**1. Introduction**

Defensins are a family of antimicrobial peptides that are part of the innate and adaptive immune system. They provide protection against too broad spectrum of pathogens, viruses, bacteria and fungi [1]. The defensins are small cationic peptides of 3–4 kb, and its structure is composed of beta sheets, six cysteines joined by disulfide bonds. In humans, it is classified in two groups: α- and β-defensins [2, 3]. The β-defensin-2 (HBD2) is found in the second group and it is a peptide of 41 amino acids; it is expressed mainly in the epithelial cells, mucous and skin [1, 4, 5]. It was isolated in 1997 from skin lesions in patients with psoriasis; later, it was detected in the epithelium of almost entire human body [6–14]. In recent years, HBD2 has been considered as a multifunctional peptide with antimicrobial activity and with immunomodulatory functions [15–17]. On the other hand, the HBD2 is expressed throughout the respiratory epithelium from the mouth to the lungs; it is believed that this defensin has a very important role in the defense against respiratory infections [2]. The alteration of the expression of the HBD2 in the respiratory epithelium has been associated with the pathogenesis of several respiratory diseases such as asthma, pulmonary fibrosis, pneumonia, tuberculosis, rhinitis, etc. [2, 9, 17–20].

The acute respiratory infections caused by viruses are the main cause of morbidity and mortality in the world, and HBD2 has got antiviral activity against some

respiratory viruses (influenza, respiratory syncytial virus, rhinovirus) [21–23]. The mechanisms of viral inactivation vary and include not only direct binding of the virus to the peptide but also indirect methods of inactivation via intracellular modulation of the viral replication, modulation of signaling pathways necessary for antiviral effects, and recruitment of immune cells that contribute to antiviral activity [2, 22]. This revision chapter focuses on the structural and general characteristics of HBD2, multifunctional activities and expression in respiratory diseases. We present some studies concerning the effect of respiratory viruses and their relationship with HBD2, mechanisms of action and their relevance as therapeutic agents.
