Editorial Commentary: Host and Viral Factors in Emergent Influenza Virus Infections

Clinical Infectious Diseases, Apr 2014

David S. Hui, Frederick G. Hayden

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Editorial Commentary: Host and Viral Factors in Emergent Influenza Virus Infections

David S. Hui 1 Frederick G. Hayden 0 0 Division of Infectious Diseases and International Health, Department of Medicine, University of Virginia School of Medicine , Charlottesville 1 Department of Medicine and Therapeutics, Chinese University of Hong Kong , Shatin - Human cases of avian influenza A (H5N1) virus infection were first documented in Hong Kong in 1997 [1, 2]; the virus reemerged in 2003 to spread intercontinentally and become entrenched in poultry in other parts of Asia and Egypt. Sporadic human cases with an estimated case fatality rate close to 60% continue to occur [3]. Influenza A(H1N1) pdm09 virus first emerged in 2009 as a novel swine-origin strain that rapidly led to a pandemic [4] and remains a common circulating strain. Human infections with the novel avian influenza A(H7N9) virus, first reported in China in March 2013 and subsequently declining after closure of live poultry markets, have reemerged since October 2013 in mainland China and spread to Hong Kong in December 2013 [5]. All 3 types of influenza viruses continue to pose significant threats to human health globally. The retrospective cohort study published by Wang et al in this issue of Clinical Infectious Diseases [6] compares the demographic features, risk factors, presenting clinical characteristics, and outcomes of patients hospitalized in China and Vietnam with laboratory-confirmed avian A(H7N9), avian A(H5N1), or A(H1N1) pdm09 virus infection. The authors have combined and compared data derived from selected studies with somewhat differing designs and time frames. For example, data from Vietnamese patients with A (H1N1)pdm09 or with A(H5N1) infection from April 2009 onward are not included [6], and population-based data on baseline comorbidities were not available for Vietnam. Such disparities might have resulted in populations with differences in variables of interest being combined or missing for analysis. Secular changes in case management are also potential confounders with regard to outcomes such as intensive care unit admission and mortality. In the current report, the frequency of mechanical ventilation was slightly higher in patients with A (H7N9), all of whom were admitted within the past year, than in A(H5N1) patients, whereas the case fatality rate was substantially higher for A(H5N1). The analysis of risk factors compares their proportions in the general Chinese population to those in the hospitalized influenza patients. The findings confirm prior studies highlighting the older age and male predominance of A(H7N9) patients [7], the broad similarities in clinical and laboratory features of severely ill A (H7N9) and A(H5N1) patients [8, 9], and the findings that obesity, asthma, and chronic obstructive pulmonary disease are significant risk factors in hospitalization for A(H1N1)pdm09 virus infections [4]. The finding that chronic heart disease was associated with an increased risk of A (H7N9) hospitalization is unsurprising, given the older age of these patients and chronic heart diseases strong association with seasonal influenza complications, although only 11% of patients with A (H7N9) reportedly had chronic heart disease [6]. Recent retrospective analyses examining the effects of influenza-specific interventions have highlighted the importance of influenza infections as predisposing to serious cardiovascular events. Both seasonal influenza vaccine receipt [10] and neuraminidase inhibitor treatment for clinically diagnosed influenza [11, 12] have been associated with significant reductions in subsequent acute cardiac and stroke diagnoses. Both viral and host factors contribute to disease severity and outcomes across influenza subtypes. The younger age, infrequent presence of comorbidities (11% of cases), and higher mortality of A(H5N1) patients (55%) presumably reflects the greater intrinsic virulence of A(H5N1) viruses, although these viruses also show substantial genetic diversity and differences in virulence and treatment response in ferrets [13] and perhaps in patients [14]. Although the absolute risk of severe disease is thankfully much lower for A (H1N1)pdm09 infection compared with A(H5N1) and A(H7N9), younger age was also a risk factor for increased likelihood of hospitalization and mortality, relative to seasonal influenza, during the first year of the pandemic [15]. Of note, the pattern of excess deaths in those aged <65 years may continue up to a decade after introduction of a pandemic strain [16], consistent with recent reports of severe A (H1N1)pdm09 virus infections in the United States (http://emergency.cdc.gov/ HAN/han00359.asp) and elsewhere. One counterintuitive observation in the current report was an apparent protective effect of smoking on hospitalization across all 3 virus subtype cohorts. One possible hypothesis is that nicotinerelated anti-inflammatory effects might alter influenza severity in humans. Chronic infusion of nicotine at doses chosen to model plasma levels of those fou (...truncated)


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David S. Hui, Frederick G. Hayden. Editorial Commentary: Host and Viral Factors in Emergent Influenza Virus Infections, Clinical Infectious Diseases, 2014, pp. 1104-1106, 58/8, DOI: 10.1093/cid/ciu054