Fig. 49.3.

Outline of the pathogenesis of measles virus (MV) from the time of infection through recovery.

(A) MV infection is initiated in the respiratory tract and spreads systemically to infect multiple organs, including lymphoid tissue, liver, lungs, and skin. Epithelial cells, endothelial cells, B and T cells, monocytes/macrophages, and dendritic cells can be infected. MV clearance begins with the onset of the rash. Clearance of MV is complete 20 days after infection; however, viral RNA (dashed line) persists at multiple sites. (B) Clinical signs and symptoms begin approximately 10 days after infection, with prodromal symptoms of fever, conjunctivitis, and oral Koplik's spots, followed by a maculopapular rash for 3–5 days. (C) The rash represents adaptive immune responses with infiltration of CD4⁺ and CD8⁺ T cells into sites of MV replication and clearance. There is a rapid activation, expansion, and then contraction of MV-specific CD8⁺ T cells. CD4⁺ T cell responses appear at the same time, but activation is prolonged. MV-specific IgM appears with the rash, and this is commonly used for diagnostic purposes. This is followed by the sustained MV-specific IgG synthesis. Immune suppression is evident during acute disease and for many weeks after recovery. (D) Cytokines and chemokines produced during infection are found in plasma in elevated amounts. Early, IL-8 is increased. During the rash, IFN-γ and IL-2 are γ and IL-2 are produced by activated T_H1-like, CD4⁺ and CD8⁺ T cells. After rash resolution, T_H2-like T cells and regulatory CD4⁺ T cells produce IL-4, IL-10, and IL-13.

Figure reproduced from Griffin DE. Measles virus-induced suppression of immune responses. Immunol Rev 2010;236:176–89 ©2010 John Wiley & Sons A/S.