Protective Effect of Surfactant Protein D in Pulmonary Vaccinia Virus Infection: Implication of A27 Viral Protein

Viruses

Julien Perino²  Nicole M. Thielens⁴  Erika Crouch³  Danièle Spehner¹  Jean-Marc Crance² 

[1] IGBMC; CNRS, UMR 7104; Inserm U 596; Illkirch, F-67400 France; Université Louis Pasteur, Strasbourg, F-67000 France; E-Mail:;Laboratoire de Virologie, Institut de Recherche Biomédicale des Armées- Antenne du Centre de Recherches du Service de Santé des Armées, 38702 La Tronche cedex, France; E-Mails:;Dept of Pathology and Immunology, Washington University School of Medicine, Saint Louis, MO, USA; E-Mail:;Institut de Biologie Structurale, CNRS, CEA, Université Joseph Fourier, Grenoble, France; E-Mail:

关键词: orthopoxvirus;    surfactant protein D;    vaccinia virus;    A27 protein;    pulmonary infection;    innate immunity;    surfactant protein A;    KO mice;    Ca²⁺;    sugars;   

DOI  :  10.3390/v5030928

来源: mdpi

【 摘 要 】

Vaccinia virus (VACV) was used as a surrogate of variola virus (VARV) (genus Orthopoxvirus), the causative agent of smallpox, to study Orthopoxvirus infection. VARV is principally transmitted between humans by aerosol droplets. Once inhaled, VARV first infects the respiratory tract where it could encounter surfactant components, such as soluble pattern recognition receptors. Surfactant protein D (SP-D), constitutively present in the lining fluids of the respiratory tract, plays important roles in innate host defense against virus infection. We investigated the role of SP-D in VACV infection and studied the A27 viral protein involvement in the interaction with SP-D. Interaction between SP-D and VACV caused viral inhibition in a lung cell model. Interaction of SP-D with VACV was mediated by the A27 viral protein. Binding required Ca²⁺ and interactions were blocked in the presence of excess of SP-D saccharide ligands. A27, which lacks glycosylation, directly interacted with SP-D. The interaction between SP-D and the viral particle was also observed using electron microscopy. Infection of mice lacking SP-D (SP-D^-/-) resulted in increased mortality compared to SP-D^+/+ mice. Altogether, our data show that SP-D participates in host defense against the vaccinia virus infection and that the interaction occurs with the viral surface protein A27.

【 授权许可】

CC BY   
© 2013 by the authors; licensee MDPI, Basel, Switzerland.