Abstract
Measles is an acute systemic viral infection with immune system interactions that play essential roles in multiple stages of infection and disease. Measles virus (MeV) infection does not induce type 1 interferons, but leads to production of cytokines and chemokines associated with nuclear factor kappa-light-chain-enhancer of activated B cells (NFκB) signaling and activation of the NACHT, LRR and PYD domains-containing protein (NLRP3) inflammasome. This restricted response allows extensive virus replication and spread during a clinically silent latent period of 10–14 days. The first appearance of the disease is a 2–3 day prodrome of fever, runny nose, cough, and conjunctivitis that is followed by a characteristic maculopapular rash that spreads from the face and trunk to the extremities. The rash is a manifestation of the MeV-specific type 1 CD4+ and CD8+ T cell adaptive immune response with lymphocyte infiltration into tissue sites of MeV replication and coincides with clearance of infectious virus. However, clearance of viral RNA from blood and tissues occurs over weeks to months after resolution of the rash and is associated with a period of immunosuppression. However, during viral RNA clearance, MeV-specific antibody also matures in type and avidity and T cell functions evolve from type 1 to type 2 and 17 responses that promote B cell development. Recovery is associated with sustained levels of neutralizing antibody and life-long protective immunity.
Highlights
Measles is a highly contagious systemic viral infection that remains one of the most important causes of worldwide morbidity and mortality in children despite the availability of a safe and effective live attenuated virus vaccine [1,2,3]
Measles virus (MeV), the causative agent of measles, is a human virus without an animal reservoir that is efficiently transmitted by aerosol or respiratory droplets
Nonhuman primate populations are too small to sustain MeV transmission, study of macaques experimentally infected with wild type (WT) strains of MeV has provided much of our detailed knowledge of measles pathogenesis [8,9]
Summary
Measles is a highly contagious systemic viral infection that remains one of the most important causes of worldwide morbidity and mortality in children despite the availability of a safe and effective live attenuated virus vaccine [1,2,3]. After introduction of MeV into the respiratory tract, immature pulmonary dendritic cells (DCs) or alveolar macrophages capture and transport MeV to regional lymph nodes (LNs) where the immune response is initiated, virus is amplified and spread of infection facilitated [10,11]. TheThe initial innate immune response is restricted due to inhibition of the interferon (IFN). The rash is a manifestation of the MeV-specific adaptive cellular immune cellularand immune response and coincides with clearance of infectious virus. The period of RNA1).persistence with decreased host with decreased host resistance to infection that can be prolonged [19]. (MeV) clearance clearance and Schematic and immune immuneresponses responsesininrhesus rhesus macaques. MeV results in viremia (infectious virus) and rash. Infection with wild type (WT) MeV results in viremia (infectious virus) and rash. T cellsTthat quickly after the viremia prolonged phase slowclearance viral RNA clearance fromblood peripheral blood viremia There is cleared. From Lin et al [9,20]
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