FIGURE 2 | Macrophage infection and antibody-dependent enhancement of virus entry in infection with feline infectious peritonitis virus.

From the following article:

Immunopathogenesis of coronavirus infections: implications for SARS

Ajai A. Dandekar & Stanley Perlman

Nature Reviews Immunology 5, 917-927 (December 2005)

doi:10.1038/nri1732

Immunopathogenesis of coronavirus infections: implications for SARS

a | Infection of macrophages and possibly dendritic cells (DCs) results in both dissemination of feline infectious peritonitis virus (FIPV) infection and dysregulation of these cells, leading to lymphocyte apoptosis. b | FIPV usually infects cells through the binding of the spike protein to its cellular receptor, CD13. The virus is then internalized and released into the cytoplasm. c | In antibody-dependent entry, specific antibodies bind the spike protein. The antibody-opsonized FIPV virions then interact with FcgammaRs (receptors for IgG). Some evidence indicates that this process augments the normal spike–CD13 interaction. After binding of the opsonized virions to FcgammaRs, the virus is internalized and released into the cytoplasm. Antigen–antibody complexes are also deposited in the vasculature, resulting in complement activation. Activation of complement contributes to the development of vasculitis and oedema, with death of the animal occurring soon after. C3, complement component 3; IL-10, interleukin-10; TH2 cell, T helper 2 cell; TNF, tumour-necrosis factor.

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