Infection of Pulmonary Vascular Endothelial Cells by H5N1 Avian Influenza Virus and its Role in Pathogenesis

Abstract

Evaluation of: Zeng H, Pappas C, Belser JA et al. Human pulmonary microvascular endothelial cells support productive replication of highly pathogenic avian influenza viruses: possible involvement in the pathogenesis of human H5N1 virus infection. J. Virol. 86(2), 667–678 (2012). The H5N1 highly pathogenic avian influenza (HPAI) virus is still a major threat for pandemic influenza. The severity of the infection, with mortality reaching up to 60%, is of particular concern, and the detailed mechanism of this high pathogenicity is not fully understood. While alveolar epithelial cells are considered to be the main target cells in humans, Zeng et al. reported that human pulmonary vascular endothelial cells were more susceptible to the H5N1 HPAI virus than to seasonal, pandemic or low pathogenic avian influenza viruses. Infection induced the endothelial cells to produce a number of proinflammatory cytokines, which raised the possibility of a new virulence mechanism that may link to the systemic dissemination of the infection in humans. However, there are still many unanswered questions regarding the determinants of the higher infectivity of H5N1 HPAI in this cell type and the role of the infection of this cell type in the pathogenesis of H5N1 HPAI.