Influenza viruses are a group of RNA viruses belonging to family Orthomyxoviridae. They are classified into three distinct genera: influenza A, B and C. Influenza A can be further divided into various subtypes depending upon expression pattern of 2 viral genes—haemagglutinin (which mediate viral attachment) and neuraminidase (which mediate viral release). There are 16 types of haemagglutinin and 9 types of neuraminidase variants. So H1N1 implies haemagglutinin1 neuraminidase 1 variant of influenza A. Influenza B and C do not have any subtype. Both influenza A and B cause seasonal viral flu, and dominant strain is included in annual vaccination programme. Influenza C typically causes only mild respiratory illness. In 2009, WHO originally called H1N1 influenza “swine flu” because its genetic appearance is similar to that of viruses that infect pigs in North America. However, further investigation revealed that this new virus is more complex. The new H1N1 virus is a quadruple human reassortant comprising two strains of avian and swine (North American and Eurasian) influenza virus [3, 6, 7].

The current literature from the recent pandemic and previous outbreaks of H1N1 shows that pregnant women in the second and third trimesters are four times more likely than the general population to be hospitalized, in addition to having a significantly higher mortality rate [4, 5]. Moreover, 8–16 % of all deaths from H1N1 infection in the USA occurred in pregnant women, although this group represented only 1 % of the general population [8]. In Brazil, 156 (9.6 %) of the 1632 total deaths reported during the 2009 pandemic were among pregnant women [9].

The worldwide pandemic of 2009 is the result of infection of influenza A (H1N1 strain) that had not been previously recognized either in pig or in humans. The CDC therefore choose the term novel H1N1 influenza A infection, a term that reflects the unique genetic make-up of virus, a genetic reassortment of several swine strain, a human strain and an avian strain. In contrast to genetic drift, which occurs when mutation create antigen variant similar to older strain, while genetic shift (reassortment) lead to a completely new antigen, thereby limiting the capacity of immune system to identify and destroy virus [6, 7]. Seasonal flu and smaller epidemics are due to genetic drift, while genetic shift leads to pandemics. The novel H1N1 virus infection carries various gene segments similar to Spanish flu influenza virus in 1918. Limited immunity contributes to more susceptibility of H1N1 infection. Recent research suggest that swine H1N1 virus replicates more efficiently in human and lead to more severe pathologic lesion in lung, including diffuse alveolar damage.

Patients with H1N1 infection typically present with symptoms of acute respiratory illness as sore throat, cough, rhinorrhoea and fever. Other complaints may include headache, fatigue, vomiting and diarrhoea. Their clinical presentation may be complicated by superimposed bacterial infection as pneumonia. Symptoms commonly develop 1 week after the exposure, and patients remain contagious for 8 days [10, 11].

The risk of morbidity with influenza is higher among pregnant women. Pregnancy-related complication of H1N1 influenza virus includes non-reassuring foetal status (most commonly foetal tachycardia) and febrile morbidity. Hyperthermia in early pregnancy leads to neural tube defect and congenital heart disease, and fever during labour and birth is a risk factor for neonatal seizure, neonatal encephalopathy, cerebral palsy and death. Due to H1N1 viral infection, pregnant women may land up in spontaneous abortion, preterm labour and preterm premature rupture of membrane.