Differences in the Epidemiology of Human Cases of Avian Influenza A(H7N9) and A(H5N1) Viruses Infection

Abstract

The results are consistent with an ascertainment bias towards severe and older cases for sporadic H7N9 but not for H5N1. The lack of evidence for ascertainment bias in sporadic H5N1 cases, the more pronounced clustering of cases, and the higher risk of infection in blood-related contacts, support the hypothesis that susceptibility to H5N1 may be limited and familial. This analysis suggests the potential pandemic risk may be greater for H7N9 than H5N1.

Sero‐epidemiologic study of influenza A(H7N9) infection among exposed populations, China 2013‐2014

“…In addition, our study only included close contacts of the early subset of all human influenza A(H7N9) cases. Although we found no evidence of infection among close contacts in our study, several clusters among close contacts of later cases were detected, indicating that the first generation of human‐to‐human transmission likely occurred on multiple occasions, although we did not detect evidence of this in our sample23, 24. With respect to our serologic study of poultry workers, we do not know what proportion of workers in our study were exposed to H7N9 in their workplaces, as several LPMs, including those where the two poultry workers with seropositive samples worked, had not been tested for influenza A(H7N9) avian influenza virus.…”

Potent protection against H5N1 and H7N9 influenza via childhood hemagglutinin imprinting

“…H5N1 and H7N9 are particularly concerning avian-origin IAVs, each having caused hundreds of severe or fatal human cases (1). Despite commonalities in their reservoir hosts and epidemiology, these viruses show puzzling differences in age distribution of observed human cases (1,2).…”

“…H5N1 and H7N9 are particularly concerning avian-origin IAVs, each having caused hundreds of severe or fatal human cases (1). Despite commonalities in their reservoir hosts and epidemiology, these viruses show puzzling differences in age distribution of observed human cases (1,2). Existing explanations, including possible protection against H5N1 among older birth-year cohorts exposed to the neuraminidase of H1N1 as children (3,4) or age biases in exposure to infected poultry (5–7), cannot fully explain these opposing patterns of severe disease and mortality.…”

“…Existing explanations, including possible protection against H5N1 among older birth-year cohorts exposed to the neuraminidase of H1N1 as children (3,4) or age biases in exposure to infected poultry (5–7), cannot fully explain these opposing patterns of severe disease and mortality. Another idea is that severity of H5N1 and H7N9 differs by age, leading to case ascertainment biases (1), but no explanatory mechanism has been proposed.…”

Mammalian Pathogenesis and Transmission of H7N9 Influenza Viruses from Three Waves, 2013-2015

“…Asymptomatic H7N9 virus-infected chickens appear to be central to the persistence and expansion of this outbreak (3); accordingly, poultry contact and visitation of live poultry markets has been linked with H7N9 virus infection (4,5), and the closure of live poultry markets has been associated with a decline of new human infections in 2013 and 2014 (6,7). Limited family clusters of H7N9 virus infection have been reported (8,9), but human-tohuman transmission has remained a rarely documented and unsustainable event (10), while human infections continue to occur following exposure to H7N9 viruses circulating in avian reservoirs (11).…”