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Pregnancy and differences in the presentation of various risk factors contribute to the worse outcome of infection in women. Vaccination and antiviral treatment efficacy also vary in a sex-dependent manner. Finally, sex-specific genetic and hormonal differences may contribute to the severity of influenza and the clearance of viral infection. The contribution of sex and gender to influenza can only be determined by a greater consideration of these factors in clinical and epidemiological studies and increased research into the biological basis underlying these differences. Sex, gender and pregnancy in the H1N1 pandemic Sex and gender differences can affect exposure to pathogens, vulnerability to infectious diseases, health seeking behaviours and immune responses to pathogens, resulting in differences between males and females in the incidence, duration, severity and case fatality rates following an infection [ 12 ].
Sex refers to the biological and physiological characteristics that define males and females, whereas gender refers to the roles, behaviours, activities and attributes that individual societies consider appropriate for men and women. The impact of sex and gender on infection is tied to the age of the individual, as both biological and cultural factors can change dramatically with age. Consideration of these factors can result in a more effective public health response to infectious diseases, including influenza, and yet they are often inadequately addressed in clinical and basic research studies.
A systematic review of the literature regarding sex, gender, pregnancy and the H1N1 pandemic indicates these are important factors which alter the severity of the disease as well as the prevention and treatment measures. A greater awareness of how sex and gender impact upon the biology of H1N1 infection could provide important insights into the unique morbidity and mortality patterns associated with this pandemic. It was the dominant influenza A virus strain circulating in the northern hemisphere for the entire influenza season, effectively outcompeting both seasonal influenza A virus strains [ 3 ].
Biological factors associated with severe H1N1 infection The pandemic has been termed mild due to the relatively low mortality. Confirmed influenza virus infections, however, have increased substantially compared to recent years and the US Center for Disease Control CDC estimates of the number of people infected with H1N1 are greater than what would be expected in a standard influenza season [ 3 ]. In contrast, H1N1 has not been associated with a large number of infections in this age group but has the highest attack and hospitalization rates in individuals between the ages of Presence of co-morbidities or risk factors for severe disease Several populations are at risk for severe disease from seasonal as well as H1N1 infection [ 4 ], including individuals who have pre-existing illnesses or medical conditions, pregnant women, immunosuppressed individuals either through treatment, HIV infection, or as a result of a pre-existing immunosuppressive disorder and children aged years.
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Medical conditions associated with an increased risk of severe disease include chronic respiratory disorders for example, asthma, bronchitis, chronic obstructive pulmonary disease [COPD] and cystic fibrosisneuromuscular disorders for example, cerebral palsy, myasthenia gravis and muscular dystrophymetabolic diseases for example, diabetes and chronic renal, heart or liver disorders [ 3 ]. Factors such as obesity and hypertension are not normally associated with severe disease from seasonal influenza but have been suggested as risk factors for severe disease from H1N1 in some studies [ 5 - 7 ]. Host immune responses The protective immunity induced by influenza vaccinations is mediated primarily by antibodies that recognize the viral haemagglutinin protein and neutralize virus infectivity.
After virus infection, host innate immune responses, including production of cytokines and chemokines, are activated which initiate a cascade of immunological events that lead to the development of specific immune responses to the virus.