Jci_page_head_homepage_01 Jci_page_head_homepage_02
Anne Moscona
Published in Volume 115, Issue 7
J Clin Invest. 2005; 115(7):1688–1698 doi:10.1172/JCI25669
Abstract | Full text | PDF
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Figure 5

Sites or steps within the viral life cycle that represent potential targets for antiviral molecules. (A) Agents directed at blocking the ability of the HN protein to recruit inflammatory cells to the lung and subsequent cytokine expression may reduce the inflammatory response to the HN protein and ameliorate disease. (B) Molecules that fit into the binding pocket on the HN globular head may inhibit HN-receptor binding and the subsequent F protein triggering action of the HN protein stalk. On the left, the HN protein is shown bound with an inhibitor, precluding the scenario shown on the right, in which the HN protein’s binding to the cell has led to its activation of F protein. (C) F protein peptides may be designed to prevent the refolding event that is essential to fusion during virus entry into the host cell. In addition, the F protein could perhaps be prematurely triggered and become incapacitated before it reaches the target host cell membrane. (D) Finally, the HN protein has NA activity and thus the ability to cleave the sialic acid moieties of the cellular receptors, promoting the release of new virions from the host cell surface. Specific inhibition of this activity may prevent virion entry into additional uninfected cells.