporal pandemic patterns in mortality were compared with the genetic drift of the influenza viruses by analyzing hemagglutinin and neuraminidase sequences from GenBank. Results In North America, the majority of influenza-related deaths in 1968/1969 and 1969/1970 occurred during the first pandemic season (United States, 70%; Canada, 54%). Conversely, in Europe and Asia, the pattern was reversed: 70% of deaths occurred during the second pandemic season. The second pandemic season coincided with a drift in the neuraminidase antigen. Conclusion We found a consistent pattern of mortality being delayed until the second pandemic season of A/H3N2 circulation in Europe and Asia. We hypothesize that this phenomenon may be explained by higher preexisting neuraminidase immunity (from the A/H2N2 era) in Europe and Asia than in North America, combined with a subsequent drift in the neuraminidase antigen during 1969/1970.

The traditional method for assessing the severity of influenza seasons is to estimate the associated increase (i.e., excess) in pneumonia and influenza (PI) mortality. In this study, excess PI hospitalizations were estimated from National Hospital Discharge Survey Data from 26 influenza seasons (1970-1995). The average seasonal rate of excess PI hospitalization was 49 (range, 8-102) /100,000 persons, but average rates were twice as high during A(H3N2) influenza seasons as during A(H1N1)/B seasons. Persons aged65 years had 57% of all influenza-related hospitalizations; however, the average seasonal risk for influenza-related PI hospitalizations was much higher in the elderly than in persons aged65 years. The 26 pairs of excess PI hospitalization and mortality rates were linearly correlated. During the A(H3N2) influenza seasons after the 1968 pandemic, excess PI hospitalizations declined among persons aged65 years but not among the elderly. This suggests that influenza-related hospitalizations will increase disproportionately among younger persons in future pandemics.

[Extract] To the Editor—In learning from history, the infectious diseases community needs to be cognizant of the consequences of swine influenza vaccination. In 1976, a considerable number of patients in the United States died of H1N1/NJ/76 vaccine–induced Guillan-Barre Syndrome (GBS). We were pleased to read the recent article by Evans et al that highlights this issue, and we wish to further explore the pathogenesis of this vaccine-related severe adverse effect. By doing so we wish to call on vaccine producers to concentrate their efforts on reassuring the medical community and therapeutic product regulators that current vaccines against pandemic H1N1 will be unlikely to induce GBS.

Almost all deaths related to current influenza epidemics occur among the elderly. However, mortality was greatest among the young during the 1918-1919 pandemic. This study compared the age distribution of influenza-related deaths in the United States during this century's three influenza A pandemics with that of the following epidemics. Half of influenza-related deaths during the 1968-1969 influenza A (H3N2) pandemic and large proportions of influenza-related deaths during the 1957-1958 influenza A (H2N2) and the 1918-1919 influenza A (H1N1) pandemics occurred among persons

During the 20th century, indisputable pandemics of influenza occurred in 1918, 1957, and 1968. The pandemics of 1957 (A/H2N2) and 1968 (A/H3N2) were associated with major antigenic changes in the virus, probably reflecting introduction by recombination of animal virus genes. The 1918 epidemic is beyond the reach of modern virology but, based on seroarcheology, appears to have been caused by a virus very similar to present swine (A/H1N1) influenza viruses. Changes in both principal antigens of the A/H1N1 subtype in 1947 resulted in total vaccine failure and pandemic spread of virus. On the basis of three periods of prevalence in the 20th century, A/H1N1 may be the "default" human virus, although the 39-year persistence of A/H3N2 to the present challenges this view. Only H1, H2, and H3 and N1 and N2 antigens have been found in human influenza viruses, but virologic history is too brief to preclude the contribution of other antigens to future pandemics.

It has also witnessed the emergence of man from the straitjacket of his earthbound state. Brave men have hazarded their lives in space and have taken the first steps on the moon. Extraterrestrial radiation has proved a lesser hazard than skin sensitivity and the common cold. Those who have spent their lives in attempts to further the conquest of infectious disease are humiliated by the contrast between the success of the astronauts and the fail

Influenza in swine was first recognized as an epizootic disease in 1918. During that same year influenza virus in humans caused the worst pandemic on record. The virus of swine influenza was isolated in 1930. Swine influenza virus was first isolated from humans in 1974. Since then, including the cases at Fort Dix, there have been a total of nine viral isolations from humans in the United States. Serologic evidence of infections with swine influenza virus in humans has also been obtained. Evidence for transmission of swine influenza virus to humans before 1974 is minimal and circumstantial. Recent recognition of infections with swine influenza virus may be the result of better surveillance, increased numbers of susceptible humans, or increased viral infectivity for humans. Nevertheless, the apparent frequency of human infections and the declining levels of antibodies to swine influenza virus in the human population suggest that influenza viruses of swine may be a potential sources of epidemic disease for humans.

Influenza A/New Jersey/76 virus was detected at Fort Dix from January 19 through February 9, 1976 and infected at least 230 military personnel. Thirteen hospital admissions for acute respiratory disease were associated with influenza A/New Jersey infection, and additional members of index training companies may have been hospitalized with influenza A/New Jersey. This virus was likely introduced into the reception center by an incoming trainee. Although our studies could not eliminate the possibility that influenza A/New jersey strains are inherently less transmissible in humans than H3N2 viruses, the simultaneous transmission of influenza A/Victoria/75 virus and the unusual environment in basic combat training may explain why influenza A/New Jersey did not spread significantly outside of this training population.