This review article discusses the clinical aspects of the 2009 pandemic influenza A (H1N1) virus. The virus, which originated from swine, caused widespread human infection and acute respiratory illness, leading to the first influenza pandemic since 1968. It spread globally, resulting in over 17,700 deaths reported to the World Health Organization (WHO) by March 2010. The virus is antigenically distinct from other human and swine influenza A (H1N1) viruses but has been antigenically homogeneous, with the A/California/7/2009 strain being representative of most isolates. The virus has a higher pulmonary replication rate than seasonal influenza A (H1N1) viruses in experimentally infected animals, but it generally lacks mutations associated with increased pathogenicity. The 2009 H1N1 virus caused acute, self-limited illnesses, with the highest attack rates among children and young adults. The relative sparing of adults over 60 years of age is likely due to prior exposure to antigenically related influenza viruses. The case fatality rate was less than 0.5%, with estimates ranging from 0.0004 to 1.47%. Most severe illnesses occurred in children and nonelderly adults, with approximately 90% of deaths occurring in those under 65 years of age. The virus spreads primarily through person-to-person contact, with household transmission being highest among children. The basic reproduction number (R0) ranges from 1.3 to 1.7, with higher values in crowded settings. Risk groups for severe disease include pregnant women, immunosuppressed individuals, and those with neurologic disorders. Severe obesity also increases the risk of hospitalization and death. The 2009 H1N1 virus causes a broad spectrum of clinical syndromes, ranging from mild upper respiratory illness to severe viral pneumonia. The principal clinical syndrome leading to hospitalization and intensive care is diffuse viral pneumonitis associated with severe hypoxemia, ARDS, and sometimes shock and renal failure. The virus replicates in various cell types and is susceptible to neuraminidase inhibitors such as oseltamivir and zanamivir. Oseltamivir is especially important for high-risk patients, including pregnant women and those with severe or progressive illness. Oseltamivir is effective in reducing the duration of hospitalization and the risk of progression to severe disease. However, resistance to oseltamivir has been reported, particularly in immunosuppressed patients. Intravenous zanamivir is preferred for hospitalized patients with oseltamivir-resistant infections. The article also discusses the importance of early antiviral treatment and the need for continued surveillance for antigenic changes, viral reassortment, antiviral resistance, and altered virulence. It highlightsThis review article discusses the clinical aspects of the 2009 pandemic influenza A (H1N1) virus. The virus, which originated from swine, caused widespread human infection and acute respiratory illness, leading to the first influenza pandemic since 1968. It spread globally, resulting in over 17,700 deaths reported to the World Health Organization (WHO) by March 2010. The virus is antigenically distinct from other human and swine influenza A (H1N1) viruses but has been antigenically homogeneous, with the A/California/7/2009 strain being representative of most isolates. The virus has a higher pulmonary replication rate than seasonal influenza A (H1N1) viruses in experimentally infected animals, but it generally lacks mutations associated with increased pathogenicity. The 2009 H1N1 virus caused acute, self-limited illnesses, with the highest attack rates among children and young adults. The relative sparing of adults over 60 years of age is likely due to prior exposure to antigenically related influenza viruses. The case fatality rate was less than 0.5%, with estimates ranging from 0.0004 to 1.47%. Most severe illnesses occurred in children and nonelderly adults, with approximately 90% of deaths occurring in those under 65 years of age. The virus spreads primarily through person-to-person contact, with household transmission being highest among children. The basic reproduction number (R0) ranges from 1.3 to 1.7, with higher values in crowded settings. Risk groups for severe disease include pregnant women, immunosuppressed individuals, and those with neurologic disorders. Severe obesity also increases the risk of hospitalization and death. The 2009 H1N1 virus causes a broad spectrum of clinical syndromes, ranging from mild upper respiratory illness to severe viral pneumonia. The principal clinical syndrome leading to hospitalization and intensive care is diffuse viral pneumonitis associated with severe hypoxemia, ARDS, and sometimes shock and renal failure. The virus replicates in various cell types and is susceptible to neuraminidase inhibitors such as oseltamivir and zanamivir. Oseltamivir is especially important for high-risk patients, including pregnant women and those with severe or progressive illness. Oseltamivir is effective in reducing the duration of hospitalization and the risk of progression to severe disease. However, resistance to oseltamivir has been reported, particularly in immunosuppressed patients. Intravenous zanamivir is preferred for hospitalized patients with oseltamivir-resistant infections. The article also discusses the importance of early antiviral treatment and the need for continued surveillance for antigenic changes, viral reassortment, antiviral resistance, and altered virulence. It highlights