Pathogenesis and Pathophysiology of Measles virus
المؤلف:
Baijayantimala Mishra
المصدر:
Textbook of Medical Virology
الجزء والصفحة:
2nd Edition , p183
2025-10-22
58
Measles virus enters through infected respiratory droplets and primarily infects the oropharynx, tracheal and bronchial epithelial cells. The initial replication for 2–4 days occurs in the respiratory mucosa after which the virus spreads to draining lymph nodes. Replication continues in the lymph nodes and then the virus spreads to the blood leading to primary viremia and through blood disseminates to reticuloendothelial system. Extensive replication of virus continues in the lymph nodes and leads to over flow of virus to blood leading to secondary viremia. Through infected lymphocytes and monocytes in the blood, the infection then spreads to the various organs including spleen, lymph node, kidney, skin, brain, etc. as well as to the respiratory tract. Replication in these organs primarily occurs in the endothelial cells, epithelial cells and monocytes or macrophage.
The thin epithelial layer of the respiratory tract and conjunctiva gets destroyed due to the process of virus infection and starts breaking down and along with the inflammatory process it leads to the development of prodromal symptoms, such as cough, coryza, congestion and conjunctivitis.
During the prodromal period, Koplik’s spot appears. This is the pathognomonic feature of measles. It appears as a raised spot with white center and erythematous base on buccal mucosa. This marks the beginning of the delayed type hypersensitivity.
The maculopapular rashes in measles are characterized by vascular congestion, oedema, epithelial necrosis and round cell infiltrates. Measles virus antigen is absent in the skin lesions unlike other sites. However, the viral antigens are concentrated in the blood vessel and in the endothelial cells of the dermal capillaries. Thus, virus is not present in the skin lesion and there is no shedding of virus from the skin surface. The containment of skin infection occurs due to development of cytotoxic T cells which is thought to be responsible for damage to the infected tissue and production of interferon causing cellular resistance to infection.
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