Adenovirus serotype 3 utilizes CD80 (B7.1) and CD86 (B7.2) as cellular attachment receptors

• Published in: Virology (New York, N.Y.) Vol. 322; no. 2; pp. 349 - 359
• Main Authors: Short, Joshua J, Pereboev, Alexander V, Kawakami, Yosuke, Vasu, Chenthamarakshan, Holterman, Mark J, Curiel, David T
• Format: Journal Article
• Language: English
• Published: United States Elsevier Inc 01.05.2004
• Subjects: Adenovirus; Adenoviruses, Human - classification; Adenoviruses, Human - genetics; Adenoviruses, Human - metabolism; Adenoviruses, Human - pathogenicity; Amino Acid Sequence; Animals; Antigens, CD - chemistry; Antigens, CD - genetics; Antigens, CD - metabolism; B7-1 Antigen - chemistry; B7-1 Antigen - genetics; B7-1 Antigen - metabolism; B7-2 Antigen; CD80; CD86; CHO Cells; Co-stimulatory molecules; Cricetinae; Dendritic Cells - virology; Genetic Vectors; HeLa Cells; Human adenovirus 3; Humans; Membrane Glycoproteins - chemistry; Membrane Glycoproteins - genetics; Membrane Glycoproteins - metabolism; Molecular Sequence Data; Peptides - metabolism; Protozoan Proteins; Receptor; Serotyping; Subgroup B; CD86; Ad5Luc1; Ad; Adenovirus; CD80; sCD86; Subgroup B; DC-sign; Ad5/3Luc1; CHO; Ad2; Ad3; Co-stimulatory molecules; Ad5; Receptor; Ad7; CAR; 6-HIS; UAB; Ad37; sCD80; vp; Ad11
• ISSN: 0042-6822; 1096-0341
• DOI: 10.1016/j.virol.2004.02.016

Most viruses exploit a variety of host cellular proteins as primary cellular attachment receptors in the context of successful execution of infection. Furthermore, many viral agents have evolved precise mechanisms to subvert host immune recognition to achieve persistence. Herein we present data indicating that adenovirus (Ad) serotype 3 utilizes CD80 (B7.1) and CD86 (B7.2) as cellular attachment receptors. CD80 and CD86 are co-stimulatory molecules that are present on mature dendritic cells and B lymphocytes and are involved in stimulating T-lymphocyte activation. To our knowledge, this is one of the first demonstrations of a virus utilizing immunologic accessory molecules as a primary means of cellular entry. This finding suggests a mechanism whereby viral exploitation of these proteins as receptors may achieve both goals of cellular entry and evading the immune system.